Strain Name:

C;129S-Ngfrtm1Jae/J

Stock Number:

002124

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Mice homozygous for the Ngfrtm1Jae mutation display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Pineal glands lack sympathetic innervation, and innervation to sweat glands on foot pads is either reduced or absent. p75-deficient dorsal root ganglion and superior cervical ganglion neurons show a 2- to 3-fold decrease in sensitivity to nerve growth factor at embryonic day 15 and postnatal day 3, respectively.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
 
Donating InvestigatorDr. Rudolf Jaenisch,   Whitehead Institute (MIT)

Appearance
white-bellied agouti
Related Genotype: Aw/Aw

Description
Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by 4 months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death.

Development
The Ngfrtm1Jae mutant strain was developed in the laboratory of Dr. Rudolf Jaenisch at the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology. The 129/Sv-derived J1 ES cell line was used.

Control Information

  Control
   See control note: There are no appropriate physiological controls for this mutant strain. However, if you must have a control you may use either 129S3/SvImJ (Stock No. 002448) or BALB/cJ mice (Stock No. 000651) These strains also serve as DNA controls.
   002448 129S1/SvImJ (approximate)
   000651 BALB/cJ (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Ngfrtm1Jae allele
002213   B6.129S4-Ngfrtm1Jae/J
View Strains carrying   Ngfrtm1Jae     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ngfrtm1Jae/Ngfrtm1Jae

        involves: 129 * BALB/c
  • nervous system phenotype
  • abnormal axon extension
    • reduced inhibition by myelin of neurite outgrowth from dorsal root ganglion neurons, but not cerebellar neurons, compared to heterozygous controls, indicating that mutant neurons are much less sensitive to myelin   (MGI Ref ID J:96121)
    • reduced inhibition by Nogo-66 (Rtn4) peptide of neurite outgrowth from P7 cerebellar neurons compared with heterozygous controls, however homozygotes did not show enhanced regeneration of corticospinal tract axons in comparison with wild-type after spinal dorsal hemisection   (MGI Ref ID J:96121)
  • cellular phenotype
  • abnormal axon extension
    • reduced inhibition by myelin of neurite outgrowth from dorsal root ganglion neurons, but not cerebellar neurons, compared to heterozygous controls, indicating that mutant neurons are much less sensitive to myelin   (MGI Ref ID J:96121)
    • reduced inhibition by Nogo-66 (Rtn4) peptide of neurite outgrowth from P7 cerebellar neurons compared with heterozygous controls, however homozygotes did not show enhanced regeneration of corticospinal tract axons in comparison with wild-type after spinal dorsal hemisection   (MGI Ref ID J:96121)

Ngfrtm1Jae/Ngfrtm1Jae

        involves: 129S4/SvJae * BALB/c
  • nervous system phenotype
  • abnormal dorsal root ganglion morphology
    • mice exhibit a loss of myelinated fibers in the dorsal root ganglion   (MGI Ref ID J:53825)
    • abnormal proprioceptive neuron morphology
      • mice exhibit a 50% loss of proprioreceptive neurons in L4 of the dorsal root ganglion   (MGI Ref ID J:53825)
    • small L4 dorsal root ganglion
      • at E14.5, L4 is smaller than in wild-type mice due to a 7.5-fold increase in apoptosis   (MGI Ref ID J:53825)
  • abnormal sensory neuron innervation pattern
    • the dermis of fore- and hindlimb paws either lacks or have reduced numbers of Pde6a+ sensory fibers and small-diameter nerves are absent   (MGI Ref ID J:43748)
    • only a few single fibers are present in the subepidermis and none are detected in the epidermis of fore- and hindlimb paws   (MGI Ref ID J:43748)
    • reduced innervation is not restricted to hairless patches   (MGI Ref ID J:43748)
    • however, sympathetic innervation of the iris and salivary glands is normal   (MGI Ref ID J:43748)
    • at 3 to 5 months, Pde6a+ pulpal neurons are decreased   (MGI Ref ID J:42087)
  • decreased muscle spindle number
    • spindle density in the soleus, but no the medial gastrocnemius, plantaris and lumbrical muscles, is reduced 50% compared to in wild-type mice   (MGI Ref ID J:53825)
  • muscle phenotype
  • abnormal muscle morphology
    • muscles exhibit fewer myelinated fibers than in wild-type mice (36+/-2 compared to 76+/-2 in wild-type mice)   (MGI Ref ID J:53825)
    • decreased muscle spindle number
      • spindle density in the soleus, but no the medial gastrocnemius, plantaris and lumbrical muscles, is reduced 50% compared to in wild-type mice   (MGI Ref ID J:53825)
  • behavior/neurological phenotype
  • abnormal sensory capabilities/reflexes/nociception
    • prolonged latency in hot plate test   (MGI Ref ID J:43748)
  • homeostasis/metabolism phenotype
  • extremity edema
    • at 4 months of age, mice exbihit edema in the fore- and hindlimb paws   (MGI Ref ID J:43748)
  • limbs/digits/tail phenotype
  • ulcerated paws
    • at 4 months of age, fore- and hindlimb paws become edematous and develop severe ulcers   (MGI Ref ID J:43748)
    • ulcers progress more proximally   (MGI Ref ID J:43748)
    • ulcers are complicated by secondary infections that result in the lose of toenails and hair   (MGI Ref ID J:43748)
    • epidermis and epidermal structures are lost from areas affected by ulcers   (MGI Ref ID J:43748)
    • excessive epidermal proliferation is present at the edges of ulcers   (MGI Ref ID J:43748)
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype
    • unlike in studies using p75NGFR oligonucleotide knockdown, kidney function is normal   (MGI Ref ID J:43748)
  • craniofacial phenotype
  • abnormal mouth morphology
    • the height of the oral cavity is reduced   (MGI Ref ID J:42087)
    • abnormal tooth morphology
      • increased signs of wear on molars   (MGI Ref ID J:42087)
      • abnormal molar morphology
        • mandibular molar occlusal facets are longer than in wild-type mice   (MGI Ref ID J:42087)
        • abnormal molar crown morphology
          • maxillary molar crown height is reduced by 15%   (MGI Ref ID J:42087)
          • however, full height of teeth is normal   (MGI Ref ID J:42087)
  • integument phenotype
  • absent hair follicles
    • loss of follicles, at distal extremities, progressive to more proximal regions   (MGI Ref ID J:43748)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Ngfrtm1Jae/Ngfr+

        B6.129S4-Ngfrtm1Jae
  • nervous system phenotype
  • abnormal neuron differentiation
    • nerve coverage is less than in wild-type mice but not as severely reduced as in Ngfrtm1Jae homozygotes   (MGI Ref ID J:127639)
    • abnormal axon extension
      • neurons exhibit an intermediate effect to Sema3a repulsion that is more sensitive than wild-type neurons but not as sensitive as Ngfrtm1Jae homozygotes   (MGI Ref ID J:127639)
  • respiratory system phenotype
  • decreased airway responsiveness
    • unlike in wild-type mice, no airway hyper-responsiveness was observed following exposure to Ach and ovalbumin (50% brionchiorestriction occurs at 580 ug per kg for Ach and 586 ug per kg ovalbulmin compared to 552 ug per kg Ach and 62.5 ug per kg ovalbumin for wild-type mice)   (MGI Ref ID J:115419)
    • total leukocytes, eosinophils and lymphocytes do not increase as in wild-type following exposure to provocation agent   (MGI Ref ID J:115419)
    • unlike in exposed wild-type mice, no pulmonary eosinophilic inflammation is observed   (MGI Ref ID J:115419)
    • unlike in exposed wild-type mice IL-4 and IL-5 production is not increased   (MGI Ref ID J:115419)
    • while IgE levels increase following exposure to provocation they do not increase as much as in wild-type mice   (MGI Ref ID J:115419)
    • however, interferon-gamma production following exposure to provocation agent is normal   (MGI Ref ID J:115419)
  • cellular phenotype
  • abnormal neuron differentiation
    • nerve coverage is less than in wild-type mice but not as severely reduced as in Ngfrtm1Jae homozygotes   (MGI Ref ID J:127639)
    • abnormal axon extension
      • neurons exhibit an intermediate effect to Sema3a repulsion that is more sensitive than wild-type neurons but not as sensitive as Ngfrtm1Jae homozygotes   (MGI Ref ID J:127639)

Ngfrtm1Jae/Ngfrtm1Jae

        C;129S-Ngfrtm1Jae/J
  • nervous system phenotype
  • abnormal neuron apoptosis
    • reduced levels of neuronal cell death   (MGI Ref ID J:46125)
  • cellular phenotype
  • abnormal neuron apoptosis
    • reduced levels of neuronal cell death   (MGI Ref ID J:46125)

