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Stock Number | Name | Common Name | Description |
---|---|---|---|
037394 | C57BL/6-Ctnna3em1Cgot/J | Ctnna3 |
Ctnna3KO mice harbor a membrane associated eGFP construct inserted into exon 2 of the catenin (cadherin associated protein), alpha 3 gene (Ctnna3). These mice express eGFP-caax under the Ctnna3 promoter, while knocking-out endogenous Ctnna3 expression. These mice may be useful for studying localization and function of CTNNA3 at the subcellular level in the heart, brain and testes. |
037502 | C57BL/6NJ-Gaaem2Jhng/J | Gaa |
Gaac.1935C>A mice carry a CRISPR/Cas9 generated aspartic acid to glutamic acid change at amino acid 645 (Asp645Glu) in the glucosidase, alpha, acid (Gaa) gene, making this strain useful when studying Infantile Onset Pompe Disease (IOPD). |
037512 | B6.Cg-Slc17a7tm1.1(cre)Hze/J | Slc17a7-IRES2-Cre-D or Vglut1-IRES2-Cre-D | Slc17a7-IRES2-Cre-D knock-in mice have Cre recombinase expression directed to Vglut1-expressing cells, without disrupting endogenous vesicular glutamate transporter 1 expression. These mice may be useful for studying glutamatergic synaptic vesicle trafficking and vesicle-bound, sodium-dependent phosphate transportation. Stock No. 037512 is a C57BL/6J-congenic Slc17a7-IRES2-Cre-D knock-in mouse line. Of note, the same allele is also available on a B6;129S genetic background as Stock No. 023527. |
037592 | B6;129S4-Cdh8tm2c(KOMP)Wtsi/DlbeJ | Cdh8 |
Cdh8FL/FL mice have loxP sites flanking exon 3 of the cadherin 8 gene, making them useful for studying synaptic adhesion, axon outgrowth and guidance. |
037627 | STOCK Nrp1tm1.1Chgu/J | Nrp1 |
Nrp1VEGF- carry a D320K mutation in exon 6 of the mouse neuropilin 1 (Nrp1) gene that selectively disrupts binding to VEGF (vascular endothelial growth factor), a key regulator of angiogenesis. |
037647 | C57BL/6-Ch25htm1.1Syfu/J | Ch25h floxed | Ch25h floxed mice possess loxP sites flanking the only exon of the cholesterol 25-hydroxylase (Ch25h) gene. These mice may be useful for studying the role of Ch25h in lipid metabolism, inflammation, and innate immune responses. |
037658 | C57BL/6-Tg(Myh11-cre/ERT2)F31Gko/J | Myh11-CreER |
Myh11-CreERT2-RAD transgenic mice allow sufficient Myh11-driven tamoxifen-inducible cre expression in smooth muscle cells (SMCs) in the brachiocephalic artery (BCA) and aorta. This transgene integrated into mouse Chromosome 2 in a region devoid of other genes [Chr2:178,826,578-178,826,802 (GRCm39)]. Of note, Stock No. 019079 and Stock No. 036935 each contain a similar BAC transgene inserted on the Y chromosome and X Chromosome, respectively. |
037673 | B6.129S-Atxn1em3Hzo/J | Atxn1<154Q[V591A;S602D]/2Q> | Atxn1154Q[V591A;S602D]/2Q mice carry a 154Q repeat as well as V591A and S602D (mouse V566A and S577D) mutations in the mouse Atxn1 (ataxin 1) gene. Protein interactions with transcriptional repressor CIC (capicua) are disrupted. Heterozygotes display phenotypes similar to the Atxn1154Q/2Q model of spinocerebellar ataxia type 1 (SCA1) (Stock No. 005601), however they are less severe. |
037674 | B6.129S7-Atxn1em4Hzo/J | Atxn1<2Q[V591A;S602D]/2Q> | Atxn12Q[V591A;S602D]/2Q mice carry CRISPR/Cas9-generated V591A and S602D (mouse V566A and S577D) mutations in the wildtype Atxn12Q (ataxin 1) allele. Homozygotes demonstrate no ATXN1 binding to CIC (capicua). This strain has been useful in studies of spinocerebellar ataxia type 1 (SCA1), and acts as a potential control for Atxn1154Q[V591A;S602D]/2Q mice (Stock No. 037673). These mice will also be useful for the study of ATXN1-CIC protein interactions, independent of SCA1 disease. |
037700 | B6.129P2-Gata2tm1.1Dzk/J | Gata2Venus | Gata2Venus knock-in mice have an IRES and a Venus sequence inserted in the 3' UTR of the Gata2 gene. These mice are useful for studying real-time transcription and protein expression of Gata2 in vivo without affecting hematopoietic development or function. |
