型号:GM-J#035186 -Cryorecovery
应用:In these 5-HT3A cKO mice, exon 2 of the mouse Htr3a (5-hydroxytryptamine (serotonin) receptor 3A; also called 5-HT3A) gene was replaced by a cassette consisting of two versions of exon 2: FLP-mediated recombination converts it randomly into HA-mVenus tagged exon 2 or FLAG tagged exon 2. Cre-mediated recombination is anticipated to result in deletion of exon 2 and a knock-out of the gene (not yet confirmed - April, 2020). This is a tool mouse line that will be useful for the community for identification of 5HT3A-receptor positive interneurons.
型号:GM-J#035178 -Cryorecovery
应用:HA-RARalpha KI knock-in mice express hemagglutinin-tagged mouse RARA (retinoic acid receptor, alpha) protein. Cre recombinase-mediated excision of floxed exons 4 and 5 results in the production of hemagglutinin-tagged RARA protein lacking the DNA binding domain.
型号:GM-J#035169 -Available
应用:The inducible KPC:APC mouse model of KRAS mutated colorectal cancer combines the oncogenic conditional KrasG12D allele, the conditional Apcfl allele and a tamoxifen inducible Cre recombinase (CDX2-Cre-ERT2) with cre expression in adult epithelium of the distal intestinal tract. Mice develop malignant colonic tumors 25-30 days post tamoxifen induction.
型号:GM-J#035136 -Cryorecovery
应用:Cre-inducible-Mps1-Knock-in-TA (CiMKiTA) mice carry a Cre-inducible point mutation (T649A) in exon 17 of the Ttk protein kinase (Ttk) gene, expression of which is blocked by the presence of a loxP-flanked cDNA cassette encoding exons 17-22 and a stop codon. This mutation results in a mutant protein similar to that found in human cell lines with a mild chromosomal instability (CIN) phenotype. This strain may be useful when studying oncogenic potential due to the degree and site of chromosomal instability.
型号:GM-J#035093 -Cryorecovery
应用:Krt6-CreERmice have a CRISPR/Cas9 generated insertion of an IRES-Cre/ERT2-SV40pA cassette inserted into the 3' UTR of the Krt6a gene, without disrupting endogenous gene expression. These mice may be used to generate tamoxifen-induced conditional mutations for studying gain-or-loss of function and/or fate mapping related to KRT6A expression during stem cell differentiation.
型号:GM-J#035092 -Available
应用:Sox9-CreER mice have a CRISPR/Cas9 generated insertion of an IRES-Cre/ERT2-SV40pA cassette inserted into the 3' UTR of the Sox9 gene, without disrupting endogenous gene expression. These mice may be used to generate tamoxifen-induced conditional mutations for studying gain-or-loss of function and/or fate mapping related to SOX9 expression during stem cell differentiation.
型号:GM-J#035046 -Cryorecovery
应用:NK1R-CreER knock-in/knock-out mice have the endogenous tachykinin receptor 1 promoter/enhancer sequences directing expression of tamoxifen-inducible Cre recombinase. These mice are a Cre-lox tool allowing inducible Cre recombination in Tacr-expressing cells/tissues (including neurons of the amygdala, hypothalamus, cortex, and spinal cord), and may be useful in studying Substance P signaling, inflammatory responses, and pain.
型号:GM-J#035045 -Cryorecovery
应用:KOR-Cre knock-in/knock-out mice have the endogenous kappa opioid receptor promoter/enhancer sequences directing expression of Cre recombinase. These mice are a Cre-lox tool allowing Cre recombination in Oprk1-expressing cells/tissues (including neurons of the cortex and striatum, retina, lung, liver, and kidney), and may be useful in studying reward, pain, and nociception.
型号:GM-J#034918 -Cryorecovery
应用:Nur77RFP BAC transgenic mice express turbo red/orange fluorescent protein (tRFP) from the mouse Nr4a1 (nuclear receptor subfamily 4, group A, member 1; Nur77) promoter. These mice are useful in studying thymocyte selection as well as lymphocyte activation, and can be used as a reporter of T cell receptor signaling strength.
型号:GM-J#034875 -Cryorecovery
应用:Ndnf-IRES-CreERT2 knock-in mice have a cre/ERT2 fusion gene inserted into the 3' UTR in exon 4 of the neuron-derived neurotrophic factor (Ndnf) gene. These mice retain endogenous Ndnf expression and may be used to generate conditional mutations for studying gain-or-loss of function, fate mapping and/or circuit dissection of NDNF+ cell populations.