| Status | Available to order |
| EMMA ID | EM:14894 |
| International strain name | B6N.129-Loxtm1Soin/Oulu |
| Alternative name | B6.129-LoxtmSoin/Oulu |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Loxtm1Soin |
| Gene/Transgene symbol | Lox |
| Provider | Joni Mäki |
| Provider affiliation | University of Oulu |
| Genetic information | Lysyl oxidase (Lox) gene was inactivated by deleting its 1st exon in mouse embryonic stem (ES) cells. ES cells carrying the inactivated Lox gene were generated by two-step targeting method comprising homologous recombination followed by cre recombination. The presently submitted strain (EMMA ID EM:14894) is on C57BL/6N background to provide a wider background for this animal model. The same mutation is also carried by the previously submitted EM:07434 EMMA strain, which is on C57BL/6JOlaHsd background. The C57BL/6JOlaHsd substrain differs from other C57BL/6J substrains, as it carries a deletion in the Snca gene that is not present in any other B6 substrain. The Snca mutation may be of importance e.g. for studies on Parkinson’s disease. Most C57BL/6J mice have a deletion in Nnt gene that results in inappropriate glucose homeostasis in B6J male mice. Regarding this gene the C57BL/6JOlaHsd substrain resembles C57BL/6N lines, which do not carry this mutation. |
| Phenotypic information | Homozygous:Perinatal death, cardiovascular defects, pulmonary defects, muscular defects, bone abnormalities, collagen and elastin abnormalities. Heterozygous:Viable. No defects observed. |
| Breeding history | The Lox mouse line is backcrossed to C57BL/6N for hundreds of generations. |
| References |
|
| Homozygous fertile | no |
| Homozygous viable | no |
| Homozygous matings required | no |
| Immunocompromised | no |
| Archiving centre | University of Oulu, Oulu, Finland |
Orphanet associated rare diseases, based on orthologous gene matching
