# Skinbase

##### Mouse Skin and Hair Database

## Aryl Hydrocarbon receptor null (Ahr) Chr12

- Relatively normal skin (left) with marked papillary epidermal hyperplasia (pseudoepitheliomatous hyperplasia) associated with onset of anagen in an aryl hydrocarbon receptor null mutant mouse.
- Marked transistion from relatively normal (left) to pseudoepitheliomatous hyperplasia in an aryl hydrocarbon receptor null mutant mouse.
- Marked pseudoepitheliomatous hyperplasia in an aryl hydrocarbon receptor null mutant mouse.

Aryl-hydrocarbon receptor-deficient (Ahr<tm1Gonz) mice, Chr 12, 18.0cM, NCBI Build 33 Ensemble annotation: 30530046-30566510
The aryl-hydrocarbon receptor (Ahr) is a ligand-activated transcription factor. It is a member of the basic-helix-loop-helix superfamily of DAN-binding proteins. It is activated by ligand binding and dimerization with the aryl-hydrocarbon receptor nuclear translocator (Arnt). The protein appears to be required to generate the harmful effects of toxic environmental chemicals such as dioxin, benzo-{a}pyrene in cigarette smoke, polychlorinated biphenyls, and polybrominated biphenyls.
Four spontaneous and 5 targeted mutations of the aryl-hydrocarbon receptor gene are reported. The illustrations provided here are from a limited longitudinal study of the B6;129-Ahr<tm1Gonz>/Ahr<tm1Gonz> targeted (null) mutant allele.
The B6;129-Ahr<tm1Gonz>/Ahr<tm1Gonz> mice developed progressive, severe, focal lesions on the dorsal skin that in some mice extended to the ears and lateral aspects of the abdomen. These lesions usually started with alopecia of the affected areas that progressed to ulcers of various degrees of severity. None of these changes were observed in age-, stock-, and gender-matched controls. Similar lesions were not seen in other mouse strains and stocks maintained in the same animal facility. The ventral skin was usually spared.
The skin consisted of widely separated individual dystrophic hair. The piliary canals were markedly dilated and contained structurally abnormal hair fibers. Alternatively, ruptured hair follicles were present associated with a mixed inflammatory cell infiltrate. Lesions progressed to acute ulcers of various sizes. These healed by pseudoepitheliomatous hyperplasia of the peripheral epidermis and dermal scarring.

### References

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