Ngfrtm1Jae/Ngfrtm1Jae

        B6.129S4-Ngfrtm1Jae
  • nervous system phenotype
  • abnormal innervation pattern to muscle
    • areas of the epithelium of the tongue lack innervation and the filiform papillae are sparsely innervated   (MGI Ref ID J:90280)
    • the axons in the tongue display reduced branching and smaller terminal arbors   (MGI Ref ID J:90280)
  • abnormal neuron morphology
    • like wild-type neurons, cultured superior cervical ganglion neurons are resistant to apoptosis induced by pro-NGF and pro-BDNF   (MGI Ref ID J:128451)
    • the number of sympathetic neurons is increased 33% at P4 and 39% at P15 compared to in wild-type mice   (MGI Ref ID J:128451)
    • at 60 weeks sympathetic neuron cell bodies are 25% smaller than in wild-type mice   (MGI Ref ID J:128451)
    • unlike in wild-type mice, superior cervical ganglion are protected from age-related apoptosis   (MGI Ref ID J:128451)
    • abnormal neuron differentiation
      • peripheral nerves in the hindlimb, forelimb, and trigeminal ganglia are severely stunted compared to in wild-type mice   (MGI Ref ID J:127639)
      • abnormal axon extension
        • growth cones from dorsal root ganglion neurons are more sensitive to Sema3A repulsion than wild-type neurons   (MGI Ref ID J:127639)
        • when treated with 15 pM Sema3A outgrowth rate inhibition is increased (15 um per hour compared to 35 um per hour for wild-type neurons)   (MGI Ref ID J:127639)
        • however, increased sensitivity to Sema3A repulsion is alleviated in a double heterozygote cross of Ngfr and Sema3A   (MGI Ref ID J:127639)
    • abnormal sensory neuron innervation pattern
      • innervation of the somatosensory prominences is reduced   (MGI Ref ID J:90280)
      • innervation of the fungiform papillae are reduced   (MGI Ref ID J:90280)
      • at P0 there are 35% fewer geniculate ganglion neurons that supply taste neurons to the fungiform papillae in homozygotes compared to wild-type mice   (MGI Ref ID J:90280)
    • increased neuron number
      • the number of sympathetic neurons is increased 33% at P4 and 39% at P15 compared to in wild-type mice   (MGI Ref ID J:128451)
      • increased retinal photoreceptor cell number
        • after 2 weeks of light exposure, the number of rows of photoreceptors is 4.6+/-0.31 rows compared to 2.3+/-0.25 in wild-type mice and 21.2+/-0.25 in homozygous mice   (MGI Ref ID J:115542)
        • after 3 weeks of light exposure, the number of rows of photoreceptors is 3.0+/-0.41 rows compared to 1.5+/-0.24 in wild-type mice and 0.9+/-0.28 in homozygous mice   (MGI Ref ID J:115542)
  • digestive/alimentary phenotype
  • abnormal tongue epithelium morphology
    • at P7 the gustatory epithelium of the vallate trench is thicker than normal blocking direct access of the ectopic tastse buds in the trench to taste solutions   (MGI Ref ID J:90280)
    • abnormal circumvallate papillae morphology
      • the vallate papilla is deformed and small in neonatal mutants   (MGI Ref ID J:90280)
      • at P7 the vallate trench is only 60% as deep as in wild-type mice   (MGI Ref ID J:90280)
  • cardiovascular system phenotype
  • abnormal Kupffer cell morphology
    • after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice   (MGI Ref ID J:120368)
  • abnormal vascular wound healing
    • formation of neointimal lesions is enhanced 2 and 4 weeks after ligation compared to in wild-type mice such that there is a 2- to 4-fold increase in intimal to medial ratio at 500 um and 1.0 mm proximal to the ligation   (MGI Ref ID J:109753)
    • however, infiltration of inflammatory cells is normal   (MGI Ref ID J:109753)
    • apoptosis in neointimal lesions is decreased by 60% to 70%   (MGI Ref ID J:109753)
  • taste/olfaction phenotype
  • abnormal gustatory papillae taste bud morphology
    • at P7 homozygous mice have 26% fewer vallate taste buds than wild-type mice   (MGI Ref ID J:90280)
    • homozygous mice have fewer fungiform taste buds than wild-type mice   (MGI Ref ID J:90280)
  • immune system phenotype
  • abnormal Kupffer cell morphology
    • after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice   (MGI Ref ID J:120368)
  • increased susceptibility to experimental autoimmune encephalomyelitis
    • mice have an increased risk of developing severe experimental autoimmune encephalomyelitis compared to wild-type mice   (MGI Ref ID J:112769)
    • B220+ B cells make up 6% of cells in the inflammatory cuffs compared to 15% in wild-type mice immunized with MOG35-55   (MGI Ref ID J:112769)
    • the population of Iba-1+ cells in the inflammatory cuffs is reduced by 10% compared to in wild-type mice immunized with MOG35-55   (MGI Ref ID J:112769)
    • polymorphonuclear cells are reduced by half compared to in wild-type mice immunized with MOG35-55   (MGI Ref ID J:112769)
    • microglial/macrophage and neutrophil numbers in the inflammatory infiltrate are reduced 68% to 40% while the size of the inflitratory cuffs is normal or even larger than in wild-type mice   (MGI Ref ID J:112769)
    • however, the number of double-positive (monocyte) cells is normal   (MGI Ref ID J:112769)
    • mice display considerable infiltration of fibronectin into the spinal cord parenchyma   (MGI Ref ID J:112769)
  • homeostasis/metabolism phenotype
  • abnormal vascular wound healing
    • formation of neointimal lesions is enhanced 2 and 4 weeks after ligation compared to in wild-type mice such that there is a 2- to 4-fold increase in intimal to medial ratio at 500 um and 1.0 mm proximal to the ligation   (MGI Ref ID J:109753)
    • however, infiltration of inflammatory cells is normal   (MGI Ref ID J:109753)
    • apoptosis in neointimal lesions is decreased by 60% to 70%   (MGI Ref ID J:109753)
  • liver/biliary system phenotype
  • abnormal Kupffer cell morphology
    • after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice   (MGI Ref ID J:120368)
  • vision/eye phenotype
  • increased retinal photoreceptor cell number
    • after 2 weeks of light exposure, the number of rows of photoreceptors is 4.6+/-0.31 rows compared to 2.3+/-0.25 in wild-type mice and 21.2+/-0.25 in homozygous mice   (MGI Ref ID J:115542)
    • after 3 weeks of light exposure, the number of rows of photoreceptors is 3.0+/-0.41 rows compared to 1.5+/-0.24 in wild-type mice and 0.9+/-0.28 in homozygous mice   (MGI Ref ID J:115542)
  • hematopoietic system phenotype
  • abnormal Kupffer cell morphology
    • after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice   (MGI Ref ID J:120368)
  • craniofacial phenotype
  • abnormal tongue epithelium morphology
    • at P7 the gustatory epithelium of the vallate trench is thicker than normal blocking direct access of the ectopic tastse buds in the trench to taste solutions   (MGI Ref ID J:90280)
    • abnormal circumvallate papillae morphology
      • the vallate papilla is deformed and small in neonatal mutants   (MGI Ref ID J:90280)
      • at P7 the vallate trench is only 60% as deep as in wild-type mice   (MGI Ref ID J:90280)
  • cellular phenotype
  • abnormal neuron differentiation
    • peripheral nerves in the hindlimb, forelimb, and trigeminal ganglia are severely stunted compared to in wild-type mice   (MGI Ref ID J:127639)
    • abnormal axon extension
      • growth cones from dorsal root ganglion neurons are more sensitive to Sema3A repulsion than wild-type neurons   (MGI Ref ID J:127639)
      • when treated with 15 pM Sema3A outgrowth rate inhibition is increased (15 um per hour compared to 35 um per hour for wild-type neurons)   (MGI Ref ID J:127639)
      • however, increased sensitivity to Sema3A repulsion is alleviated in a double heterozygote cross of Ngfr and Sema3A   (MGI Ref ID J:127639)

Ngfrtm1Jae/Ngfrtm1Jae

        B6.129S4-Ngfrtm1Jae/J
  • hearing/vestibular/ear phenotype
  • cochlear hair cell degeneration
    • by 6 months, male homozygotes exhibit absence or damage of cochlear HCs in both the basal and upper turns   (MGI Ref ID J:110434)
    • however, IHCs are still present and morphologically normal at 4 months, suggesting that SGN's dendrites connecting the IHCs are damaged earlier than IHCs   (MGI Ref ID J:110434)
  • increased or absent threshold for auditory brainstem response
    • at 4 months of age, male homozygotes exhibit a significant elevation (>33 dB SPL) in click-evoked ABR thresholds relative to wild-type males   (MGI Ref ID J:110434)
    • at 6 months and 1 year, male homozygotes continue to display significant increases in ABR thresholds relative to age-matched wild-type males (100 and 126 dB SPL, respectively)   (MGI Ref ID J:110434)
    • however, no significant differences in click-evoked ABR thresholds are observed at 1 month, consistent with a normal cochlear structure at this age   (MGI Ref ID J:110434)
  • increased susceptibility to age-related hearing loss
    • starting at 4 months, male homozygotes display an age-related progressive hearing loss relative to age-matched wild-type males   (MGI Ref ID J:110434)
    • by 1 year of age, homozygotes are unresponsive to click stimuli at the maximum level (136 dB SPL)   (MGI Ref ID J:110434)
  • organ of Corti degeneration
    • at 1 month of age, male homozygotes exhibit a grossly normal organ of the Corti, except for a slight reduction in the number of SGNs   (MGI Ref ID J:110434)
    • by 6 months, male homozygotes show complete degeneration of the organ of Corti in the basal turns   (MGI Ref ID J:110434)
  • sensorineural hearing loss
    • male homozygotes show progressive hearing loss at 4 months, when both SGN degeneration and hair cell loss are observed in the basal cochlear turn   (MGI Ref ID J:110434)
  • nervous system phenotype
  • cochlear ganglion degeneration
    • starting at 1 month, male homozygotes show a slight (15.7%) but progressive loss of SGNs from the basal to the apical cochlear turns   (MGI Ref ID J:110434)
    • at 4 months, male homozygotes display significant SGN degeneration in the basal cochlear turn and swelling of the afferent dendrites below IHCs in the middle turns   (MGI Ref ID J:110434)
    • by 6 months, the density of SGNs is significantly reduced in the middle and basal turns, with a 59.8% loss of SGNs in the most basal turns   (MGI Ref ID J:110434)
  • cochlear hair cell degeneration
    • by 6 months, male homozygotes exhibit absence or damage of cochlear HCs in both the basal and upper turns   (MGI Ref ID J:110434)
    • however, IHCs are still present and morphologically normal at 4 months, suggesting that SGN's dendrites connecting the IHCs are damaged earlier than IHCs   (MGI Ref ID J:110434)
  • cardiovascular system phenotype
  • decreased myocardial infarction size
    • 10 days after myocardial ischemic/reperfusion injury   (MGI Ref ID J:190893)
  • homeostasis/metabolism phenotype
  • decreased myocardial infarction size
    • 10 days after myocardial ischemic/reperfusion injury   (MGI Ref ID J:190893)

Ngfrtm1Jae/Ngfrtm1Jae

        involves: 129S4/SvJae * C57BL/6J
  • nervous system phenotype
  • abnormal peripheral nervous system regeneration
    • motor axonal regeneration is increased in the tibial nerve cross-suture   (MGI Ref ID J:116954)
  • decreased motor neuron number
    • the number of motor neurons in tibial nerve is reduced   (MGI Ref ID J:116954)

