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Thyroid abnormalities and hepatocellular carcinoma in mice transgenic for v‐erbA.
Author(s) -
Barlow C.,
Meister B.,
Lardelli M.,
Lendahl U.,
Vennström B.
Publication year - 1994
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1994.tb06744.x
Subject(s) - biology , hepatocellular carcinoma , transgene , genetically modified mouse , carcinoma , cancer research , thyroid , thyroid carcinoma , medicine , endocrinology , genetics , gene
The v‐erbA oncogene consists of an avian retroviral gag gene fused to a mutated thyroid hormone receptor. To define better its role as an oncogene in mammals and its ability to function as a dominant negative transcription factor, transgenic mice expressing v‐erbA ubiquitously were generated. The effects of v‐erbA are pleiotropic, tissue‐specific and dose dependent. Mice have breeding disorders, abnormal behavior, reduced adipose tissue, hypothyroidism with inappropriate TSH response, and enlarged seminal vesicles. This provides an animal model consistent with the proposal that v‐ErbA functions as a dominant negative receptor by transcriptional interference or squelching of normal receptors or associated proteins. Finally, male animals develop hepatocellular carcinoma, demonstrating that v‐erbA can promote neoplasia in mammals.