JAX Mice Database - Mouse/Human Gene Homologs

New strains under development - Research area: Mouse/Human Gene Homologs

View a Full List of New Strains Under Development Sorted by Gene Symbol.
Go Back To REGISTER INTEREST: New Strains Under Development.
Select another Research Area.

Strains Newly Available for all Mouse/Human Gene Homologs models.

View all Research Models for Mouse/Human Gene Homologs

Search JAX^® Mice Database

How to Register Interest

Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

Mouse/Human Gene Homologs

Allele Symbol Strain Description	Stock Number	Strain Name (link to Data Sheet)
Atcay^ji	008140 Under Development for Production	B6.C(Cg)-Atcay^ji/BurJ
Mice homozygous for the spontaneous mutation, jittery (ji) in Atcay (ataxia, cerebellar, Cayman type homolog), exhibit severe, progressive ataxia and die at approximately 4 weeks of age. This mutant mouse strain represents a model that may be useful in studies of congenital ataxia.
Foxp3^sf	006775 On Hold	NOD.Cg-Foxp3^sf/DoiJ

Fxn^tm1Mkn	008398 Under Development for Production	B6.Cg-Fxn^tm1Mkn Tg(FXN)YG8Pook/J
Mice that are homozygous for the Fxn^tm1Mkn (frataxin) targeted allele and hemizygous for the Tg(FXN)YG8Pook (frataxin, human) transgene, display an age dependent, tissue specific expansion of the GAA repeat, with expansion accumulation in the CNS (particularly cerebellum), similar to the human pathology of Friedreich Ataxia. This strain is maintained heterozygous for the targeted mutation and hemizygous for the transgene.
Mecp2^tm1Bird	006847 Under Development for Production	B6;129P2-Mecp2^tm1Bird/J
Mice with this X-linked floxed mutation of the methyl CpG binding protein 2 gene may be useful in neurological and developmental studies of Rett syndrome.
Myo5a^d	006255 Under Development for Production	BXD25/TyJRwwJ
The BXD# recombinant inbred (RI) strains originate from crosses between C57BL/6J and DBA/2J. They may be used to study the genetics of behavioral phenotypes (including alcohol and drug addiction, stress, and locomotor activity) and complex or potentially complex physiologic phenotypes (including differences in organ weight and bone mineral density).
Ncf1^m1J	004742 On Hold	B6(Cg)-Ncf1^m1J/J

Pomc^tm2Ute	008115 Under Development for Production	B6.129X1-Pomc^tm2Ute/J
These mutant mice lack pro-opiomelanocortin-alpha (POMC) and all POMC-derived peptides. Homozygotes are twice the weight of wildtype controls and have no detectable serum adrenocorticotropic hormone (ACTH), corticosterone, or aldosterone. This mutant mouse strain may be useful in studies of obesity, energy homeostasis and endocrinology.
Sgca^tm2Kcam	008275 Under Development for Production	B6.129S6-Sgca^tm2Kcam/J
A loxP-flanked neomycin resistance cassette blocks expression of a His77Cys (H77C) missense mutation introduced to exon 3 of the gene. The mice develop progressive muscular dystrophy shortly as early as six weeks of age with typical pathological changes in skeletal muscle and an elevation of serum creatine kinase activity. After germline- or striated muscle-specific Cre-mediated excision of the floxed neomycin cassette, the locus expresses a transcript bearing the H77C missense mutation. The mutant protein is expressed in the sarcolemma of striated muscles, and homozygotes do not show any sign of muscular dystrophy as late as 88 weeks of age.
Sox10^Dom	000290 On Hold	B6C3Fe a/a-Sox10^Dom/J

Trp53^tm2Xu	007218 Under Development for Production	B6.129S6-Trp53^tm2Xu/J
This targeted mutation of Trp53 (transformation related protein 53) contains two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes from mice homozygous for this allele. This mutant mouse strain may be useful in studies of phosphorylation events, cancer development and apoptosis.
a	000290 On Hold	B6C3Fe a/a-Sox10^Dom/J