Ngfrtm1Jae/Ngfrtm1Jae

        involves: 129S4/SvJae
  • nervous system phenotype
  • abnormal axon guidance
    • when given the choice between strips that contain Eph47-Fc or Fc, retinal axons fail to avoid EPHA7-Fc stripes or exhibit a preference for the Fc stripes unlike wild-type axons   (MGI Ref ID J:145459)
    • however, avoidance of stripes with EPHA5-Fc is normal   (MGI Ref ID J:145459)
  • abnormal cholinergic neuron morphology
    • increased size of cholinergic forebrain neurons   (MGI Ref ID J:62379)
  • abnormal retinal ganglion cell morphology
    • 50% of mice exhibit ectopic branches and arbors along the anterior posterior length of the nasal RGC axons in the superior colliculus unlike in wild-type mice   (MGI Ref ID J:145459)
    • the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice   (MGI Ref ID J:145459)
    • at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice   (MGI Ref ID J:145459)
  • abnormal sensory neuron innervation pattern
    • absence of sensory innervation to pineal and sweat glands   (MGI Ref ID J:43749)
  • abnormal superior colliculus morphology
    • however, total area of the superior colliculus is normal   (MGI Ref ID J:145459)
    • the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice   (MGI Ref ID J:145459)
    • at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice   (MGI Ref ID J:145459)
  • abnormal trigeminal ganglion morphology
    • ophthalmic branch of the trigeminal ganglion is severely truncated at E12.5   (MGI Ref ID J:157604)
  • decreased neuron apoptosis
    • at E12 and E14, neuron apoptosis is reduced 72% and 70%, respectively, compared to in wild-type mice   (MGI Ref ID J:123022)
    • nearly all neurons cultured with NT4 survive unlike wild-type neurons   (MGI Ref ID J:123022)
  • behavior/neurological phenotype
  • abnormal spatial learning
    • spatial learning is improved compared to in wild-type mice without deterioration with age   (MGI Ref ID J:62379)
  • vision/eye phenotype
  • abnormal eye physiology
    • mice subjected to intraocular injection of the pro form of nerve growth factor are protected from induced retinal ganglion cell death   (MGI Ref ID J:157549)
  • abnormal retinal ganglion cell morphology
    • 50% of mice exhibit ectopic branches and arbors along the anterior posterior length of the nasal RGC axons in the superior colliculus unlike in wild-type mice   (MGI Ref ID J:145459)
    • the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice   (MGI Ref ID J:145459)
    • at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice   (MGI Ref ID J:145459)
  • homeostasis/metabolism phenotype
  • abnormal tumor necrosis factor level
    • the pro form of nerve growth factor fails to induce TNF expression in retinas   (MGI Ref ID J:157549)
  • immune system phenotype
  • abnormal tumor necrosis factor level
    • the pro form of nerve growth factor fails to induce TNF expression in retinas   (MGI Ref ID J:157549)
  • cellular phenotype
  • abnormal axon guidance
    • when given the choice between strips that contain Eph47-Fc or Fc, retinal axons fail to avoid EPHA7-Fc stripes or exhibit a preference for the Fc stripes unlike wild-type axons   (MGI Ref ID J:145459)
    • however, avoidance of stripes with EPHA5-Fc is normal   (MGI Ref ID J:145459)
  • decreased neuron apoptosis
    • at E12 and E14, neuron apoptosis is reduced 72% and 70%, respectively, compared to in wild-type mice   (MGI Ref ID J:123022)
    • nearly all neurons cultured with NT4 survive unlike wild-type neurons   (MGI Ref ID J:123022)

Ngfrtm1Jae/Ngfrtm1Jae

        involves: 129S4/SvJae * C57BL/6
  • nervous system phenotype
  • abnormal axon extension
    • axons of mutant neurons grown in vitro in the presence of NGF grow equally well regardless if they are stimulated or not in contrast to wild-type neurons where stimulated axons out compete non-stimulated axons   (MGI Ref ID J:139381)
    • this lack of growth disadvantage in non-stimulated axons is due to less axon degeneration than occurs to wild-type neurons   (MGI Ref ID J:139381)
  • abnormal axon pruning
    • sympathetic neurons of the superior cervical ganglion (SCG) have improper pruning of axons from neurons that reach into both eye compartments   (MGI Ref ID J:139381)
    • SCG neurons in wild-type mice reduce through axon pruning the number of neurons projecting to both eyes from 78% at p20 to 20% at p50   (MGI Ref ID J:139381)
    • mutant mice have a similar percentage of SCG neurons that connect to both eyes at P20 but this percentage does not decrease with age   (MGI Ref ID J:139381)
    • at p35 where SCG neurons are actively pruning exons in wild-type mice, mutant mice have significantly less degenerating SCG axons than in wild-type mice   (MGI Ref ID J:139381)
  • cellular phenotype
  • abnormal axon extension
    • axons of mutant neurons grown in vitro in the presence of NGF grow equally well regardless if they are stimulated or not in contrast to wild-type neurons where stimulated axons out compete non-stimulated axons   (MGI Ref ID J:139381)
    • this lack of growth disadvantage in non-stimulated axons is due to less axon degeneration than occurs to wild-type neurons   (MGI Ref ID J:139381)
  • abnormal axon pruning
    • sympathetic neurons of the superior cervical ganglion (SCG) have improper pruning of axons from neurons that reach into both eye compartments   (MGI Ref ID J:139381)
    • SCG neurons in wild-type mice reduce through axon pruning the number of neurons projecting to both eyes from 78% at p20 to 20% at p50   (MGI Ref ID J:139381)
    • mutant mice have a similar percentage of SCG neurons that connect to both eyes at P20 but this percentage does not decrease with age   (MGI Ref ID J:139381)
    • at p35 where SCG neurons are actively pruning exons in wild-type mice, mutant mice have significantly less degenerating SCG axons than in wild-type mice   (MGI Ref ID J:139381)

Ngfrtm1Jae/Ngfrtm1Jae

        involves: 129S1/Sv * 129S4/SvJae
  • nervous system phenotype
  • abnormal retinal ganglion cell morphology
    • the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice   (MGI Ref ID J:145459)
    • at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice   (MGI Ref ID J:145459)
  • abnormal superior colliculus morphology
    • the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice   (MGI Ref ID J:145459)
    • at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice   (MGI Ref ID J:145459)
  • vision/eye phenotype
  • abnormal retinal ganglion cell morphology
    • the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice   (MGI Ref ID J:145459)
    • at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice   (MGI Ref ID J:145459)
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Research Applications
This mouse can be used to support research in many areas including:

Sensorineural Research
Nociception

Ngfrtm1Jae related

Apoptosis Research
Death Receptors

Neurobiology Research
Neurotrophic Factor Defects
Receptor Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ngfrtm1Jae
Allele Name targeted mutation 1, Rudolf Jaenisch
Allele Type Targeted (knock-out)
Common Name(s) NGFRtm1Jac; Ngfr-; p75(III)-; p75-; p75-KO; p75NGFR; p75NTR-; p75NTR KO; p75NTRexon3-null; p75exonIII-; p75NTR-; p75NTR/ExonIII-; p75e3-;
Mutation Made ByDr. Rudolf Jaenisch,   Whitehead Institute (MIT)
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Ngfr, nerve growth factor receptor (TNFR superfamily, member 16)
Chromosome 11
Gene Common Name(s) CD271; Gp80-LNGFR; LNGFR; RNNGFRR; TNFRSF16; p75; p75 neurotrophin receptor; p75(NTR); p75NGFR; p75NTR;
Molecular Note A neomycin selection cassette was inserted into the third exon of the gene, disrupting the sequences encoding cysteine repeats 2, 3, and 4. Northern blot analysis revealed that the mutant gene did not yield a full length mRNA, however subsequent RT-PCR analysis, described in J:71955, detected an endogenous alternative transcript which lacks exon 3. Western blot analysis showed that the full length isoform was absent in homozygous mutant mice, but an isoform lacking cysteine repeats 2, 3, and 4 was present in both wild and mutant mice. In vitro experiments showed the persisting isoform to be a transmembrane protein that cannot bind neurotrophins but interacts with tyrosine kinase receptors. [MGI Ref ID J:43748] [MGI Ref ID J:71955]

Genotyping

Genotyping Information

Genotyping Protocols

NEOTD (Generic Neo), Standard PCR
Ngfrtm1Jae, Melt Curve Analysis
Ngfrtm1Jae, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Lee KF; Li E; Huber LJ; Landis SC; Sharpe AH; Chao MV; Jaenisch R. 1992. Targeted mutation of the gene encoding the low affinity NGF receptor p75 leads to deficits in the peripheral sensory nervous system. Cell 69(5):737-49. [PubMed: 1317267]  [MGI Ref ID J:43748]

Additional References

Lee KF; Bachman K; Landis S; Jaenisch R. 1994. Dependence on p75 for innervation of some sympathetic targets. Science 263(5152):1447-9. [PubMed: 8128229]  [MGI Ref ID J:43749]

Lee KF; Davies AM; Jaenisch R. 1994. p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF. Development 120(4):1027-33. [PubMed: 7600951]  [MGI Ref ID J:43751]

McQuillen PS; DeFreitas MF; Zada G; Shatz CJ. 2002. A novel role for p75NTR in subplate growth cone complexity and visual thalamocortical innervation. J Neurosci 22(9):3580-93. [PubMed: 11978834]  [MGI Ref ID J:76254]

Ward NL; Stanford LE; Brown RE; Hagg T. 2000. Cholinergic medial septum neurons do not degenerate in aged 129/Sv control or p75(NGFR)-/-mice(*) Neurobiol Aging 21(1):125-34. [PubMed: 10794857]  [MGI Ref ID J:62452]

Ngfrtm1Jae related

Agerman K; Baudet C; Fundin B; Willson C; Ernfors P. 2000. Attenuation of a caspase-3 dependent cell death in NT4- and p75-deficient embryonic sensory neurons. Mol Cell Neurosci 16(3):258-68. [PubMed: 10995552]  [MGI Ref ID J:123022]

