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: 19081072 
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Rutkowski DT, et al. (2008) UPR pathways combine to prevent hepatic steatosis caused by ER stress-mediated suppression of transcriptional master regulators. Dev Cell 15, 829-40 19081072
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

S473-p - Akt1 (mouse) ▲
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  liver cancer
 Relevant cell lines - cell types - tissues:  Fao (hepatic), hepatocyte-liver [eIF2-alpha (mouse), homozygous knockout]
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
tunicamycin ATF6 (mouse) increase
tunicamycin tunicamycin ATF6 (mouse) ATF6 (mouse) inhibit treatment-induced increase ATF6 -/- mice

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:  liver cancer
 Relevant cell lines - cell types - tissues:  Fao (hepatic), hepatocyte-liver [eIF2-alpha (mouse), homozygous knockout]
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IRE1 (mouse) no change compared to control IRE1 wild-type
IRE1 (mouse) increase IRE1 -/-
tunicamycin IRE1 (mouse) increase IRE1 wild-type
tunicamycin IRE1 (mouse) no effect upon treatment-induced increase IRE1 -/- mice
no change compared to control EIF2 S51A heterozygous
no change compared to control EIF2A 51A homozygous
no change compared to control EIF2A 51A heterozygous, transgene deleted
tunicamycin increase EIF2A 51A heterozygous, transgene deleted
tunicamycin no change compared to control EIF2A 51A homozygous, transgene deleted
tunicamycin increase p58IPK wild-type
tunicamycin augment treatment-induced decrease p58IPK -/-


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.