Description

Strain Information

Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Generation +N1   Donating Investigator Rudolf Jaenisch,   Massachusetts Institute of Technology

Appearance
white-bellied agouti
Related Genotype: A^w/A^w

Description
Mice homozygous for the Ngfr^tm1Jae 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 Ngfr^tm1Jae 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
	002448 129S1/SvImJ	(approximate)
	000651 BALB/cJ	(approximate)
		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.
Considerations for Choosing Controls

Related Strains

Strains carrying   Ngfr^tm1Jae allele

002213

B6.129S4-Ngfrtm1Jae/J

View Strains carrying   Ngfr^tm1Jae     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Ngfr^tm1Jae/Ngfr^tm1Jae

        involves: 129 * BALB/c

• nervous system phenotype
• abnormal axon outgrowth (MGI Ref ID J:96121)
  • 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
  • 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

Ngfr^tm1Jae/Ngfr^tm1Jae

        involves: 129S4/SvJae * BALB/c

• nervous system phenotype
• abnormal dorsal root ganglion morphology (MGI Ref ID J:53825)
  • mice exhibit a loss of myelinated fibers in the dorsal root ganglion
• abnormal proprioceptive neuron morphology (MGI Ref ID J:53825)
  • mice exhibit a 50% loss of proprioreceptive neurons in L4 of the dorsal root ganglion
• small L4 dorsal root ganglion (MGI Ref ID J:53825)
  • at E14.5, L4 is smaller than in wild-type mice due to a 7.5-fold increase in apoptosis
• abnormal sensory neuron innervation (MGI Ref ID J:43748)
  • the dermis of fore- and hindlimb paws either lacks or have reduced numbers of Pde6a+ sensory fibers and small-diameter nerves are absent
  • only a few single fibers are present in the subepidermis and none are detected in the epidermis of fore- and hindlimb paws
  • reduced innervation is not restricted to hairless patches
  • however, sympathetic innervation of the iris and salivary glands is normal
  • at 3 to 5 months, Pde6a+ pulpal neurons are decreased
• decreased muscle spindle number (MGI Ref ID J:53825)
  • spindle density in the soleus, but no the medial gastrocnemius, plantaris and lumbrical muscles, is reduced 50% compared to in wild-type mice
• muscle phenotype
• abnormal muscle morphology (MGI Ref ID J:53825)
  • muscles exhibit fewer myelinated fibers than in wild-type mice (36+/-2 compared to 76+/-2 in wild-type mice)
• decreased muscle spindle number (MGI Ref ID J:53825)
  • spindle density in the soleus, but no the medial gastrocnemius, plantaris and lumbrical muscles, is reduced 50% compared to in wild-type mice
• behavior/neurological phenotype
• abnormal sensory capabilities/reflexes/nociception (MGI Ref ID J:43748)
  • prolonged latency in hot plate test
• homeostasis/metabolism phenotype
• extremity edema (MGI Ref ID J:43748)
  • at 4 months of age, mice exbihit edema in the fore- and hindlimb paws
• limbs/digits/tail phenotype
• ulcerated paws (MGI Ref ID J:43748)
  • at 4 months of age, fore- and hindlimb paws become edematous and develop severe ulcers
  • ulcers progress more proximally
  • ulcers are complicated by secondary infections that result in the lose of toenails and hair
  • epidermis and epidermal structures are lost from areas affected by ulcers
  • excessive epidermal proliferation is present at the edges of ulcers
• renal/urinary system phenotype
• *normal* renal/urinary system phenotype (MGI Ref ID J:43748)
  • unlike in studies using p75^NGFR oligonucleotide knockdown, kidney function is normal
• skin/coat/nails phenotype
• abnormal hair follicle structure/orientation (MGI Ref ID J:43748)
  • loss of follicles, at distal extremities, progressive to more proximal regions
• craniofacial phenotype
• abnormal mouth morphology (MGI Ref ID J:42087)
  • the height of the oral cavity is reduced
• abnormal tooth morphology (MGI Ref ID J:42087)
  • increased signs of wear on molars
• abnormal molar morphology (MGI Ref ID J:42087)
  • mandibular molar occlusal facets are longer than in wild-type mice
• abnormal molar crown morphology (MGI Ref ID J:42087)
  • maxillary molar crown height is reduced by 15%
  • however, full height of teeth is normal

