2cp9: Difference between revisions

<table><tr><td colspan='2'>[[2cp9]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2CP9 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2CP9 FirstGlance]. <br>

</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2cp9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2cp9 OCA], [http://pdbe.org/2cp9 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2cp9 RCSB], [http://www.ebi.ac.uk/pdbsum/2cp9 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2cp9 ProSAT], [http://www.topsan.org/Proteins/RSGI/2cp9 TOPSAN]</span></td></tr>

[[http://www.uniprot.org/uniprot/EFTS_HUMAN EFTS_HUMAN]] Defects in TSFM are the cause of combined oxidative phosphorylation deficiency type 3 (COXPD3) [MIM:[http://omim.org/entry/610505 610505]]. Defects in the mitochondrial oxidative phosphorylation system result in devastating, mainly multisystem, diseases. COXPD3 symptoms include severe metabolic acidosis with encephalomyopathy or with hypertrophic cardiomyopathy. Patients show a severe defect in mitochondrial translation leading to a failure to assemble adequate amounts of three of the oxidative phosphorylation complexes.<ref>PMID:17033963</ref>   

[[http://www.uniprot.org/uniprot/EFTS_HUMAN EFTS_HUMAN]] Associates with the EF-Tu.GDP complex and induces the exchange of GDP to GTP. It remains bound to the aminoacyl-tRNA.EF-Tu.GTP complex up to the GTP hydrolysis stage on the ribosome (By similarity).[HAMAP-Rule:MF_03135]