Andres R; Herraez-Baranda LA; Thompson J; Wyatt S; Davies AM. 2008. Regulation of sympathetic neuron differentiation by endogenous nerve growth factor and neurotrophin-3. Neurosci Lett 431(3):241-6. [PubMed: 18162309]  [MGI Ref ID J:141631]

Andsberg G; Kokaia Z; Lindvall O. 2001. Upregulation of p75 neurotrophin receptor after stroke in mice does not contribute to differential vulnerability of striatal neurons. Exp Neurol 169(2):351-63. [PubMed: 11358448]  [MGI Ref ID J:118035]

Atwal JK; Pinkston-Gosse J; Syken J; Stawicki S; Wu Y; Shatz C; Tessier-Lavigne M. 2008. PirB is a functional receptor for myelin inhibitors of axonal regeneration. Science 322(5903):967-70. [PubMed: 18988857]  [MGI Ref ID J:141065]

Baeza-Raja B; Eckel-Mahan K; Zhang L; Vagena E; Tsigelny IF; Sassone-Corsi P; Ptacek LJ; Akassoglou K. 2013. p75 neurotrophin receptor is a clock gene that regulates oscillatory components of circadian and metabolic networks. J Neurosci 33(25):10221-34. [PubMed: 23785138]  [MGI Ref ID J:199564]

Baeza-Raja B; Li P; Le Moan N; Sachs BD; Schachtrup C; Davalos D; Vagena E; Bridges D; Kim C; Saltiel AR; Olefsky JM; Akassoglou K. 2012. p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. Proc Natl Acad Sci U S A 109(15):5838-43. [PubMed: 22460790]  [MGI Ref ID J:183530]

Bamji SX; Majdan M; Pozniak CD; Belliveau DJ; Aloyz R; Kohn J; Causing CG; Miller FD. 1998. The p75 neurotrophin receptor mediates neuronal apoptosis and is essential for naturally occurring sympathetic neuron death. J Cell Biol 140(4):911-23. [PubMed: 9472042]  [MGI Ref ID J:46125]

Bath KG; Mandairon N; Jing D; Rajagopal R; Kapoor R; Chen ZY; Khan T; Proenca CC; Kraemer R; Cleland TA; Hempstead BL; Chao MV; Lee FS. 2008. Variant brain-derived neurotrophic factor (Val66Met) alters adult olfactory bulb neurogenesis and spontaneous olfactory discrimination. J Neurosci 28(10):2383-93. [PubMed: 18322085]  [MGI Ref ID J:132776]

Ben-Zvi A; Ben-Gigi L; Klein H; Behar O. 2007. Modulation of Semaphorin3A activity by p75 neurotrophin receptor influences peripheral axon patterning. J Neurosci 27(47):13000-11. [PubMed: 18032673]  [MGI Ref ID J:127639]

Bengoechea TG; Chen Z; O'Leary D; Masliah E; Lee KF. 2009. p75 reduces beta-amyloid-induced sympathetic innervation deficits in an Alzheimer's disease mouse model. Proc Natl Acad Sci U S A 106(19):7870-5. [PubMed: 19416837]  [MGI Ref ID J:148402]

Benson MD; Romero MI; Lush ME; Lu QR; Henkemeyer M; Parada LF. 2005. Ephrin-B3 is a myelin-based inhibitor of neurite outgrowth. Proc Natl Acad Sci U S A 102(30):10694-9. [PubMed: 16020529]  [MGI Ref ID J:100179]

Bentley CA; Lee KF. 2000. p75 is important for axon growth and schwann cell migration during development J Neurosci 20(20):7706-15. [PubMed: 11027232]  [MGI Ref ID J:65134]

Bergmann I; Priestley JV; McMahon SB; Brocker EB; Toyka KV; Koltzenburg M. 1997. Analysis of cutaneous sensory neurons in transgenic mice lacking the low affinity neurotrophin receptor p75. Eur J Neurosci 9(1):18-28. [PubMed: 9042565]  [MGI Ref ID J:128203]

Bergmann I; Reiter R; Toyka KV; Koltzenburg M. 1998. Nerve growth factor evokes hyperalgesia in mice lacking the low-affinity neurotrophin receptor p75. Neurosci Lett 255(2):87-90. [PubMed: 9835221]  [MGI Ref ID J:54742]

Bertrand MJ; Kenchappa RS; Andrieu D; Leclercq-Smekens M; Nguyen HN; Carter BD; Muscatelli F; Barker PA; De Backer O. 2008. NRAGE, a p75NTR adaptor protein, is required for developmental apoptosis in vivo. Cell Death Differ 15(12):1921-9. [PubMed: 18772898]  [MGI Ref ID J:157604]

Bonanomi D; Chivatakarn O; Bai G; Abdesselem H; Lettieri K; Marquardt T; Pierchala BA; Pfaff SL. 2012. Ret Is a Multifunctional Coreceptor that Integrates Diffusible- and Contact-Axon Guidance Signals. Cell 148(3):568-82. [PubMed: 22304922]  [MGI Ref ID J:180801]

Bono F; Lamarche I; Bornia J; Savi P; Della Valle G; Herbert JM. 1999. Nerve growth factor (NGF) exerts its pro-apoptotic effect via the P75NTR receptor in a cell cycle-dependent manner. FEBS Lett 457(1):93-7. [PubMed: 10486571]  [MGI Ref ID J:115312]

Botchkarev VA; Botchkareva NV; Albers KM; Chen LH; Welker P; Paus R. 2000. A role for p75 neurotrophin receptor in the control of apoptosis-driven hair follicle regression. FASEB J 14(13):1931-42. [PubMed: 11023977]  [MGI Ref ID J:118020]

Botchkareva NV; Botchkarev VA; Chen LH; Lindner G; Paus R. 1999. A role for p75 neurotrophin receptor in the control of hair follicle morphogenesis. Dev Biol 216(1):135-53. [PubMed: 10588868]  [MGI Ref ID J:58865]

Boyd JG; Gordon T. 2001. The neurotrophin receptors, trkB and p75, differentially regulate motor axonal regeneration. J Neurobiol 49(4):314-25. [PubMed: 11745667]  [MGI Ref ID J:116954]

Brennan C; Rivas-Plata K; Landis SC. 1999. The p75 neurotrophin receptor influences NT-3 responsiveness of sympathetic neurons in vivo. Nat Neurosci 2(8):699-705. [PubMed: 10412058]  [MGI Ref ID J:56521]

Cao L; Dhilla A; Mukai J; Blazeski R; Lodovichi C; Mason CA; Gogos JA. 2007. Genetic modulation of BDNF signaling affects the outcome of axonal competition in vivo. Curr Biol 17(11):911-21. [PubMed: 17493809]  [MGI Ref ID J:124050]

Capsoni S; Tiveron C; Vignone D; Amato G; Cattaneo A. 2010. Dissecting the involvement of tropomyosin-related kinase A and p75 neurotrophin receptor signaling in NGF deficit-induced neurodegeneration. Proc Natl Acad Sci U S A 107(27):12299-304. [PubMed: 20566851]  [MGI Ref ID J:162075]

Carter AR; Berry EM; Segal RA. 2003. Regional expression of p75NTR contributes to neurotrophin regulation of cerebellar patterning. Mol Cell Neurosci 22(1):1-13. [PubMed: 12595234]  [MGI Ref ID J:82192]

Catts VS; Al-Menhali N; Burne TH; Colditz MJ; Coulson EJ. 2008. The p75 neurotrophin receptor regulates hippocampal neurogenesis and related behaviours. Eur J Neurosci 28(5):883-92. [PubMed: 18717734]  [MGI Ref ID J:142287]

Chu GK; Yu W; Fehlings MG. 2007. The p75 neurotrophin receptor is essential for neuronal cell survival and improvement of functional recovery after spinal cord injury. Neuroscience 148(3):668-82. [PubMed: 17706365]  [MGI Ref ID J:128395]

Coome GE; Elliott J; Kawaja MD. 1998. Sympathetic and sensory axons invade the brains of nerve growth factor transgenic mice in the absence of p75NTR expression. Exp Neurol 149(1):284-94. [PubMed: 9454638]  [MGI Ref ID J:45485]

Copray S; Kust B; Emmer B; Lin MY; Liem R; Amor S; de Vries H; Floris S; Boddeke E. 2004. Deficient p75 low-affinity neurotrophin receptor expression exacerbates experimental allergic encephalomyelitis in C57/BL6 mice. J Neuroimmunol 148(1-2):41-53. [PubMed: 14975585]  [MGI Ref ID J:101824]

Culmsee C; Gerling N; Lehmann M; Nikolova-Karakashian M; Prehn JH; Mattson MP; Krieglstein J. 2002. Nerve growth factor survival signaling in cultured hippocampal neurons is mediated through TrkA and requires the common neurotrophin receptor P75. Neuroscience 115(4):1089-108. [PubMed: 12453482]  [MGI Ref ID J:120043]

Davies AM; Lee KF; Jaenisch R. 1993. p75-deficient trigeminal sensory neurons have an altered response to NGF but not to other neurotrophins. Neuron 11(4):565-74. [PubMed: 8398147]  [MGI Ref ID J:43750]

Deppmann CD; Mihalas S; Sharma N; Lonze BE; Niebur E; Ginty DD. 2008. A model for neuronal competition during development. Science 320(5874):369-73. [PubMed: 18323418]  [MGI Ref ID J:133953]

Dhanoa NK; Krol KM; Jahed A; Crutcher KA; Kawaja MD. 2006. Null mutations for exon III and exon IV of the p75 neurotrophin receptor gene enhance sympathetic sprouting in response to elevated levels of nerve growth factor in transgenic mice. Exp Neurol 198(2):416-26. [PubMed: 16488412]  [MGI Ref ID J:107898]

Dickendesher TL; Baldwin KT; Mironova YA; Koriyama Y; Raiker SJ; Askew KL; Wood A; Geoffroy CG; Zheng B; Liepmann CD; Katagiri Y; Benowitz LI; Geller HM; Giger RJ. 2012. NgR1 and NgR3 are receptors for chondroitin sulfate proteoglycans. Nat Neurosci 15(5):703-12. [PubMed: 22406547]  [MGI Ref ID J:191258]

