Structural highlights
Function
YIH1_YEAST Translational regulator that ensures constant high levels of translation under amino acid starvation. Plays a role as a negative regulator of the GCN2 kinase activity; impairs GCN1-mediated GCN2 activation, and hence GCN2-mediated eIF-2-alpha phosphorylation in amino acid-starved cells and subsequent down-regulation of protein synthesis (PubMed:15126500, PubMed:15937339, PubMed:24333428). In normal conditions, it resides in a actin complex and has no activity (PubMed:15126500).[1] [2] [3]
References
- ↑ Sattlegger E, Swanson MJ, Ashcraft EA, Jennings JL, Fekete RA, Link AJ, Hinnebusch AG. YIH1 is an actin-binding protein that inhibits protein kinase GCN2 and impairs general amino acid control when overexpressed. J Biol Chem. 2004 Jul 16;279(29):29952-62. Epub 2004 May 4. PMID:15126500 doi:http://dx.doi.org/10.1074/jbc.M404009200
- ↑ Pereira CM, Sattlegger E, Jiang HY, Longo BM, Jaqueta CB, Hinnebusch AG, Wek RC, Mello LE, Castilho BA. IMPACT, a protein preferentially expressed in the mouse brain, binds GCN1 and inhibits GCN2 activation. J Biol Chem. 2005 Aug 5;280(31):28316-23. doi: 10.1074/jbc.M408571200. Epub 2005 , Jun 2. PMID:15937339 doi:http://dx.doi.org/10.1074/jbc.M408571200
- ↑ Cambiaghi TD, Pereira CM, Shanmugam R, Bolech M, Wek RC, Sattlegger E, Castilho BA. Evolutionarily conserved IMPACT impairs various stress responses that require GCN1 for activating the eIF2 kinase GCN2. Biochem Biophys Res Commun. 2014 Jan 10;443(2):592-7. doi:, 10.1016/j.bbrc.2013.12.021. Epub 2013 Dec 11. PMID:24333428 doi:http://dx.doi.org/10.1016/j.bbrc.2013.12.021