037713 | STOCK Igdmrem1Yste/J | IG-CGI |
IG-CGIf mice possess loxP sites flanking the CpG island (IG-CGI) located at the 5prime portion of an intergenic differentially methylated region (IG-DMR), which controls imprinting across the Dlk1-Dio3 domain. This strain may be useful for studying DNA methylation and genomic imprinting. |
037723 | STOCK Dmrt1em1Zark/J | Dmrt1 |
Dmrt1R111G knock-in mice express the R109G (aspargine to glycine amino acid substitution in the Dmrt1 (doublesex and mab-3 related transcription factor 1) locus. The R109G mutation is equivalent to the R111G mutation in humans. Male heterozygotes have gonadal dysgenesis with partial feminization of the transcriptome and are infertile. These mice may be useful in studies of male germ cells development as well as dominant complete gonadal dysgenesis and 46,XY sex reversal. |
037781 | C57BL/6J-Tg(Prnp-CHCHD10)U34Dkan/J | CHCHD10-WT | CHCHD10-WT mice harbor the human wildtype coiled-coil-helix-coiled-coil-helix domain containing 10 (CHCHD10) transgene driven by the endogenous prion (Prnp) promoter. These mice may be useful for studying amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and mitochondrial myopathies. These CHCHD10-WT mice may be used as controls for CHCHD10-R15L (Stock No. 037782) and CHCHD10-S59L (Stock No. 037783) transgenic models. |
037782 | C57BL/6J-Tg(Prnp-CHCHD10*R15L)U2Dkan/J | CHCHD10-R15L | CHCHD10-R15L mice harbor the human R15L mutation in the coiled-coil-helix-coiled-coil-helix domain containing 10 (CHCHD10) transgene driven by the endogenous prion (Prnp) promoter. These mice may be useful for studying amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and mitochondrial myopathies. The donating laboratory has made multiple Prnp-CHCHD10 transgenic lines available: CHCHD10-WT (Stock No. 037781), CHCHD10-R15L (Stock No. 037782) and CHCHD10-S59L (Stock No. 037783). |
037783 | C57BL/6J-Tg(Prnp-CHCHD10*S59L)U1Dkan/J | CHCHD10-S59L | CHCHD10-S59L mice harbor the human S59L mutation in the coiled-coil-helix-coiled-coil-helix domain containing 10 (CHCHD10) transgene driven by the endogenous prion (Prnp) promoter. These mice may be useful for studying amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and mitochondrial myopathies. The donating laboratory has made multiple Prnp-CHCHD10 transgenic lines available: CHCHD10-WT (Stock No. 037781), CHCHD10-R15L (Stock No. 037782) and CHCHD10-S59L (Stock No. 037783). |
037787 | C57BL/6J-Kcnma1em1Alme/J | KCNMA1-N999S | KCNMA1-N999S knock-in mice express a gain-of-function (GOF) asparagine to serine substitution at position 999 of the potassium large conductance calcium-activated channel, subfamily M, alpha member 1 gene. Mice exhibit increased channel activity, decreased seizure thresholds, and become immobile following (stress) restraint. These mice may be useful as a model for paroxysmal nonkinesigenic dyskinesia (PNKD3) with increased seizure propensity. Additional strains with patient-associated PKND3 mutations include KCNMA1-D434G (Stock No. 037788) and KCNMA1-H444Q (Stock No. 037789). |
037788 | C57BL/6J-Kcnma1em2Alme/J | KCNMA1-D434G | KCNMA1-D434G knock-in mice express a gain-of-function (GOF) autosomal dominant aspartic acid to glycine substitution at position 434 of the potassium large conductance calcium-activated channel, subfamily M, alpha member 1 (Kcnma) gene. Mice exhibit increased BK channel activity and decreased seizure thresholds. These mice may be useful for studying paroxysmal nonkinesigenic dyskinesia (PNKD3) with increased seizure propensity. Additional strains with patient-associated PKND3 mutations include KCNMA1-N999S (Stock No. 037787) and KCNMA1-H444Q (Stock No. 037789). |