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

Ngfr^tm1Jae/Ngfr⁺

        B6.129S4-Ngfr^tm1Jae

• nervous system phenotype
• abnormal neurogenesis (MGI Ref ID J:127639)
  • nerve coverage is less than in wild-type mice but not as severely reduced as in Ngfr^tm1Jae homozygotes
• abnormal axon outgrowth (MGI Ref ID J:127639)
  • neurons exhibit an intermediate effect to Sema3a repulsion that is more sensitive than wild-type neurons but not as sensitive as Ngfr^tm1Jae homozygotes
• respiratory system phenotype
• decreased airway responsiveness (MGI Ref ID J:115419)
  • 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)
  • total leukocytes, eosinophils and lymphocytes do not increase as in wild-type following exposure to provocation agent
  • unlike in exposed wild-type mice, no pulmonary eosinophilic inflammation is observed
  • unlike in exposed wild-type mice IL-4 and IL-5 production is not increased
  • while IgE levels increase following exposure to provocation they do not increase as much as in wild-type mice
  • however, interferon-gamma production following exposure to provocation agent is normal

Ngfr^tm1Jae/Ngfr^tm1Jae

        C;129S-Ngfr^tm1Jae/J

• nervous system phenotype
• abnormal neuron apoptosis (MGI Ref ID J:46125)
  • reduced levels of neuronal cell death

