The Insulin Receptor and Insulin like Growth Factor Receptor 5' UTRs Support Translation Initiation Independently of EIF4G1.

Autor:	Clark NK; Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, USA.; mRNA Center of Excellence, Sanofi, Waltham, Massachusetts, USA., Harris MT; Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, USA.; Myeloid Therapeutics, Cambridge, Massachusetts, USA., Dahl WB; Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, USA., Knotts Z; Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, USA., Marr MT 2nd; Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, USA.
Jazyk:	angličtina
Zdroj:	Molecular and cellular biology [Mol Cell Biol] 2023; Vol. 43 (10), pp. 485-499. Date of Electronic Publication: 2023 Oct 11.
DOI:	10.1080/10985549.2023.2255120
Abstrakt:	IRES mediated translation initiation requires a different repertoire of factors than canonical cap-dependent translation. Treatments that inhibit the canonical translation factor EIF4G1 have little or no effect on the ability of the Insr and Igf1r cellular IRESes to promote translation. Transcripts for two cellular receptors contain RNA elements that facilitate translation initiation without intact EIF4G1. Cellular IRES mechanisms may resemble viral type III IRESes allowing them to promote translate with a limited number of initiation factors allowing them to work under stress conditions when canonical translation is repressed.
Databáze:	MEDLINE
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