Allele Symbol Strain Description
Stock Number
Strain Name (link to Data Sheet)
Cacna1ftm1.2Sdie
017762Under Development for Cryo
B6(Cg)-Cacna1ftm1.2Sdie /J
These mice carry the I756T point mutation in exon 17, and loxP sites flanking exons 14 through 17, of the Cacna1f (calcium channel, voltage-dependent, alpha 1F subunit). This mutant mouse strain may be useful in studies of calcium channelopathies, an inherited retinal disorder, photoreceptor electrophysiology, and the role of the Cav1.4 channel in survival of naive T cells.
Cacna1ftm1Sdie
017760Under Development for Cryo
B6(Cg)-Cacna1ftm1Sdie /J
These I756T+neo mice carry the I756T point mutation in exon 17 of the Cacna1f , calcium channel, voltage-dependent, alpha 1F subunit, (756 is the mouse equivalent to residue 745 in human CACNA1F ) as well as a FRT flanked NEO selection cassette and loxP sites flanking exons 14 through 17. This mutant mouse strain may be useful in studies of calcium channelopathies, incomplete congenital stationary night blindness, photoreceptor electrophysiology, and the role of the Cav1.4 channel in survival of naive T cells.
Cln3tm1.1Mem
017895In Progress
B6.129(Cg)-Cln3tm1.1Mem /J
These Cln3Δex7/8 knock in mice exhibit sensorimotor deficits, retinal degeneration, metabolic, hematological abnormalities, and accumulate mitochondrial ATPase subunit c, and may be useful in studies of juvenile onset neuronal ceroid lipofuscinosis (JNCL), also known as Batten or Spielmeyer-Vogt disease.
Cmahtm1Avrk
017929Awaiting Transfer from the Donor
B10.Cg-Cmahtm1Avrk Dmdmdx /PtmJ
These Cmah-mdx mice are useful for studying how human-like CMAH-deficiency accelerates the onset and severity of the Duchenne muscular dystrophy (DMD) seen in Dmdmdx mice. These mice are useful for studying the metabolic accumulation of dietary N -glycolylneuraminic acid (Neu5Gc; a foreign sialyl-containing glycan in humans and Cmah-deficient mice), the subsequent generation of Neu5Gc-specific antibodies and the deposition of activated (C5b-9) complement on muscle fibers. These Cmah-mdx mice represent a new small animal model for DMD that better approximates the human glycome and its contributions to muscular dystrophy.
Dmdmdx
017929Awaiting Transfer from the Donor
B10.Cg-Cmahtm1Avrk Dmdmdx /PtmJ
These Cmah-mdx mice are useful for studying how human-like CMAH-deficiency accelerates the onset and severity of the Duchenne muscular dystrophy (DMD) seen in Dmdmdx mice. These mice are useful for studying the metabolic accumulation of dietary N -glycolylneuraminic acid (Neu5Gc; a foreign sialyl-containing glycan in humans and Cmah-deficient mice), the subsequent generation of Neu5Gc-specific antibodies and the deposition of activated (C5b-9) complement on muscle fibers. These Cmah-mdx mice represent a new small animal model for DMD that better approximates the human glycome and its contributions to muscular dystrophy.
Dmdmdx
018018Awaiting Transfer from the Donor
B10ScSn.Cg-Prkdcscid Dmdmdx /J
MDX/SCID mice exhibit necrosis, centrally located nuclei and and the muscle degeneration characteristic of DMD and may be used a dystrophic model for the transplantation of human donor cells to evaluate skeletal muscle regeneration.
Dmdmdx
013141Awaiting Transfer from the Donor
D2.B10-Dmdmdx /J
These Dmdmdx mutant mice may be useful for studying Duchenne muscular dystrophy (DMD).
Eya4TgTn(Prm1-sb10,sb-Tyr)1739AOve
017594Awaiting Transfer from the Donor
FVB;B6-Eya4TgTn(Prm1-sb10,sb-Tyr)1739AOve /J
These OVE1739A mice harbor a mutation created by random insertion of co-injected transgenes pT-Tybs-3'E and Prm-SB10. Using inverse PCR analysis, the
integration site of the co-injected transgenes is near the eyes absent 4 homolog [Drosophila] locus (Eya4 ) on mouse chromosome 10. These OVE1739A mice may be useful for studying cleft palate, as well as middle ear morphology, otitis media, and incomplete fusion of palatal bones during skull development.
Hfe2tm1Nca
017788In Progress
129S-Hfe2tm1Nca /J
These Hfe2 knockout mice exhibit iron loading and have applications in studies of juvenile or Type2A hemochromatosis, iron homeostasis and iron-induced oxidative damage.
Prkdcscid
018018Awaiting Transfer from the Donor
B10ScSn.Cg-Prkdcscid Dmdmdx /J
MDX/SCID mice exhibit necrosis, centrally located nuclei and and the muscle degeneration characteristic of DMD and may be used a dystrophic model for the transplantation of human donor cells to evaluate skeletal muscle regeneration.
Prom1tm1(cre/ERT2)Gilb
017743In Progress
B6N;129S-Prom1tm1(cre/ERT2)Gilb /J
A CreERT2 fusion protein and β-galactosidase (lacZ ) gene knocked into the ATG start codon of Prom1 abolishes gene function in these mice. Useful applications include visualizing and tracking adult stem cell lineages.
Sema5btm1.2Alk
017534Awaiting Transfer from the Donor
B6.129(Cg)-Sema5btm1.2Alk /J
This knockout strain of the Sema5b gene exhibits no obvious abnormal phenotype, but when mated with a Sema5a knockout mouse, development of the neural tissue of the eye is impacted in the offspring.
Slc26a4tm1Egr
018424Awaiting Transfer from the Donor
129S-Slc26a4tm1Egr /AjgJ
Pds-/- mice are useful for studying deafness and vestibular dysfunction associtated with Pendred syndrome.
Tas1r2tm1Csz
013065In Progress
B6.129-Tas1r2tm1Csz /J
This strain carries a targeted mutation of the Tas1r2 (taste receptor, type 1, member 2) gene which encodes a component of the heterodimeric G-protein coupled sweet receptor. Sweet (D-amino acids, sucrose, maltose, glucose, saccharin) tastant responses are severely defective. This strain may be useful in studies of taste and nutrient sensing.
018064Awaiting Transfer from the Donor
B6.129S1-Plcb2tm1Dwu /J
Plcb2 (phospholipase C, beta 2) knockout mice show enhanced resistance to viral and bacterial infection, and lack sweet and bitter taste reception.
017761Under Development for Cryo
C57BL/6-Cacna1ftm1.1Sdie /J
These mice carry a targeted mutation with exons 14 through 17 of the Cacna1f (calcium channel, voltage-dependent, alpha 1F subunit) gene deleted. This mutant mouse strain may be useful in studies of calcium channelopathies, incomplete congenital stationary night blindness, photoreceptor electrophysiology, and the role of the Cav1.4 channel in survival of naive T cells.