| Status | Available to order |
| EMMA ID | EM:09859 |
| International strain name | B6.129-Scnn1btm1Wsh/Ph |
| Alternative name | bmENaC |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Scnn1btm1Wsh, |
| Gene/Transgene symbol | Scnn1b |
| Provider | Michael Welsh |
| Provider affiliation | Pappajohn Biomedical Institute, The University of Iowa |
| Additional owner | Prof. Michael Welsh, The University of Iowa, Iowa City, USA and Prof. Fiona McDonald, University of Otaga, Dunedin, New Zealand |
| Genetic information | The bmENaC (Scnn1b) targeting vector was introduced into R1 ES cells by electroporation, and surviving G418 and ganciclovir resistant clones were screened by Southern blotting. |
| Phenotypic information | Homozygous:The bENaC-deficient mice (-/-) show normal prenatal development but die within 2 days after birth, most likely of hyperkalemia. The phenotype of the bENaC-deficient mice is similar to that of humans with pseudohypoaldosteronism type 1.Heterozygous:The bENaC heterozygous mice (+/-) are viable and fertile. |
| Breeding history | The line was maintained by crossing bmENaC +/- with bmENaC +/- or by crossing bmENaC +/- with wild-type (C57BL/6) mice. |
| References |
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| Homozygous fertile | no |
| Homozygous viable | no |
| Homozygous matings required | no |
| Immunocompromised | no |
| Archiving centre | Institute of Molecular Genetics, Prague, Czech Republic |
| Animals used for archiving | heterozygous 0 |
MGI allele-associated human disease models
Orphanet associated rare diseases, based on orthologous gene matching