037789 | C57BL/6-Kcnma1em3Alme/J | KCNMA1-H444Q | KCNMA1-H444Q knock-in mice express a loss-of-function (LOF) histidine to glutamine substitution at position 444 of the potassium large conductance calcium-activated channel, subfamily M, alpha member 1 (Kcnma1) gene. Mice exhibit locomotor dysfunction and hyperactive dyskinesia. These mice may be useful for studying paroxysmal nonkinesigenic dyskinesia (PNKD3). Additional strains with patient-associated PKND3 mutations include KCNMA1-N999S (Stock No. 037787) and KCNMA1-D434G (Stock No. 037788). |
037790 | B6N.Cg-Cd40tm1.1Wgnr/HodeJ | CD40 |
CD40fl/fl mice have loxP sites flanking exon 1 of the Cd40 gene. These mice may be useful when studying the progression of autoimmune diseases by CD40-driven effector programs in B cells and dendritic cells. |
037797 | C57BL/6J-Il33tm1Cln/J | Il33 |
Il33cherry knock-in/knock-out mice harbor an H2B-mCherry reporter cassette inserted between exons 4 and 5 of the interleukin 33 (Il33) locus. These mice may be useful for studying and tracking interleukin 33 activity. |
037800 | B6.129X1(Cg)-Nfkbiatm1.1Pjc/J | IκBα |
IκBαM knock-in mice harbor mutations in two NF-κB binding sites (M1 and M2) and 4 NF-κB-like binding sites (M3-M6) in the promoter region of the nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha gene (Nfkbia). These mice may be useful in studying the regulatory role of Nfkbia on NF-κB activity and autoimmune diseases. |
037803 | B6.Cg-H2-K1em1Tyj/AjgrJ | KStrep | KbStrep knock-in mice have an inverted StrepTagII, flanked by two pairs of inward-facing heterospecific Lox sites, inserted into intron 1 of the H2-K1 gene. Upon cre induction, recombination of the Lox sites results in the inversion of the StrepTagII into the correct transcriptional orientation. These mice may be useful for the selective purification of MHC-I peptide antigens from cell type(s) of interest from intact tissues. |
037804 | B6.Cg-Clec9atm4.1(cre/ERT2)Crs/J | Clec9a |
Clec9aCreERT2 knock-in mice have a P2A peptide fused to a cre/ERT2 sequence inserted into the C-terminal of the Clec9a gene. This strain is useful for dendritic cell lineage fate mapping and for studying adaptive immune responses to antigens in apoptotic and necrotic cells. |
037805 | B6.Cg-Clec9atm5.1Crs/J | Clec9a |
Clec9atdTomato knock-in/knock-out mice have tdTomato with a BGH_pA inserted into the ATG in exon 1 of the Clec9a gene. This strain is useful for dendritic cell lineage fate mapping and for studying adaptive immune responses to antigens in apoptotic and necrotic cells. |
037827 | B6.129(Cg)-Ep300tm1.1Kahn/J | p300 S89A | p300 S89A mice have a serine to alanine mutation (S89A) in exon 2 of the Ep300 gene. This mutation removes a highly conserved phosphorylation site at S89 making these mice useful when studying p300 signaling and its effects on intestinal homeostasis and repair. |
037835 | C57BL/6J-Kcnb1em1Sesf/J | Kcnb1 |
R312H knock-in (KI) is a CRISPR/Cas9 generated mutant of the potassium voltage gated channel, Shab-related subfamily, member 1 (Kcnb1) gene carrying the R312H knock-in mutation. These mice may be useful for studying the role of Kcnb1 in neocortical growth and Developmental and Epileptic Encephalopathies (DEEs). |
037836 | B6(FVB)-Il1bem1Mora/J | IL-1β |
IL-1βfl mice possess loxP sites flanking exon 4 of the Interleukin 1 beta (Il1b) gene. These mice may be useful in studying inflammation and autoimmune disease. |
037843 | C57BL/6-Agpat5tm1Thor/J | Agpat5 |
Exon 3 of the mouse Agpat5 (1-acylglycerol-3-phosphate O-acyltransferase 5 (lysophosphatidic acid acyltransferase, epsilon) gene is flanked by lox2272/loxP sites in these Agpat5flox mice. Cre recombinase-mediated excision of the floxed region results in a knock-out allele and expression of a tdTomato reporter useful in studies of agouti-related peptide neurons and their roles in insulin-induced hypoglycemia sensing and glucagon secretion. |
