B6.129P2-Vti1btm1Gfvm/Ieg
| Status | Available to order |
| EMMA ID | EM:15086 |
| Citation information | RRID:IMSR_EM:15086 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-Vti1btm1Gfvm/Ieg |
| Alternative name | Vti1b-/- |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Vti1btm1Gfvm |
| Gene/Transgene symbol | Vti1b |
Information from provider
| Provider | Gabriele Fischer von Mollard |
| Provider affiliation | Chemie, Biochemie III, Universität Bielefeld |
| Genetic information | A neomycin resistance cassette has been inserted into exon 4 of Vti1b, encoding amino acid residues 123-180, by homologous recombination in ES cells. |
| Phenotypic information | Homozygous:Vti1b-/- mice are viable without overt phenotypes. Subtle phenotypes can be observed such as reduced amounts of the SNARE partner syntaxin 8 and slower maturation of cytotoxic T-cells to secrete lytic granules. Vti1b is functionally redundant with Vti1a as Vti1a-/- Vti1b-/- embryos die perinatally.Heterozygous:Vti1b+/- mice are indistinguishable from wild-type mice. |
| Breeding history | The ES cell line E14.1 from 129Ola was used. Offspring was mated with C57BL/6 mice. Mouse strains were maintained with a mixed C57BL/6 x 129/Sv background for several years. Mice were backcrossed to C57BL/6 for 10 generations. Vti1b-/- mice were crossed with Vti1a-/- mice and are now bred as a single strain with Vti1a+/- Vti1b+/-, Vti1a-/- Vti1b+/- and Vti1a+/- Vti1b-/- mice. C57BL/6 is crossed in once or twice a year. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Helmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH), Oberschleißheim, Germany |
| Animals used for archiving | homozygous C57BL/6JRj males |
Literature references
- Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development.;Kunwar Ajaya J, Rickmann Michael, Backofen Bianca, Browski Sascha M, Rosenbusch Joachim, Schöning Susanne, Fleischmann Thomas, Krieglstein Kerstin, Fischer von Mollard Gabriele, ;2011;Proceedings of the National Academy of Sciences of the United States of America;108;2575-80; 21262811
- The exocytosis of lytic granules is impaired in Vti1b- or Vamp8-deficient CTL leading to a reduced cytotoxic activity following antigen-specific activation.;Dressel Ralf, Elsner Leslie, Novota Peter, Kanwar Namita, Fischer von Mollard Gabriele, ;2010;Journal of immunology (Baltimore, Md. : 1950);185;1005-14; 20543108
- Deletion of the SNARE vti1b in mice results in the loss of a single SNARE partner, syntaxin 8.;Atlashkin Vadim, Kreykenbohm Vera, Eskelinen Eeva-Liisa, Wenzel Dirk, Fayyazi Afshin, Fischer von Mollard Gabriele, ;2003;Molecular and cellular biology;23;5198-207; 12861006