B6.129P2(Cg)-Kcnj8tm1.2Geno/H
| Status | Available to order |
| EMMA ID | EM:13464 |
| Citation information | RRID:IMSR_EM:13464 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | B6.129P2(Cg)-Kcnj8tm1.2Geno/H |
| Alternative name | Kir6.1 Global KO |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Kcnj8tm1.2Geno |
| Gene/Transgene symbol | Kcnj8 |
Information from provider
| Provider | Andrew Tinker |
| Provider affiliation | William Harvey Research Institute, QMUL |
| Genetic information | In collaboration with Genoway (Lyon, France; project number genOway/EV/TIN1-Kcnj8070206), we targeted exon 2 of the mouse Kcnj8 (Kir6.1) gene. Using homologous recombination a lox P site together with a FRT flanked neomycin selection cassette was inserted within intron 1 upstream of exon 2. Exon 2 contains the ATG translation initiation codon and another loxP was inserted distal to exon 2 in intron 2. The targeting construct was transfected into E14Tg2a ES cells derived from 129P2/Ola mice and one positive clone was isolated that had the intended 5’ and 3’ homologous recombination event in one allele. There were no other randomly integrated copies of the targeting vector. This ES cell clone was injected into C57BL/6J blastocysts and implanted into pseudo-pregnant females. A number of male chimaeras were bred with Flp deleter mice to remove the neomycin cassette and generate Kir6.1(+/flx) mice. |
| Phenotypic information | Homozygous:Knock-out mice will likely die from sudden cardiac death (SCD) at adulthood.Heterozygous:Normal |
| Breeding history | The Kir6.1(+/flx) were crossed with C57BL/6 cre deleter mice (which ubiquitously express the cre recombinase) to develop mice with global genetic deletion of one allele of Kir6.1 (Kir6.1 +/-). Kir6.1 +/- and Kir6.1(+/flx) were backcrossed onto a C57BL/6 background for at least six generations. Homozygous knock-out (Kir6.1 -/-) mice were generated by cross-breeding of the Kir6.1 +/- heterozygous mice. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | not known |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Literature references
- The ATP-sensitive potassium channel subunit, Kir6.1, in vascular smooth muscle plays a major role in blood pressure control.;Aziz Qadeer, Thomas Alison M, Gomes John, Ang Richard, Sones William R, Li Yiwen, Ng Keat-Eng, Gee Lorna, Tinker Andrew, ;2014;Hypertension (Dallas, Tex. : 1979);64;523-9; 24914196
- Vascular KATP channels protect from cardiac dysfunction and preserve cardiac metabolism during endotoxemia.;Aziz Qadeer, Chen Jianmin, Moyes Amie J, Li Yiwen, Anderson Naomi A, Ang Richard, Aksentijevic Dunja, Sebastian Sonia, Hobbs Adrian J, Thiemermann Christoph, Tinker Andrew, ;2020;Journal of molecular medicine (Berlin, Germany);98;1149-1160; 32632751
- A critical role for the ATP-sensitive potassium channel subunit KIR6.1 in the control of cerebral blood flow.;Hosford Patrick S, Christie Isabel N, Niranjan Arun, Aziz Qadeer, Anderson Naomi, Ang Richard, Lythgoe Mark F, Wells Jack A, Tinker Andrew, Gourine Alexander V, ;2019;Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism;39;2089-2095; 29862863