Ngfr^tm1Jae/Ngfr^tm1Jae

        B6.129S4-Ngfr^tm1Jae

• nervous system phenotype
• abnormal muscle innervation (MGI Ref ID J:90280)
  • areas of the epithelium of the tongue lack innervation and the filiform papillae are sparsely innervated
  • the axons in the tongue display reduced branching and smaller terminal arbors
• abnormal neurogenesis (MGI Ref ID J:127639)
  • peripheral nerves in the hindlimb, forelimb, and trigeminal ganglia are severely stunted compared to in wild-type mice
• abnormal axon outgrowth (MGI Ref ID J:127639)
  • growth cones from dorsal root ganglion neurons are more sensitive to Sema3A repulsion than wild-type neurons
  • 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)
  • however, increased sensitivity to Sema3A repulsion is alleviated in a double heterozygote cross of Ngfr and Sema3A
• abnormal neuron morphology (MGI Ref ID J:128451)
  • like wild-type neurons, cultured superior cervical ganglion neurons are resistant to apoptosis induced by pro-NGF and pro-BDNF
  • the number of sympathetic neurons is increased 33% at P4 and 39% at P15 compared to in wild-type mice
  • at 60 weeks sympathetic neuron cell bodies are 25% smaller than in wild-type mice
  • unlike in wild-type mice, superior cervical ganglion are protected from age-related apoptosis
• abnormal gustatory papillae taste buds (MGI Ref ID J:90280)
  • at P7 homozygous mice have 26% fewer vallate taste buds than wild-type mice
  • homozygous mice have fewer fungiform taste buds than wild-type mice
• abnormal sensory neuron innervation (MGI Ref ID J:90280)
  • innervation of the somatosensory prominences is reduced
  • innervation of the fungiform papillae are reduced
  • at P0 there are 35% fewer geniculate ganglion neurons that supply taste neurons to the fungiform papillae in homozygotes compared to wild-type mice
• increased neuron number (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
• increased retinal photoreceptor cell number (MGI Ref ID J:115542)
  • 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
  • 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
• digestive/alimentary phenotype
• abnormal tongue epithelium morphology (MGI Ref ID J:90280)
  • 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
• abnormal circumvallate papillae (MGI Ref ID J:90280)
  • the vallate papilla is deformed and small in neonatal mutants
  • at P7 the vallate trench is only 60% as deep as in wild-type mice
• cardiovascular system phenotype
• abnormal blood vessel healing (MGI Ref ID J:109753)
  • 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
  • however, infiltration of inflammatory cells is normal
  • apoptosis in neointimal lesions is decreased by 60% to 70%
• taste/olfaction phenotype
• abnormal gustatory papillae taste buds (MGI Ref ID J:90280)
  • at P7 homozygous mice have 26% fewer vallate taste buds than wild-type mice
  • homozygous mice have fewer fungiform taste buds than wild-type mice
• immune system phenotype
• abnormal Kupffer cell morphology (MGI Ref ID J:120368)
  • after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice
• increased susceptibility to experimental autoimmune encephalomyelitis (MGI Ref ID J:112769)
  • mice have an increased risk of developing severe experimental autoimmune encephalomyelitis compared to wild-type mice
  • B220+ B cells make up 6% of cells in the inflammatory cuffs compared to 15% in wild-type mice immunized with MOG35-55
  • the population of Iba-1+ cells in the inflammatory cuffs is reduced by 10% compared to in wild-type mice immunized with MOG35-55
  • polymorphonuclear cells are reduced by half compared to in wild-type mice immunized with MOG35-55
  • 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
  • however, the number of double-positive (monocyte) cells is normal
  • mice display considerable infiltration of fibronectin into the spinal cord parenchyma
• homeostasis/metabolism phenotype
• abnormal blood vessel healing (MGI Ref ID J:109753)
  • 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
  • however, infiltration of inflammatory cells is normal
  • apoptosis in neointimal lesions is decreased by 60% to 70%
• liver/biliary system phenotype
• abnormal Kupffer cell morphology (MGI Ref ID J:120368)
  • after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice
• vision/eye phenotype
• increased retinal photoreceptor cell number (MGI Ref ID J:115542)
  • 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
  • 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
• hematopoietic system phenotype
• abnormal Kupffer cell morphology (MGI Ref ID J:120368)
  • after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice

Ngfr^tm1Jae/Ngfr^tm1Jae

        B6.129S4-Ngfr^tm1Jae/J

• hearing/vestibular/ear phenotype
• cochlear hair cell degeneration (MGI Ref ID J:110434)
  • by 6 months, male homozygotes exhibit absence or damage of cochlear HCs in both the basal and upper turns
  • however, IHCs are still present and morphologically normal at 4 months, suggesting that SGN's dendrites connecting the IHCs are damaged earlier than IHCs
• decreased brainstem auditory evoked potential (MGI Ref ID J:110434)
  • at 4 months of age, male homozygotes exhibit a significant elevation (>33 dB SPL) in click-evoked ABR thresholds relative to wild-type males
  • 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)
  • however, no significant differences in click-evoked ABR thresholds are observed at 1 month, consistent with a normal cochlear structure at this age
• increased susceptibility to age-related hearing loss (MGI Ref ID J:110434)
  • starting at 4 months, male homozygotes display an age-related progressive hearing loss relative to age-matched wild-type males
  • by 1 year of age, homozygotes are unresponsive to click stimuli at the maximum level (136 dB SPL)
• organ of Corti degeneration (MGI Ref ID J:110434)
  • 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
  • by 6 months, male homozygotes show complete degeneration of the organ of Corti in the basal turns
• sensorineural hearing loss (MGI Ref ID J:110434)
  • male homozygotes show progressive hearing loss at 4 months, when both SGN degeneration and hair cell loss are observed in the basal cochlear turn
• nervous system phenotype
• cochlear ganglion degeneration (MGI Ref ID J:110434)
  • starting at 1 month, male homozygotes show a slight (15.7%) but progressive loss of SGNs from the basal to the apical cochlear turns
  • 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
  • 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
• cochlear hair cell degeneration (MGI Ref ID J:110434)
  • by 6 months, male homozygotes exhibit absence or damage of cochlear HCs in both the basal and upper turns
  • however, IHCs are still present and morphologically normal at 4 months, suggesting that SGN's dendrites connecting the IHCs are damaged earlier than IHCs

