B6;129S2-Crh^tm1Maj/J

Stock number: 002783
Product name: CRH-
Research areas: Developmental Biology Research, Endocrine Deficiency Research, Immunology, Inflammation and Autoimmunity Research, Neurobiology Research

Description

These Crh knock-out mice exhibit reduced adrenocortical secretion following stress and may be susceptible to complications from hypoglycemia when fasting. They may be useful in applications related to the study of role of glucocorticoid during development.

Detailed description

Mice homozygous for the Crh^tm1Maj targeted mutation are viable and fertile. Pups born to homozygous mothers must be supplemented with corticosterone in the drinking water (10-30ug/ml) from day 12 of gestation until weaning. Homozygous mutant mice have reduced adrenocortical secretion following stress. They may be susceptible to complications from hypoglycemia when fasting. Heterozygous mice are phenotypically indistinguishable from wildtype siblings.

Development

This strain was developed in the laboratory of Dr. Joseph Majzoub at Children's Hospital, Boston. The vector containing Pgk-neo replaced the entire coding region of the Crh gene. The 129-derived D3 ES cell line was used.

Allele

Symbol: Crh^tm1Maj
Name: targeted mutation 1, Joseph Majzoub
MGI accession ID: MGI:1857392
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Crh
Marker name: corticotropin releasing hormone
Chromosome: 3
Strain of origin: 129S2/SvPas
Molecular note: The sequences encoding the pre-propeptide region were replaced by a neomycin resistance cassette. RT-PCR analysis demonstrated that the transcript was absent in whole brain RNA derived from homozygous mice. Immunohistochemical analysis demonstrated that the protein was not detectable in sections of the amygdala and cerebral cortex of brains of homozygous mice.