037848 | C57BL/6J-Kcnb1em2Sesf/J | Kcnb1 null | The Kcnb1 null allele is a CRISPR/Cas9 generated mutant of the potassium voltage gated channel, Shab-related subfamily, member 1 (Kcnb1) gene resulting in expression of a non-functional 337 amino acids truncated KCNB1 protein. These mice may be useful for studying the role of Kcnb1 in neocortical growth and Developmental and Epileptic Encephalopathies (DEEs). |
037864 | STOCK Atp5if1tm1c(EUCOMM)Wtsi/RtiJ | ATPIF1-floxed | Exon 3 of the Atp5if1 (ATPase 5 inhibitory factor 1) gene is flanked by loxP sites in this conditional mutant strain. These mice may be useful in Cre-lox studies of cardiac hypertrophy. |
037882 | C57BL/6J-Slc6a2em1(cre)Lbrl/J | Slc6a2-p2a-Cre | CRISPR-generated Slc6a2-p2a-Cre knock-in mice express cre recombinase from the mouse solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2 (Slc6a2) promoter. This strain has been useful in studies of area postrema excitatory neurons as they relate to nausea-associated behaviors. |
037894 | B6.Cg-Kcnq2em3Frk/Mmjax | Kcnq2-T274M | Kcnq2em3Frk is a CRISPR/Cas9 generated knock-in mutant to the Kcnq2 (potassium voltage-gated channel, subfamily Q, member 2) gene carrying the T274M (ACC to ATG) and T277T (silent PAM deleter) mutations. These mice may be useful in studying epilepsy. |
037912 | C57BL/6-Gt(ROSA)26Sortm1.1(CAG-Nfatc*,-tdTomato)Znlab/Mmjax | iNFATuation | iNFATuation knock-in mice conditionally express a peptide inhibitor (VIVIT) and tdTomato reporter. VIVIT selectively inhibits calcineurin/NFATC1-4 (nuclear factor of activated T cells, cytoplasmic, calcineurin dependent) interaction. iNFATuation mice maybe used for studies involving NFAT inhibition in a cell-type specific manner. |
037919 | B6.129S4(FVB)-Nos3tm2.1Plh/J | eNos S1176A | eNos S1176A knock-in mice harbor an amino acid substitution of serine to alanine in exon 26 of the nitric oxide synthase 3, endothelial cell (Nos3 or eNos) gene. These mice may be useful for studying the role of eNos in cardiovascular disease, hypertension, and metabolic syndrome. The donating laboratory also created a phosphomimetic eNos knock-in mouse line, S1176D (Stock No. 037920), which may be utilized as a positive control to the eNos S1176A knock-in mice. |
037920 | B6.129S4(FVB)-Nos3tm3.1Plh/J | eNos S1176D | eNos S1176D knock-in mice harbor an amino acid substitution of serine to aspartate in exon 26 of the nitric oxide synthase 3, endothelial cell (eNos) gene. These mice may be useful for studying the role of eNos in cardiovascular disease, hypertension, and metabolic syndrome. The donating laboratory also created a nonphosphorylatable eNos knock-in mouse line, S1176A (Stock No. 037919), which may be utilized as a negative control to the eNos S1176D knock-in mice. |
037930 | B6.Cg-Grb10tm1.1Esze/J | Grb10 |
Grb10P2A-H2B-Venus knock-in mice have a bicistronic reporter replacing the stop codon of exon 18 of the Grb10 gene. Specifically, this vector includes (from 5' to 3') an in frame replacement of the endogenous Grb10 stop codon with a P2A-H2B-Venus non-gene disruptive reporter cassette. Endogenous Grb10 expression is as expected in the brain, with nuclear Venus expression in cells that express the imprinted Grb10 locus. These mice may be useful in studying Grb10 function and imprinted-expression patterns in cellular growth, metabolism, neurogenesis and social behavior. |
037935 | C57BL/6J-Grm3tm1.1Conn/J | Grm3 |
Grm3Fl floxed mice have loxP sites flanking exon 3 of the Grm3 gene. These mice may be useful when studying the role of mGlu3 receptors in the regulation of synaptic plasticity and cognition. |
