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: 10581258 
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.
Bulavin DV, et al. (1999) Phosphorylation of human p53 by p38 kinase coordinates N-terminal phosphorylation and apoptosis in response to UV radiation. EMBO J 18, 6845-54 10581258
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

S15-p - p53 (human) ▲
Orthologous residues
p53 (human): S15‑p, p53 (mouse): S15‑p, p53 iso2 (mouse): S18‑p, p53 (rat): S15‑p, p53 (rabbit): S15‑p, p53 (monkey): S15‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody
 Relevant cell lines - cell types - tissues:  MCF-7 (breast cell), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase

S33-p - p53 (human) ▲
Orthologous residues
p53 (human): S33‑p, p53 (mouse): P33‑p, p53 iso2 (mouse): P36‑p, p53 (rat): P33‑p, p53 (rabbit): T33‑p, p53 (monkey): S33‑p
Characterization
 Methods used to characterize site in vivo:  [32P] ATP in vitro, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  MCF-7 (breast cell), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE p38-alpha (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE p38-alpha (human)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced

S37-p - p53 (human) ▲
Orthologous residues
p53 (human): S37‑p, p53 (mouse): S34‑p, p53 iso2 (mouse): S37‑p, p53 (rat): S39‑p, p53 (rabbit): N37‑p, p53 (monkey): S37‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody
 Relevant cell lines - cell types - tissues:  MCF-7 (breast cell), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase

S46-p - p53 (human) ▲
Orthologous residues
p53 (human): S46‑p, p53 (mouse): L43‑p, p53 iso2 (mouse): L46‑p, p53 (rat): L48‑p, p53 (rabbit): S45‑p, p53 (monkey): S46‑p
Characterization
 Methods used to characterize site in vivo:  [32P] ATP in vitro, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  MCF-7 (breast cell), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE p38-alpha (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE p38-alpha (human)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase
Downstream Regulation
 Effect of modification (process):  apoptosis, induced


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.