J:NU

Stock number: 007850
Product name: outbred athymic nude
Research areas: Dermatology Research, Endocrine Deficiency Research, Immunology, Inflammation and Autoimmunity Research, Internal/Organ Research, Research Tools

Description

Outbred nude mice are immunodeficient tumor transplant hosts, and the standard in vivo model for drug efficacy testing in oncology.

Detailed description

Outbred homozygous nude (Foxn1^nu/Foxn1^nu) mice are the standard in vivo model for drug efficacy testing in oncology. Nude mice are athymic and hairless as a result of the recessive nu mutation. T cell precursors exist but development is blocked in the absence of a thymus, resulting in an immunodeficiency that permits transplantation of tumor cell xenografts. Homozygous females are poor breeders and fail to lactate. Heterozygous males and females breed well and have normal immune function. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers.

View Flow Cytometry Characterization Data for Immunodeficient JAX Strains

Development

Outbred athymic nude mice were recovered from cryopreserved NIH stocks received from the NIH Genetic Resource (now located at the University of Missouri MMRRC). These recovered stocks were then crossed with athymic nudes from NCI-Frederick using in vitro fertilization to maximize genetic diversity. The colony is maintained by a highly specialized outbred mating scheme, avoiding crosses between siblings to retain the widest possible genetic diversity and maximize animal vigor. The nude mutation was first recorded by Dr. N.R. Grist at the Virus Laboratory, Ruchill Hospital, Glasgow, Scotland.

Allele

Symbol: Foxn1^nu
Name: nude
MGI accession ID: MGI:1856108
Generation method: Spontaneous
Attributes: Null/Knockout
Synonyms: Foxnl^nu; hairless; nu; Whn^-
Marker symbol: Foxn1
Marker name: forkhead box N1
Marker synonyms: D11Bhm185e; FKHL20; Hfh11; Rnu; RONU; TIDAND; TLIND; whn
Chromosome: 11
Strain of origin: albino stock
Molecular note: A single base pair (G) deletion in exon 3 introduces a frameshift and a premature stop codon. The encoded protein is predicted to terminate upstream of the DNA-binding domain.