Ngfr^tm1Jae/Ngfr^tm1Jae

        involves: 129S4/SvJae * C57BL/6J

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

Ngfr^tm1Jae/Ngfr^tm1Jae

        involves: 129S4/SvJae

• nervous system phenotype
• abnormal cholinergic neuron morphology (MGI Ref ID J:62379)
  • increased size of cholinergic forebrain neurons
• abnormal sensory neuron innervation (MGI Ref ID J:43749)
  • absence of sensory innervation to pineal and sweat glands
• decreased neuron apoptosis (MGI Ref ID J:123022)
  • at E12 and E14, neuron apoptosis is reduced 72% and 70%, respectively, compared to in wild-type mice
  • nearly all neurons cultured with NT4 survive unlike wild-type neurons
• behavior/neurological phenotype
• abnormal spatial learning (MGI Ref ID J:62379)
  • spatial learning is improved compared to in wild-type mice without deterioration with age

Ngfr^tm1Jae/Ngfr^tm1Jae

        involves: 129S4/SvJae * C57BL/6

• nervous system phenotype
• abnormal axon outgrowth (MGI Ref ID J:139381)
  • 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
  • this lack of growth disadvantage in non-stimulated axons is due to less axon degeneration than occurs to wild-type neurons
• abnormal axon pruning (MGI Ref ID J:139381)
  • sympathetic neurons of the superior cervical ganglion (SCG) have improper pruning of axons from neurons that reach into both eye compartments
  • 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
  • mutant mice have a similar percentage of SCG neurons that connect to both eyes at P20 but this percentage does not decrease with age
  • 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

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Research Applications

This mouse can be used to support research in many areas including:

Ngfr^tm1Jae related

Apoptosis Research
Death Receptors

Neurobiology Research
Neurotrophic Factor Defects
Receptor Defects

Genes & Alleles

Gene & Allele Information

Allele Symbol		Ngfrtm1Jae
Allele Name		targeted mutation 1, Rudolf Jaenisch
Allele Type		Targeted (knock-out)
Common Name(s)		NGFRtm1Jac; Ngfr-; p75-; p75-KO; p75NGFR; p75NTR-; p75NTRexon3-null; p75exonIII-; p75NTR-; p75e3-;
Mutation Made By		Rudolf Jaenisch,   Whitehead Institute (MIT)
Strain of Origin		129S4/SvJae
ES Cell Line Name		J1
ES Cell Line Strain		129S4/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), STD PCR, vers. 1
Ngfr^tm1Jae, STD PCR, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

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]

Ngfr^tm1Jae 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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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]

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; 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]

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]

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]

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]

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

Health & Colony Maintenance Information

Colony Maintenance

Breeding & Husbandry	The 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
Diet Information	LabDiet® 5K52/5K67

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply

Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.

Supply Notes

Cryorecovery - Standard. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845. This strain is included in the Induced Mutant Resource Colony collection. Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	002448 129S1/SvImJ	(approximate)
	000651 BALB/cJ	(approximate)
		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.
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions

See Terms of Use

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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Ordering and Purchasing Information

      Purchasing Information
      JAX^® Mice Orders
      Surgical Services

Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form

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

Contracts Administration

phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (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 with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

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, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

No Liability

In no event shall The Jackson Laboratory, 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 The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.

MICE and biological materials 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 The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory 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 The Jackson Laboratory, 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 The Jackson Laboratory, 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 services by The Jackson Laboratory.