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N-terminal hamartin-binding and C-terminal GAP domain of tuberin can separate in vivo.

Authors: Momose, S  Kobayashi, T  Tada, N  Itoyama, S  Hino, O 
Citation: Momose S, etal., Biochem Biophys Res Commun. 2007 May 11;356(3):693-8. Epub 2007 Mar 13.
Pubmed: (View Article at PubMed) PMID:17379185
DOI: Full-text: DOI:10.1016/j.bbrc.2007.03.036

The Eker rat is an animal model of renal carcinogenesis and carries a transposon insertion in the Tsc2 (tuberous sclerosis-2) gene. We previously generated transgenic Eker rats and identified coding sequences in the Tsc2 gene that are responsible for suppression of renal carcinogenesis in Eker rats. Tsc2-RGH, a transgene that expresses the carboxy terminal region (amino acids 1425-1755) of the Tsc2 product (tuberin), partially suppressed renal carcinogenesis. However, Tsc2-DRG, which expresses a mutant tuberin lacking the carboxy-terminal region (Deltaaa 1425-1755), did not suppress renal carcinogenesis. Here, we found that introduction of both Tsc2-RGH and Tsc2-DRG in Eker rats completely suppressed renal carcinogenesis and rescued homozygous (Tsc2(Ek/Ek)) mutants from embryonic lethality in a complementary manner. Co-introduction of Tsc2-RGH and Tsc2-DRG, but not introduction of either alone, efficiently suppressed phosphorylation of p70 S6K. Thus, the functional domains of N-terminal hamartin binding and C-terminal tumor suppression in tuberin can separate in vivo.

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RGD Object Information
RGD ID: 1601351
Created: 2007-04-17
Species: All species
Last Modified: 2007-04-17
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.