037951 | B6.129(Cg)-Wapltm1.1Kpfe/J | Wapl |
WaplFlox mice possess loxP sites flanking the endogenous promoter and exon 2 of the WAPL cohesin release factor (Wapl) gene. The mutation results in a hypomorph with WAPL protein levels reduced by two-fold. The strain may be useful in studies of cohesion and cohesinopathies. |
037966 | C57BL/6J-Trpm4em1Sthg/J | TRPM4 |
TRPM4I1029M knock-in mice express a gain-of-function (GOF) isoleucine to methionine substitution at position 1029 of the transient receptor potential cation channel, subfamily M, member 4 (Trpm4) gene. Heterozygous mice treated with imiquimod develop a psoriasis-like dermatitis. These mice may be useful as a model for progressive systemic erythrokeratodermia (PDEK). |
037966 | C57BL/6J-Trpm4em1Sthg/J | TRPM4 |
TRPM4I1029M knock-in mice express a gain-of-function (GOF) isoleucine to methionine substitution at position 1029 of the transient receptor potential cation channel, subfamily M, member 4 (Trpm4) gene. Heterozygous mice treated with imiquimod develop a psoriasis-like dermatitis. These mice may be useful as a model for progressive systemic erythrokeratodermia (PDEK). |
037967 | C57BL/6J-Il1aem1Tdk/J | Il1a-KO |
The Il1a KOline 2 mice have a CRISPR/Cas9 generated deletion of exons 2-6 of the interleukin 1 alpha (Il1a) gene. These mice may be useful when studying inflammatory pathways, hematopoiesis and immunity. |
037968 | C57BL/6J-Pparaem1Ngwu/J | PPARα HA knock-in | PPARα HA knock-in mice express an N-terminal HA-tag under direction of the endogenous Ppara promoter. This mouse strain could be useful for studying the regulatory mechanisms required to drive the energy-burning characteristics of brown adipocytes to counter obesity. |
037969 | C57BL/6J-Cebpaem1Ngwu/J | C/EBPα HA knock-in | C/EBPα HA knock-in mice express an N-terminal HA-tag under direction of the endogenous Cebpa promoter. This mouse strain could be useful for studying the energy-burning characteristics of brown adipocytes, weight homeostasis, gluconeogenesis, and lipogenesis. |
037970 | C57BL/6J-Cebpbem1Ngwu/J | C/EBPβ HA knock-in | C/EBPβ HA knock-in mice express an N-terminal HA-tag under direction of the endogenous Cebpb promoter. This mouse strain could be useful for studying the energy-burning characteristics of brown adipocytes, adipogenesis, and immune and inflammatory responses. |
037971 | C57BL/6J-Ppargc1aem1Ngwu/J | PGC1α HisHA knock-in | PGC1α HisHA knock-in mice express a C-terminal HisHA tag immediately upstream of the stop codon of the Ppargc1a gene. This mouse strain could be useful for studying the energy-burning characteristics of brown adipocytes and the regulation of energy metabolism. |
037972 | B6;129-Tshz1tm1(flpo)Zjh/J | Tshz1-2A-FlpO | Tshz1-2A-FlpO knock-in mice are designed to have optimized Flp recombinase expression directed to teashirt zinc finger family member 1-expressing cells. These mice may be used to generate conditional mutations for studying the function of TSHZ1 in neuronal differentiation, craniofacial development, and complex cognitive pathways. |
038030 | B6(Cg)-Meis1em1Bcca/AkarJ | MEIS1-EGFP | MEIS1-EGFP mice contain a CRISPR/Cas9-generated insertion of a GFP-P2A-HA immediately downstream of the endogenous Meis1 translational start site (TSS). These mice may be useful for tracking Meis1-expressing hematopoietic cells and for exploring MEIS1 function and regulation during normal and leukemic hematopoiesis. |
038083 | C57BL/6-Is(SYNGAP1-ZBTB9)1Bpro/Mmjax | SYNGAP1 |
Humanized SYNGAP1hu knock-in/knock-out mice express human SYNGAP1. RT-qPCR analysis from the mouse cortex indicates that these mice express no detectable mouse Syngap1, but do express an equivalent level of human SYNGAP1. This strain may be useful for studies of intellectual disability (ID) and autism spectrum disorder (ASD). |