Tg(APOE-DGAT2)24Far	007744 Under Development for Production	C57BL/6-Tg(APOE-DGAT2)24Far/J
These Liv-DGAT2-low transgenic mice may be useful in studying hepatic steatosis, lipid, glucose, and insulin metabolism, as well as obesity and diabetes.
Tg(APOE-NPC1L1)20Lqyu	008408 Under Development for Production	B6;D2-Tg(APOE-NPC1L1)20Lqyu/J
These transgenic mice express the human NPC1 (Niemann-Pick disease, type C1, gene)-like 1 (NPC1L1) gene under the control of the human apolipoprotein E (APOE) promoter and hepatic control region. This mutant mouse strain exhibits decreased biliary cholesterol levels, which is associated with increased plasma cholesterol levels, and may be useful in studies related to lipid metabolism and cholesterol transport.
Tg(Ckmm-cre)5Khn	008275 Under Development for Production	B6.129S6-Sgca^tm2Kcam/J
A loxP-flanked neomycin resistance cassette blocks expression of a His77Cys (H77C) missense mutation introduced to exon 3 of the gene. The mice develop progressive muscular dystrophy shortly as early as six weeks of age with typical pathological changes in skeletal muscle and an elevation of serum creatine kinase activity. After germline- or striated muscle-specific Cre-mediated excision of the floxed neomycin cassette, the locus expresses a transcript bearing the H77C missense mutation. The mutant protein is expressed in the sarcolemma of striated muscles, and homozygotes do not show any sign of muscular dystrophy as late as 88 weeks of age.
Tg(FXN)YG8Pook	008398 Under Development for Production	B6.Cg-Fxn^tm1Mkn Tg(FXN)YG8Pook/J
Mice that are homozygous for the Fxn^tm1Mkn (frataxin) targeted allele and hemizygous for the Tg(FXN)YG8Pook (frataxin, human) transgene, display an age dependent, tissue specific expansion of the GAA repeat, with expansion accumulation in the CNS (particularly cerebellum), similar to the human pathology of Friedreich Ataxia. This strain is maintained heterozygous for the targeted mutation and hemizygous for the transgene.
Tg(HDexon1)61Gpb	007578 Under Development for Production	CBy.Cg-Tg(HDexon1)61Gpb/J
These HDexon1 mice may be useful in Huntington's Disease research.
Tg(HDexon1)62Gpb	004601 On Hold	B6CBA-Tg(HDexon1)62Gpb/2J

Tg(Ins2-IAPP)RHFSoel	008232 Under Development for Production	FVB/N-Tg(Ins2-IAPP)RHFSoel/J
These RIPHAT transgenic mice express human islet amyloid polypeptide (h-IAPP) under the regulatory control of the rat insulin II promoter and may be useful in studying the beta-cell destruction and islet amyloid deposition associated with non-insulin-dependent diabetes mellitus (NIDDM) or Type II diabetes, as well as beta-cell apoptosis and characteristics of the endoplasmic reticulum (ER) stress pathway.
Tg(MMTV-neu/OT-I/OT-II)CBnel	007962 Under Development for Production	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J
Approximately 85% of the compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neu^OT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age.
Tg(Nes-cre)1Kln	006847 Under Development for Production	B6;129P2-Mecp2^tm1Bird/J
Mice with this X-linked floxed mutation of the methyl CpG binding protein 2 gene may be useful in neurological and developmental studies of Rett syndrome.
Tg(SOD1*G37R)42Dpr	008342 Under Development for Production	B6.Cg-Tg(SOD1*G37R)42Dpr/J
These high-expressing G37R(42) (or G37R-SOD1 line 42) transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).
Tg(SOD1*G85R)148Dwc	008248 Under Development for Production	B6.Cg-Tg(SOD1*G85R)148Dwc/J
These G85R-SOD1 transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).
Tg(Thy1-APPSwDutIowa)BWevn	007027 Under Development for Production	C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/J
These transgenic mice express the human amyloid beta-precursor protein, APP gene, 770 isoform, with the Swedish K670N/M671L, Dutch E693Q and Iowa D694N mutations, under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. Plaque-like deposits of amyloid beta that are similar to the plaques observed in human patients with the Dutch and Iowa familial disorders, are initially detected at approximately 3 months of age in the subiculum, hippocampus and cortex. Amyloid beta deposits are detected throughout the forebrain by 12 months of age. This mutant mouse strain may be useful in studies of Alzheimer's disease.
Tg(Thy1-SOD1*G93A)T3Hgrd	008230 Under Development for Production	FVB(Cg)-Tg(Thy1-SOD1*G93A)T3Hgrd/J
Thy1.2-G93A (or T3) transgenic mice express human G93A mutant SOD1 (G93A-SOD1)in neurons throughout the brain and spinal cord (including spinal motor neurons), and may be useful in studying neuromuscular disorders, such as Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).
Tg(Trp53R172H)8512Jmr	007962 Under Development for Production	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J
Approximately 85% of the compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neu^OT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age.

(25 stocks)

Select another Research Area Application:

Send questions to our Technical Support team using the Express Technical Support Form.
(2.15)