Disease relevance of CRTC3

• By using a luciferase assay system, we show that TORC3 alone can enhance transcription from the HTLV-I LTR, as well as from a cellular cyclic AMP-response element (CRE) [1].

High impact information on CRTC3

• The other two members of the TORC family, TORC2 and TORC3, also strongly activated PGC-1alpha transcription [2].
• Here, we present evidence that transducer of regulated cyclic AMP-response element-binding protein 3 (TORC3), a co-activator of CREB, is involved in Tax-induced transcriptional activation from the HTLV-I LTR [1].
• Interestingly, we find that co-expression of TORC3 and Tax dramatically increased transcriptional activation at the HTLV-I LTR [1].
• Enhanced activation of tax-dependent transcription of human T-cell leukemia virus type I (HTLV-I) long terminal repeat by TORC3 [1].
• Using deletion mutant analysis, we identify the Tax interaction domain of TORC3 as a region spanning from amino acid 1 to 103, which contains a coiled-coil domain [1].

Associations of CRTC3 with chemical compounds

• We also show by glutathione S-transferase pull-down and co-immunoprecipitation experiments that TORC3 interacts with Tax [1].

References