Du Y; Fischer TZ; Clinton-Luke P; Lercher LD; Dreyfus CF. 2006. Distinct effects of p75 in mediating actions of neurotrophins on basal forebrain oligodendrocytes. Mol Cell Neurosci 31(2):366-75. [PubMed: 16356734]  [MGI Ref ID J:106882]

Dubois-Dauphin M; Poitry-Yamate C; de Bilbao F; Julliard AK; Jourdan F; Donati G. 2000. Early postnatal Muller cell death leads to retinal but not optic nerve degeneration in NSE-Hu-Bcl-2 transgenic mice. Neuroscience 95(1):9-21. [PubMed: 10619458]  [MGI Ref ID J:60078]

Fan G; Jaenisch R; Kucera J. 1999. A role for p75 receptor in neurotrophin-3 functioning during the development of limb proprioception. Neuroscience 90(1):259-68. [PubMed: 10188952]  [MGI Ref ID J:53825]

Fan L; Girnius S; Oakley B. 2004. Support of trigeminal sensory neurons by nonneuronal p75 neurotrophin receptors. Brain Res Dev Brain Res 150(1):23-39. [PubMed: 15126035]  [MGI Ref ID J:90280]

Ferri CC; Bisby MA. 1999. Improved survival of injured sciatic nerve Schwann cells in mice lacking the p75 receptor. Neurosci Lett 272(3):191-4. [PubMed: 10505613]  [MGI Ref ID J:59771]

Ferri CC; Ghasemlou N; Bisby MA; Kawaja MD. 2002. Nerve growth factor alters p75 neurotrophin receptor-induced effects in mouse facial motoneurons following axotomy. Brain Res 950(1-2):180-5. [PubMed: 12231242]  [MGI Ref ID J:134659]

Ferri CC; Moore FA; Bisby MA. 1998. Effects of facial nerve injury on mouse motoneurons lacking the p75 low-affinity neurotrophin receptor. J Neurobiol 34(1):1-9. [PubMed: 9469614]  [MGI Ref ID J:121247]

Frade JM; Barde YA. 1999. Genetic evidence for cell death mediated by nerve growth factor and the neurotrophin receptor p75 in the developing mouse retina and spinal cord. Development 126(4):683-90. [PubMed: 9895316]  [MGI Ref ID J:51990]

Fujita Y; Endo S; Takai T; Yamashita T. 2011. Myelin suppresses axon regeneration by PIR-B/SHP-mediated inhibition of Trk activity. EMBO J 30(7):1389-401. [PubMed: 21364532]  [MGI Ref ID J:171253]

Fundin BT; Silos-Santiago I; Ernfors P; Fagan AM; Aldskogius H ; DeChiara TM ; Phillips HS ; Barbacid M ; Yancopoulos GD ; Rice FL. 1997. Differential dependency of cutaneous mechanoreceptors on neurotrophins, trk receptors, and P75 LNGFR. Dev Biol 190(1):94-116. [PubMed: 9331334]  [MGI Ref ID J:43425]

Gao X; Daugherty RL; Tourtellotte WG. 2007. Regulation of low affinity neurotrophin receptor (p75(NTR)) by early growth response (Egr) transcriptional regulators. Mol Cell Neurosci 36(4):501-14. [PubMed: 17916431]  [MGI Ref ID J:126322]

Gehler S; Gallo G; Veien E; Letourneau PC. 2004. p75 neurotrophin receptor signaling regulates growth cone filopodial dynamics through modulating RhoA activity. J Neurosci 24(18):4363-72. [PubMed: 15128850]  [MGI Ref ID J:96877]

Gjerstad MD; Tandrup T; Koltzenburg M; Jakobsen J. 2002. Predominant neuronal B-cell loss in L5 DRG of p75 receptor-deficient mice. J Anat 200(Pt 1):81-7. [PubMed: 11833656]  [MGI Ref ID J:74546]

Golombek DA; Hurd MW; Lee KF; Ralph MR. 1996. Mice lacking the p75(NGFR) receptor exhibit abnormal responses to light. Biol Rhythm Res 27(3):409-418.  [MGI Ref ID J:36157]

Graham RM; Friedman M; Hoyle GW. 2001. Sensory nerves promote ozone-induced lung inflammation in mice. Am J Respir Crit Care Med 164(2):307-13. [PubMed: 11463606]  [MGI Ref ID J:133168]

Greferath U; Bennie A; Kourakis A; Bartlett PF; Murphy M; Barrett GL. 2000. Enlarged cholinergic forebrain neurons and improved spatial learning in p75 knockout mice Eur J Neurosci 12(3):885-93. [PubMed: 10762318]  [MGI Ref ID J:62379]

Gschwendtner A; Liu Z; Hucho T; Bohatschek M; Kalla R; Dechant G; Raivich G. 2003. Regulation, cellular localization, and function of the p75 neurotrophin receptor (p75NTR) during the regeneration of facial motoneurons. Mol Cell Neurosci 24(2):307-22. [PubMed: 14572455]  [MGI Ref ID J:86223]

Gumy LF; Bampton ET; Tolkovsky AM. 2008. Hyperglycaemia inhibits Schwann cell proliferation and migration and restricts regeneration of axons and Schwann cells from adult murine DRG. Mol Cell Neurosci 37(2):298-311. [PubMed: 18024075]  [MGI Ref ID J:132600]

Habecker BA; Bilimoria P; Linick C; Gritman K; Lorentz CU; Woodward W; Birren SJ. 2008. Regulation of cardiac innervation and function via the p75 neurotrophin receptor. Auton Neurosci 140(1-2):40-8. [PubMed: 18430612]  [MGI Ref ID J:139920]

Hanbury R; Chen EY; Wuu J; Kordower JH. 2003. Knockout of p75NTR does not alter the viability of striatal neurons following a metabolic or excitotoxic injury. J Mol Neurosci 20(2):93-102. [PubMed: 12794303]  [MGI Ref ID J:121246]

Hannila SS; Kawaja MD. 2003. Distribution of central sensory axons in transgenic mice overexpressing nerve growth factor and lacking functional p75 neurotrophin receptor expression. Eur J Neurosci 18(2):312-22. [PubMed: 12887413]  [MGI Ref ID J:108772]

Hannila SS; Kawaja MD. 1999. Nerve growth factor-induced growth of sympathetic axons into the optic tract of mature mice is enhanced by an absence of p75NTR expression. J Neurobiol 39(1):51-66. [PubMed: 10213453]  [MGI Ref ID J:116951]

Hannila SS; Kawaja MD. 2005. Nerve growth factor-mediated collateral sprouting of central sensory axons into deafferentated regions of the dorsal horn is enhanced in the absence of the p75 neurotrophin receptor. J Comp Neurol 486(4):331-43. [PubMed: 15846783]  [MGI Ref ID J:105175]

Hannila SS; Lawrance GM; Ross GM; Kawaja MD. 2004. TrkA and mitogen-activated protein kinase phosphorylation are enhanced in sympathetic neurons lacking functional p75 neurotrophin receptor expression. Eur J Neurosci 19(10):2903-8. [PubMed: 15147324]  [MGI Ref ID J:90300]

Harada C; Harada T; Nakamura K; Sakai Y; Tanaka K; Parada LF. 2006. Effect of p75(NTR) on the regulation of naturally occurring cell death and retinal ganglion cell number in the mouse eye. Dev Biol 290(1):57-65. [PubMed: 16343477]  [MGI Ref ID J:104804]

Harada T; Harada C; Nakayama N; Okuyama S; Yoshida K; Kohsaka S; Matsuda H; Wada K. 2000. Modification of glial-neuronal cell interactions prevents photoreceptor apoptosis during light-induced retinal degeneration [see comments] Neuron 26(2):533-41. [PubMed: 10839371]  [MGI Ref ID J:62567]

Harrison SM; Jones ME; Uecker S; Albers KM; Kudrycki KE; Davis BM. 2000. Levels of nerve growth factor and neurotrophin-3 are affected differentially by the presence of p75 in sympathetic neurons in vivo J Comp Neurol 424(1):99-110. [PubMed: 10888742]  [MGI Ref ID J:63454]

Hasan W; Woodward WR; Habecker BA. 2012. Altered atrial neurotransmitter release in transgenic p75(-/-) and gp130 KO mice. Neurosci Lett 529(1):55-9. [PubMed: 22999927]  [MGI Ref ID J:189000]

Holm MM; Nieto-Gonzalez JL; Vardya I; Vaegter CB; Nykjaer A; Jensen K. 2009. Mature BDNF, but not proBDNF, reduces excitability of fast-spiking interneurons in mouse dentate gyrus. J Neurosci 29(40):12412-8. [PubMed: 19812317]  [MGI Ref ID J:153654]

Hu Y; Lee X; Shao Z; Apicco D; Huang G; Gong BJ; Pepinsky RB; Mi S. 2013. A DR6/p75(NTR) complex is responsible for beta-amyloid-induced cortical neuron death. Cell Death Dis 4:e579. [PubMed: 23559013]  [MGI Ref ID J:205745]

Jackson AC; Park H. 1999. Experimental rabies virus infection of p75 neurotrophin receptor-deficient mice. Acta Neuropathol (Berl) 98(6):641-4. [PubMed: 10603041]  [MGI Ref ID J:59804]

Jahed A; Kawaja MD. 2005. The influences of p75 neurotrophin receptor and brain-derived neurotrophic factor in the sympathetic innervation of target tissues during murine postnatal development. Auton Neurosci 118(1-2):32-42. [PubMed: 15795176]  [MGI Ref ID J:101883]

Jansen P; Giehl K; Nyengaard JR; Teng K; Lioubinski O; Sjoegaard SS; Breiderhoff T; Gotthardt M; Lin F; Eilers A; Petersen CM; Lewin GR; Hempstead BL; Willnow TE; Nykjaer A. 2007. Roles for the pro-neurotrophin receptor sortilin in neuronal development, aging and brain injury. Nat Neurosci 10(11):1449-57. [PubMed: 17934455]  [MGI Ref ID J:128451]

