Curated Information
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
PhosphoSitePlus
HomeAbout PhosphoSiteUsing PhosphoSiteCuration ProcessContact
NIH-logos NIGMS Logo NIAAA Logo NCI Logo NIH Logo
Curated Information Page
PubMed Id: 12370288 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
Koumenis C, et al. (2002) Regulation of protein synthesis by hypoxia via activation of the endoplasmic reticulum kinase PERK and phosphorylation of the translation initiation factor eIF2alpha. Mol Cell Biol 22, 7405-16 12370288
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
Download Sites

S52-p - eIF2-alpha (human) ▲
Orthologous residues
eIF2‑alpha (human): S52‑p, eIF2‑alpha (mouse): S52‑p, eIF2‑alpha (rat): S52‑p, eIF2‑alpha (rabbit): S51‑p, eIF2‑alpha (fruit fly): S51‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast), A549 (pulmonary), AG1522 (fibroblast), HeLa (cervical), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PERK (mouse) transfection of wild-type enzyme, transfection of dominant-negative enzyme, genetic knockout/knockin of upstream enzyme, transfection of inactive enzyme, phospho-antibody, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
hypoxia increase
hypoxia/reoxygenation hypoxia inhibit treatment-induced increase
cobalt increase CoCl2
thapsigargin increase
Downstream Regulation
 Effect of modification (process):  translation, altered

S52-p - eIF2-alpha (mouse) ▲
Orthologous residues
eIF2‑alpha (human): S52‑p, eIF2‑alpha (mouse): S52‑p, eIF2‑alpha (rat): S52‑p, eIF2‑alpha (rabbit): S51‑p, eIF2‑alpha (fruit fly): S51‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  lung cancer
 Relevant cell lines - cell types - tissues:  3T3 (fibroblast), A549 (pulmonary), AG1522 (fibroblast), HeLa (cervical), MEF (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PERK (mouse) transfection of wild-type enzyme, transfection of dominant-negative enzyme, genetic knockout/knockin of upstream enzyme, transfection of inactive enzyme, phospho-antibody, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
hypoxia increase
DTT increase
thapsigargin increase


Home  |  Curator Login With enhanced literature mining using Linguamatics I2E I2E Logo Produced by 3rd Millennium  |  Design by Digizyme
©2003-2013 Cell Signaling Technology, Inc.