First Look Strains

Stock Number	Name	Common Name	Description
037394	C57BL/6-Ctnna3^em1Cgot/J	Ctnna3	Ctnna3^KO 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-Gaa^em2Jhng/J	GaaA>	Gaa^c.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-Slc17a7^{tm1.1(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-Cdh8^{tm2c(KOMP)Wtsi}/DlbeJ	Cdh8	Cdh8^FL/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 Nrp1^tm1.1Chgu/J	Nrp1	Nrp1^VEGF- 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-Ch25h^tm1.1Syfu/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-RAD	Myh11-CreER^T2-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-Atxn1^em3Hzo/J	Atxn1<154Q[V591A;S602D]/2Q>	Atxn1^{154Q[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 Atxn1^154Q/2Q model of spinocerebellar ataxia type 1 (SCA1) (Stock No. 005601), however they are less severe.
037674	B6.129S7-Atxn1^em4Hzo/J	Atxn1<2Q[V591A;S602D]/2Q>	Atxn1^{2Q[V591A;S602D]/2Q} mice carry CRISPR/Cas9-generated V591A and S602D (mouse V566A and S577D) mutations in the wildtype Atxn1^2Q (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 Atxn1^{154Q[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-Gata2^tm1.1Dzk/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 Igdmr^em1Yste/J	IG-CGI	IG-CGI^f 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 Dmrt1^em1Zark/J	Dmrt1	Dmrt1^R111G 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-Kcnma1^em1Alme/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-Kcnma1^em2Alme/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-Kcnma1^em3Alme/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-Cd40^tm1.1Wgnr/HodeJ	CD40	CD40^fl/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-Il33^tm1Cln/J	Il33	Il33^cherry 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)-Nfkbia^tm1.1Pjc/J	IκBα	IκBα^M 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-K1^em1Tyj/AjgrJ	KStrep	K^bStrep 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-Clec9a^{tm4.1(cre/ERT2)Crs}/J	Clec9a	Clec9a^CreERT2 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-Clec9a^tm5.1Crs/J	Clec9a	Clec9a^tdTomato 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)-Ep300^tm1.1Kahn/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-Kcnb1^em1Sesf/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)-Il1b^em1Mora/J	IL-1β	IL-1β^fl 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-Agpat5^tm1Thor/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 Agpat5^flox 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-Kcnb1^em2Sesf/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 Atp5if1^{tm1c(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-Slc6a2^em1(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-Kcnq2^em3Frk/Mmjax	Kcnq2-T274M	Kcnq2^em3Frk 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)26Sor^{tm1.1(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)-Nos3^tm2.1Plh/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)-Nos3^tm3.1Plh/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-Grb10^tm1.1Esze/J	Grb10-H2B-Venus	Grb10^P2A-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-Grm3^tm1.1Conn/J	Grm3	Grm3^Fl 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)-Wapl^tm1.1Kpfe/J	Wapl	Wapl^Flox 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-Trpm4^em1Sthg/J	TRPM4	TRPM4^I1029M 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-Trpm4^em1Sthg/J	TRPM4	TRPM4^I1029M 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-Il1a^em1Tdk/J	Il1a-KO	The Il1a KO^{line 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-Ppara^em1Ngwu/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-Cebpa^em1Ngwu/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-Cebpb^em1Ngwu/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-Ppargc1a^em1Ngwu/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-Tshz1^tm1(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)-Meis1^em1Bcca/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 SYNGAP1^hu 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).

View Previous Strains

First Look Strains

Featured "First Look" Platforms:

HET3

NSG Flt3KO hFLT3LG Tg

NSG-SGM3-IL15

Csf1r^ΔFIRE

K^bStrep

iPSC

First Look Strains

Featured "First Look" Platforms:

HET3

NSG Flt3KO hFLT3LG Tg

NSG-SGM3-IL15

Csf1rΔFIRE

KbStrep

iPSC

Csf1r^ΔFIRE

K^bStrep