Je HS; Yang F; Ji Y; Potluri S; Fu XQ; Luo ZG; Nagappan G; Chan JP; Hempstead B; Son YJ; Lu B. 2013. ProBDNF and mature BDNF as punishment and reward signals for synapse elimination at mouse neuromuscular junctions. J Neurosci 33(24):9957-62. [PubMed: 23761891]  [MGI Ref ID J:199166]

Jiang Y; Nyengaard JR; Zhang JS; Jakobsen J. 2004. Selective loss of calcitonin gene-related Peptide-expressing primary sensory neurons of the a-cell phenotype in early experimental diabetes. Diabetes 53(10):2669-75. [PubMed: 15448099]  [MGI Ref ID J:93188]

Jiang Y; Zhang JS; Jakobsen J. 2005. Differential effect of p75 neurotrophin receptor on expression of pro-apoptotic proteins c-jun, p38 and caspase-3 in dorsal root ganglion cells after axotomy in experimental diabetes. Neuroscience 132(4):1083-92. [PubMed: 15857712]  [MGI Ref ID J:105206]

Kerr B; Garcia-Rudaz C; Dorfman M; Paredes A; Ojeda SR. 2009. NTRK1 and NTRK2 receptors facilitate follicle assembly and early follicular development in the mouse ovary. Reproduction 138(1):131-40. [PubMed: 19357131]  [MGI Ref ID J:152505]

Kerzel S; Path G; Nockher WA; Quarcoo D; Raap U; Groneberg DA; Dinh QT; Fischer A; Braun A; Renz H. 2003. Pan-neurotrophin receptor p75 contributes to neuronal hyperreactivity and airway inflammation in a murine model of experimental asthma. Am J Respir Cell Mol Biol 28(2):170-8. [PubMed: 12540484]  [MGI Ref ID J:94616]

Kinkelin I; Stucky CL; Koltzenburg M. 1999. Postnatal loss of Merkel cells, but not of slowly adapting mechanoreceptors in mice lacking the neurotrophin receptor p75. Eur J Neurosci 11(11):3963-9. [PubMed: 10583485]  [MGI Ref ID J:59859]

Knowles JK; Rajadas J; Nguyen TV; Yang T; LeMieux MC; Vander Griend L; Ishikawa C; Massa SM; Wyss-Coray T; Longo FM. 2009. The p75 neurotrophin receptor promotes amyloid-beta(1-42)-induced neuritic dystrophy in vitro and in vivo. J Neurosci 29(34):10627-37. [PubMed: 19710315]  [MGI Ref ID J:152315]

Kohn J; Aloyz RS; Toma JG; Haak-Frendscho M; Miller FD. 1999. Functionally antagonistic interactions between the TrkA and p75 neurotrophin receptors regulate sympathetic neuron growth and target innervation. J Neurosci 19(13):5393-408. [PubMed: 10377349]  [MGI Ref ID J:120561]

Koshimizu H; Hazama S; Hara T; Ogura A; Kojima M. 2010. Distinct signaling pathways of precursor BDNF and mature BDNF in cultured cerebellar granule neurons. Neurosci Lett 473(3):229-32. [PubMed: 20219632]  [MGI Ref ID J:159904]

Kraemer R. 2002. Reduced apoptosis and increased lesion development in the flow-restricted carotid artery of p75(NTR)-null mutant mice. Circ Res 91(6):494-500. [PubMed: 12242267]  [MGI Ref ID J:109753]

Kramer BM; Van der Zee CE; Hagg T. 1999. P75 nerve growth factor receptor is important for retrograde transport of neurotrophins in adult cholinergic basal forebrain neurons. Neuroscience 94(4):1163-72. [PubMed: 10625055]  [MGI Ref ID J:118445]

Krimm RF. 2006. Mice lacking the p75 receptor fail to acquire a normal complement of taste buds and geniculate ganglion neurons by adulthood. Anat Rec A Discov Mol Cell Evol Biol 288(12):1294-302. [PubMed: 17083122]  [MGI Ref ID J:174178]

Krol KM; Crutcher KA; Kalisch BE; Rylett RJ; Kawaja MD. 2000. Absence of p75(NTR) expression reduces nerve growth factor immunolocalization in cholinergic septal neurons. J Comp Neurol 427(1):54-66. [PubMed: 11042591]  [MGI Ref ID J:120026]

Krol KM; Stein EJ; Elliott J; Kawaja MD. 2001. TrkA-expressing trigeminal sensory neurons display both neurochemical and structural plasticity despite a loss of p75NTR function: responses to normal and elevated levels of nerve growth factor. Eur J Neurosci 13(1):35-47. [PubMed: 11135002]  [MGI Ref ID J:107975]

Kuruvilla R; Zweifel LS; Glebova NO; Lonze BE; Valdez G; Ye H; Ginty DD. 2004. A neurotrophin signaling cascade coordinates sympathetic neuron development through differential control of TrkA trafficking and retrograde signaling. Cell 118(2):243-55. [PubMed: 15260993]  [MGI Ref ID J:91949]

Kust B; Mantingh-Otter I; Boddeke E; Copray S. 2006. Deficient p75 low-affinity neurotrophin receptor expression does alter the composition of cellular infiltrate in experimental autoimmune encephalomyelitis in C57BL/6 mice. J Neuroimmunol 174(1-2):92-100. [PubMed: 16519950]  [MGI Ref ID J:112769]

Le Moan N; Houslay DM; Christian F; Houslay MD; Akassoglou K. 2011. Oxygen-dependent cleavage of the p75 neurotrophin receptor triggers stabilization of HIF-1alpha. Mol Cell 44(3):476-90. [PubMed: 22055192]  [MGI Ref ID J:180679]

Lebrun-Julien F; Bertrand MJ; De Backer O; Stellwagen D; Morales CR; Di Polo A; Barker PA. 2010. ProNGF induces TNF{alpha}-dependent death of retinal ganglion cells through a p75NTR non-cell-autonomous signaling pathway. Proc Natl Acad Sci U S A 107(8):3817-22. [PubMed: 20133718]  [MGI Ref ID J:157549]

Lee KF; Bachman K; Landis S; Jaenisch R. 1994. Dependence on p75 for innervation of some sympathetic targets. Science 263(5152):1447-9. [PubMed: 8128229]  [MGI Ref ID J:43749]

Lee KF; Davies AM; Jaenisch R. 1994. p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF. Development 120(4):1027-33. [PubMed: 7600951]  [MGI Ref ID J:43751]

Lim YS; McLaughlin T; Sung TC; Santiago A; Lee KF; O'Leary DD. 2008. p75(NTR) mediates ephrin-A reverse signaling required for axon repulsion and mapping. Neuron 59(5):746-58. [PubMed: 18786358]  [MGI Ref ID J:145459]

Lin PY; Hinterneder JM; Rollor SR; Birren SJ. 2007. Non-cell-autonomous regulation of GABAergic neuron development by neurotrophins and the p75 receptor. J Neurosci 27(47):12787-96. [PubMed: 18032650]  [MGI Ref ID J:127645]

Lopez-Sanchez N; Frade JM. 2013. Genetic evidence for p75NTR-dependent tetraploidy in cortical projection neurons from adult mice. J Neurosci 33(17):7488-500. [PubMed: 23616554]  [MGI Ref ID J:197034]

Lorentz CU; Alston EN; Belcik T; Lindner JR; Giraud GD; Habecker BA. 2010. Heterogeneous ventricular sympathetic innervation, altered beta-adrenergic receptor expression, and rhythm instability in mice lacking the p75 neurotrophin receptor. Am J Physiol Heart Circ Physiol 298(6):H1652-60. [PubMed: 20190098]  [MGI Ref ID J:160249]

Lorentz CU; Parrish DC; Alston EN; Pellegrino MJ; Woodward WR; Hempstead BL; Habecker BA. 2013. Sympathetic denervation of peri-infarct myocardium requires the p75 neurotrophin receptor. Exp Neurol 249:111-9. [PubMed: 24013014]  [MGI Ref ID J:206543]

Martin LJ; Chen K; Liu Z. 2005. Adult motor neuron apoptosis is mediated by nitric oxide and Fas death receptor linked by DNA damage and p53 activation. J Neurosci 25(27):6449-59. [PubMed: 16000635]  [MGI Ref ID J:99428]

McDonald TG; Scott SA; Kane KM; Kawaja MD. 2009. Proteomic assessment of sympathetic ganglia from adult mice that possess null mutations of ExonIII or ExonIV in the p75 neurotrophin receptor gene. Brain Res 1253:1-14. [PubMed: 19046947]  [MGI Ref ID J:147806]

McNulty JA; Prechel MM; Young RA; Fox LM. 1997. Pinealocyte ultrastructure in mutant mice that lack sympathetic innervation to the pineal gland. J Submicrosc Cytol Pathol 29(3):305-11. [PubMed: 9267038]  [MGI Ref ID J:113179]

McQuillen PS; DeFreitas MF; Zada G; Shatz CJ. 2002. A novel role for p75NTR in subplate growth cone complexity and visual thalamocortical innervation. J Neurosci 22(9):3580-93. [PubMed: 11978834]  [MGI Ref ID J:76254]

Michaelsen K; Murk K; Zagrebelsky M; Dreznjak A; Jockusch BM; Rothkegel M; Korte M. 2010. Fine-tuning of neuronal architecture requires two profilin isoforms. Proc Natl Acad Sci U S A 107(36):15780-5. [PubMed: 20798032]  [MGI Ref ID J:164381]

Mirnics ZK; Yan C; Portugal C; Kim TW; Saragovi HU; Sisodia SS; Mirnics K; Schor NF. 2005. P75 neurotrophin receptor regulates expression of neural cell adhesion molecule 1. Neurobiol Dis 20(3):969-85. [PubMed: 16006137]  [MGI Ref ID J:104654]

Murray SS; Bartlett PF; Cheema SS. 1999. Differential loss of spinal sensory but not motor neurons in the p75NTR knockout mouse. Neurosci Lett 267(1):45-8. [PubMed: 10400245]  [MGI Ref ID J:107967]

Murray SS; Bartlett PF; Lopes EC; Coulson EJ; Greferath U; Cheema SS. 2003. Low-affinity neurotrophin receptor with targeted mutation of exon 3 is capable of mediating the death of axotomized neurons. Clin Exp Pharmacol Physiol 30(4):217-22. [PubMed: 12680838]  [MGI Ref ID J:103109]

Mysona BA; Al-Gayyar MM; Matragoon S; Abdelsaid MA; El-Azab MF; Saragovi HU; El-Remessy AB. 2013. Modulation of p75(NTR) prevents diabetes- and proNGF-induced retinal inflammation and blood-retina barrier breakdown in mice and rats. Diabetologia 56(10):2329-39. [PubMed: 23918145]  [MGI Ref ID J:203278]

Nakamura K; Harada C; Okumura A; Namekata K; Mitamura Y; Yoshida K; Ohno S; Yoshida H; Harada T. 2005. Effect of p75NTR on the regulation of photoreceptor apoptosis in the rd mouse. Mol Vis 11:1229-35. [PubMed: 16402023]  [MGI Ref ID J:136765]

Namekata K; Harada C; Taya C; Guo X; Kimura H; Parada LF; Harada T. 2010. Dock3 induces axonal outgrowth by stimulating membrane recruitment of the WAVE complex. Proc Natl Acad Sci U S A 107(16):7586-91. [PubMed: 20368433]  [MGI Ref ID J:159284]

Naska S; Lin DC; Miller FD; Kaplan DR. 2010. p75NTR is an obligate signaling receptor required for cues that cause sympathetic neuron growth cone collapse. Mol Cell Neurosci 45(2):108-20. [PubMed: 20584617]  [MGI Ref ID J:171326]

Naumann T; Casademunt E; Hollerbach E; Hofmann J; Dechant G; Frotscher M; Barde YA. 2002. Complete deletion of the neurotrophin receptor p75NTR leads to long-lasting increases in the number of basal forebrain cholinergic neurons. J Neurosci 22(7):2409-18. [PubMed: 11923404]  [MGI Ref ID J:76011]

Niklison-Chirou MV; Steinert JR; Agostini M; Knight RA; Dinsdale D; Cattaneo A; Mak TW; Melino G. 2013. TAp73 knockout mice show morphological and functional nervous system defects associated with loss of p75 neurotrophin receptor. Proc Natl Acad Sci U S A 110(47):18952-7. [PubMed: 24190996]  [MGI Ref ID J:202987]

Page ME; Bao L; Andre P; Pelta-Heller J; Sluzas E; Gonzalez-Alegre P; Bogush A; Khan LE; Iacovitti L; Rice ME; Ehrlich ME. 2010. Cell-autonomous alteration of dopaminergic transmission by wild type and mutant (DeltaE) TorsinA in transgenic mice. Neurobiol Dis 39(3):318-26. [PubMed: 20460154]  [MGI Ref ID J:163037]

Park KJ; Grosso CA; Aubert I; Kaplan DR; Miller FD. 2010. p75NTR-dependent, myelin-mediated axonal degeneration regulates neural connectivity in the adult brain. Nat Neurosci 13(5):559-66. [PubMed: 20348920]  [MGI Ref ID J:159671]

Passino MA; Adams RA; Sikorski SL; Akassoglou K. 2007. Regulation of hepatic stellate cell differentiation by the neurotrophin receptor p75NTR. Science 315(5820):1853-6. [PubMed: 17395831]  [MGI Ref ID J:120368]

Pehar M; Cassina P; Vargas MR; Castellanos R; Viera L; Beckman JS; Estevez AG; Barbeito L. 2004. Astrocytic production of nerve growth factor in motor neuron apoptosis: implications for amyotrophic lateral sclerosis. J Neurochem 89(2):464-73. [PubMed: 15056289]  [MGI Ref ID J:128978]

Perez-Perez M; Garcia-Suarez O; Esteban I; Germana A; Farinas I; Naves FJ; Vega JA. 2003. p75NTR in the spleen: Age-dependent changes, effect of NGF and 4-methylcatechol treatment, and structural changes in p75NTR-deficient mice. Anat Rec A Discov Mol Cell Evol Biol 270(2):117-28. [PubMed: 12524687]  [MGI Ref ID J:81509]

Peterson DA; Dickinson-Anson HA; Leppert JT; Lee KF; Gage FH. 1999. Central neuronal loss and behavioral impairment in mice lacking neurotrophin receptor p75. J Comp Neurol 404(1):1-20. [PubMed: 9886021]  [MGI Ref ID J:77289]

Peterson DA; Leppert JT; Lee KF; Gage FH. 1997. Basal forebrain neuronal loss in mice lacking neurotrophin receptor p75 [letter; comment] Science 277(5327):837-9. [PubMed: 9273702]  [MGI Ref ID J:42248]

Petrie CN; Smithson LJ; Crotty AM; Michalski B; Fahnestock M; Kawaja MD. 2013. Overexpression of nerve growth factor by murine smooth muscle cells: role of the p75 neurotrophin receptor on sympathetic and sensory sprouting. J Comp Neurol 521(11):2621-43. [PubMed: 23322532]  [MGI Ref ID J:200734]

Raiker SJ; Lee H; Baldwin KT; Duan Y; Shrager P; Giger RJ. 2010. Oligodendrocyte-myelin glycoprotein and Nogo negatively regulate activity-dependent synaptic plasticity. J Neurosci 30(37):12432-45. [PubMed: 20844138]  [MGI Ref ID J:164667]

Rice FL; Albers KM; Davis BM; Silos-Santiago I; Wilkinson GA; LeMaster AM; Ernfors P; Smeyne RJ; Aldskogius H; Phillips HS; Barbacid M; DeChiara TM; Yancopoulos GD; Dunne CE; Fundin BT. 1998. Differential dependency of unmyelinated and A delta epidermal and upper dermal innervation on neurotrophins, trk receptors, and p75LNGFR. Dev Biol 198(1):57-81. [PubMed: 9640332]  [MGI Ref ID J:107715]

Rohrer B; Matthes MT; LaVail MM; Reichardt LF. 2003. Lack of p75 receptor does not protect photoreceptors from light-induced cell death. Exp Eye Res 76(1):125-9. [PubMed: 12589782]  [MGI Ref ID J:115542]

Rosch H; Schweigreiter R; Bonhoeffer T; Barde YA; Korte M. 2005. The neurotrophin receptor p75NTR modulates long-term depression and regulates the expression of AMPA receptor subunits in the hippocampus. Proc Natl Acad Sci U S A 102(20):7362-7. [PubMed: 15883381]  [MGI Ref ID J:99236]

Sachs BD; Baillie GS; McCall JR; Passino MA; Schachtrup C; Wallace DA; Dunlop AJ; MacKenzie KF; Klussmann E; Lynch MJ; Sikorski SL; Nuriel T; Tsigelny I; Zhang J; Houslay MD; Chao MV; Akassoglou K. 2007. p75 neurotrophin receptor regulates tissue fibrosis through inhibition of plasminogen activation via a PDE4/cAMP/PKA pathway. J Cell Biol 177(6):1119-32. [PubMed: 17576803]  [MGI Ref ID J:134923]

Sarram S; Lee KF; Byers MR. 1997. Dental innervation and CGRP in adult p75-deficient mice. J Comp Neurol 385(2):297-308. [PubMed: 9268129]  [MGI Ref ID J:42087]

Sato T; Doi K; Taniguchi M; Yamashita T; Kubo T; Tohyama M. 2006. Progressive hearing loss in mice carrying a mutation in the p75 gene. Brain Res 1091(1):224-34. [PubMed: 16564506]  [MGI Ref ID J:110434]

Scott AL; Borisoff JF; Ramer MS. 2005. Deafferentation and neurotrophin-mediated intraspinal sprouting: a central role for the p75 neurotrophin receptor. Eur J Neurosci 21(1):81-92. [PubMed: 15654845]  [MGI Ref ID J:100810]

Sedy J; Szeder V; Walro JM; Ren ZG; Nanka O; Tessarollo L; Sieber-Blum M; Grim M; Kucera J. 2004. Pacinian corpuscle development involves multiple Trk signaling pathways. Dev Dyn 231(3):551-63. [PubMed: 15376326]  [MGI Ref ID J:93853]

Siao CJ; Lorentz CU; Kermani P; Marinic T; Carter J; McGrath K; Padow VA; Mark W; Falcone DJ; Cohen-Gould L; Parrish DC; Habecker BA; Nykjaer A; Ellenson LH; Tessarollo L; Hempstead BL. 2012. ProNGF, a cytokine induced after myocardial infarction in humans, targets pericytes to promote microvascular damage and activation. J Exp Med 209(12):2291-305. [PubMed: 23091165]  [MGI Ref ID J:190893]

Singh KK; Park KJ; Hong EJ; Kramer BM; Greenberg ME; Kaplan DR; Miller FD. 2008. Developmental axon pruning mediated by BDNF-p75NTR-dependent axon degeneration. Nat Neurosci 11(6):649-58. [PubMed: 18382462]  [MGI Ref ID J:139381]

Snapyan M; Lemasson M; Brill MS; Blais M; Massouh M; Ninkovic J; Gravel C; Berthod F; Gotz M; Barker PA; Parent A; Saghatelyan A. 2009. Vasculature guides migrating neuronal precursors in the adult mammalian forebrain via brain-derived neurotrophic factor signaling. J Neurosci 29(13):4172-88. [PubMed: 19339612]  [MGI Ref ID J:155654]

Sorensen B; Tandrup T; Koltzenburg M; Jakobsen J. 2003. No further loss of dorsal root ganglion cells after axotomy in p75 neurotrophin receptor knockout mice. J Comp Neurol 459(3):242-50. [PubMed: 12655507]  [MGI Ref ID J:125667]

Sotthibundhu A; Li QX; Thangnipon W; Coulson EJ. 2009. Abeta(1-42) stimulates adult SVZ neurogenesis through the p75 neurotrophin receptor. Neurobiol Aging 30(12):1975-85. [PubMed: 18374455]  [MGI Ref ID J:155160]

Sotthibundhu A; Sykes AM; Fox B; Underwood CK; Thangnipon W; Coulson EJ. 2008. Beta-amyloid(1-42) induces neuronal death through the p75 neurotrophin receptor. J Neurosci 28(15):3941-6. [PubMed: 18400893]  [MGI Ref ID J:132959]

Stucky CL; Koltzenburg M. 1997. The low-affinity neurotrophin receptor p75 regulates the function but not the selective survival of specific subpopulations of sensory neurons. J Neurosci 17(11):4398-405. [PubMed: 9151756]  [MGI Ref ID J:111181]

Syroid DE; Maycox PJ; Soilu-Hanninen M; Petratos S; Bucci T; Burrola P; Murray S; Cheema S; Lee KF; Lemke G; Kilpatrick TJ. 2000. Induction of postnatal schwann cell death by the low-affinity neurotrophin receptor in vitro and after axotomy. J Neurosci 20(15):5741-7. [PubMed: 10908614]  [MGI Ref ID J:120471]

Taniguchi J; Fujitani M; Endo M; Kubo T; Fujitani M; Miller FD; Kaplan DR; Yamashita T. 2008. Rap1 is involved in the signal transduction of myelin-associated glycoprotein. Cell Death Differ 15(2):408-19. [PubMed: 18049479]  [MGI Ref ID J:146387]

Tep C; Kim ML; Opincariu LI; Limpert AS; Chan JR; Appel B; Carter BD; Yoon SO. 2012. Brain-derived Neurotrophic Factor (BDNF) Induces Polarized Signaling of Small GTPase (Rac1) Protein at the Onset of Schwann Cell Myelination through Partitioning-defective 3 (Par3) Protein. J Biol Chem 287(2):1600-8. [PubMed: 22128191]  [MGI Ref ID J:179663]

Tisay KT; Bartlett PF; Key B. 2000. Primary olfactory axons form ectopic glomeruli in mice lacking p75NTR J Comp Neurol 428(4):656-70. [PubMed: 11077419]  [MGI Ref ID J:65849]

Tokuoka S; Takahashi Y; Masuda T; Tanaka H; Furukawa S; Nagai H. 2001. Disruption of antigen-induced airway inflammation and airway hyper-responsiveness in low affinity neurotrophin receptor p75 gene deficient mice. Br J Pharmacol 134(7):1580-6. [PubMed: 11724766]  [MGI Ref ID J:115419]

Tomita K; Kubo T; Matsuda K; Fujiwara T; Yano K; Winograd JM; Tohyama M; Hosokawa K. 2007. The neurotrophin receptor p75NTR in Schwann cells is implicated in remyelination and motor recovery after peripheral nerve injury. Glia 55(11):1199-208. [PubMed: 17600367]  [MGI Ref ID J:156304]

Trang T; Koblic P; Kawaja M; Jhamandas K. 2009. Attenuation of opioid analgesic tolerance in p75 neurotrophin receptor null mutant mice. Neurosci Lett 451(1):69-73. [PubMed: 19114089]  [MGI Ref ID J:146358]

Underwood CK; Reid K; May LM; Bartlett PF; Coulson EJ. 2008. Palmitoylation of the C-terminal fragment of p75(NTR) regulates death signaling and is required for subsequent cleavage by gamma-secretase. Mol Cell Neurosci 37(2):346-58. [PubMed: 18055214]  [MGI Ref ID J:132689]

Vaegter CB; Jansen P; Fjorback AW; Glerup S; Skeldal S; Kjolby M; Richner M; Erdmann B; Nyengaard JR; Tessarollo L; Lewin GR; Willnow TE; Chao MV; Nykjaer A. 2011. Sortilin associates with Trk receptors to enhance anterograde transport and neurotrophin signaling. Nat Neurosci 14(1):54-61. [PubMed: 21102451]  [MGI Ref ID J:170255]

Van der Zee CE; Ross GM; Riopelle RJ; Hagg T. 1996. Survival of cholinergic forebrain neurons in developing p75NGFR-deficient mice [see comments] Science 274(5293):1729-32. [PubMed: 8939868]  [MGI Ref ID J:37105]

Venkatesh K; Chivatakarn O; Sheu SS; Giger RJ. 2007. Molecular dissection of the myelin-associated glycoprotein receptor complex reveals cell type-specific mechanisms for neurite outgrowth inhibition. J Cell Biol 177(3):393-9. [PubMed: 17470639]  [MGI Ref ID J:134726]

Volosin M; Song W; Almeida RD; Kaplan DR; Hempstead BL; Friedman WJ. 2006. Interaction of survival and death signaling in basal forebrain neurons: roles of neurotrophins and proneurotrophins. J Neurosci 26(29):7756-66. [PubMed: 16855103]  [MGI Ref ID J:110652]

Walsh GS; Krol KM; Crutcher KA; Kawaja MD. 1999. Enhanced neurotrophin-induced axon growth in myelinated portions of the CNS in mice lacking the p75 neurotrophin receptor. J Neurosci 19(10):4155-68. [PubMed: 10234043]  [MGI Ref ID J:54959]

Walsh GS; Krol KM; Kawaja MD. 1999. Absence of the p75 neurotrophin receptor alters the pattern of sympathosensory sprouting in the trigeminal ganglia of mice overexpressing nerve growth factor. J Neurosci 19(1):258-73. [PubMed: 9870956]  [MGI Ref ID J:51837]

Wang YJ; Wang X; Lu JJ; Li QX; Gao CY; Liu XH; Sun Y; Yang M; Lim Y; Evin G; Zhong JH; Masters C; Zhou XF. 2011. p75NTR regulates Abeta deposition by increasing Abeta production but inhibiting Abeta aggregation with its extracellular domain. J Neurosci 31(6):2292-304. [PubMed: 21307265]  [MGI Ref ID J:169451]

Ward NL; Hagg T. 2000. SEK1/MKK4, c-Jun and NFKappaB are differentially activated in forebrain neurons during postnatal development and injury in both control and p75NGFR-deficient mice. Eur J Neurosci 12(6):1867-81. [PubMed: 10886328]  [MGI Ref ID J:108087]

Ward NL; Hagg T. 1999. p75(NGFR) and cholinergic neurons in the developing forebrain: a re-examination. Brain Res Dev Brain Res 118(1-2):79-91. [PubMed: 10611506]  [MGI Ref ID J:59195]

Ward NL; Stanford LE; Brown RE; Hagg T. 2000. Cholinergic medial septum neurons do not degenerate in aged 129/Sv control or p75(NGFR)-/-mice(*) Neurobiol Aging 21(1):125-34. [PubMed: 10794857]  [MGI Ref ID J:62452]

Wiese S; Metzger F; Holtmann B; Sendtner M. 1999. The role of p75NTR in modulating neurotrophin survival effects in developing motoneurons. Eur J Neurosci 11(5):1668-76. [PubMed: 10215920]  [MGI Ref ID J:108091]

Woo NH; Teng HK; Siao CJ; Chiaruttini C; Pang PT; Milner TA; Hempstead BL; Lu B. 2005. Activation of p75NTR by proBDNF facilitates hippocampal long-term depression. Nat Neurosci 8(8):1069-77. [PubMed: 16025106]  [MGI Ref ID J:101447]

Wright JW; Alt JA; Turner GD; Krueger JM. 2004. Differences in spatial learning comparing transgenic p75 knockout, New Zealand Black, C57BL/6, and Swiss Webster mice. Behav Brain Res 153(2):453-8. [PubMed: 15265642]  [MGI Ref ID J:91879]

Yeo TT; Chua-Couzens J; Butcher LL; Bredesen DE; Cooper JD; Valletta JS; Mobley WC; Longo FM. 1997. Absence of p75NTR causes increased basal forebrain cholinergic neuron size, choline acetyltransferase activity, and target innervation. J Neurosci 17(20):7594-605. [PubMed: 9315882]  [MGI Ref ID J:107543]

Zagrebelsky M; Holz A; Dechant G; Barde YA; Bonhoeffer T; Korte M. 2005. The p75 neurotrophin receptor negatively modulates dendrite complexity and spine density in hippocampal neurons. J Neurosci 25(43):9989-99. [PubMed: 16251447]  [MGI Ref ID J:123448]

Zheng B; Atwal J; Ho C; Case L; He XL; Garcia KC; Steward O; Tessier-Lavigne M. 2005. Genetic deletion of the Nogo receptor does not reduce neurite inhibition in vitro or promote corticospinal tract regeneration in vivo. Proc Natl Acad Sci U S A 102(4):1205-10. [PubMed: 15647357]  [MGI Ref ID J:96121]

Zhou P; Porcionatto M; Pilapil M; Chen Y; Choi Y; Tolias KF; Bikoff JB; Hong EJ; Greenberg ME; Segal RA. 2007. Polarized signaling endosomes coordinate BDNF-induced chemotaxis of cerebellar precursors. Neuron 55(1):53-68. [PubMed: 17610817]  [MGI Ref ID J:128625]

Zhou XF; Li WP; Zhou FH; Zhong JH; Mi JX; Wu LL; Xian CJ. 2005. Differential effects of endogenous brain-derived neurotrophic factor on the survival of axotomized sensory neurons in dorsal root ganglia: a possible role for the p75 neurotrophin receptor. Neuroscience 132(3):591-603. [PubMed: 15837121]  [MGI Ref ID J:105141]

von Schack D; Casademunt E; Schweigreiter R; Meyer M; Bibel M; Dechant G. 2001. Complete ablation of the neurotrophin receptor p75NTR causes defects both in the nervous and the vascular system. Nat Neurosci 4(10):977-8. [PubMed: 11559852]  [MGI Ref ID J:71955]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryThe Ngfrtm1Jae strain is maintained by mating homozygous siblings. Homozygous mice may be ordered. The feet of these mice tend to become sore and to bleed because of the loss of sensory nerves. They need to be handled very carefully to minimize these problems. The lifespan is normal. Expected coat color from breeding:White Bellied Agouti

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3175.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4127.50
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   See control note: There are no appropriate physiological controls for this mutant strain. However, if you must have a control you may use either 129S3/SvImJ (Stock No. 002448) or BALB/cJ mice (Stock No. 000651) These strains also serve as DNA controls.
   002448 129S1/SvImJ (approximate)
   000651 BALB/cJ (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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