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: 20126263 
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.
van Vugt MA, et al. (2010) A Mitotic Phosphorylation Feedback Network Connects Cdk1, Plk1, 53BP1, and Chk2 to Inactivate the G(2)/M DNA Damage Checkpoint. PLoS Biol 8, e1000287 20126263
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

S1981-p - ATM (human)
Orthologous residues
ATM (human): S1981‑p, ATM (mouse): S1987‑p, ATM (rat): S1988‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  U2OS (bone cell)
 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
ionizing radiation increase
nocodazole ionizing radiation no effect upon treatment-induced increase

T68-p - Chk2 (human)
Orthologous residues
Chk2 (human): T68‑p, Chk2 iso12 (human): T68‑p, Chk2 (mouse): T77‑p, Chk2 (rat): T76‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PLK1 (human) modification site within consensus motif, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
nocodazole ionizing radiation inhibit treatment-induced increase
BI2536 decrease

S164-p - Chk2 (human)
Orthologous residues
Chk2 (human): S164‑p, Chk2 iso12 (human): S164‑p, Chk2 (mouse): S168‑p, Chk2 (rat): S167‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PLK1 (human) modification site within consensus motif, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
BI2536 decrease
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited
 Effect of modification (process):  cell cycle regulation
 Comments:  mutation of this site impairs checkpoint recovery

T205-p - Chk2 (human)
Orthologous residues
Chk2 (human): T205‑p, Chk2 iso12 (human): T205‑p, Chk2 (mouse): T209‑p, Chk2 (rat): T208‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PLK1 (human) modification site within consensus motif, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
BI2536 decrease
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited
 Effect of modification (process):  cell cycle regulation
 Comments:  mutation of this site impairs checkpoint recovery

S210-p - Chk2 (human)
Orthologous residues
Chk2 (human): S210‑p, Chk2 iso12 (human): S210‑p, Chk2 (mouse): S214‑p, Chk2 (rat): S213‑p
Characterization
 Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PLK1 (human) modification site within consensus motif, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
BI2536 decrease
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited
 Effect of modification (process):  cell cycle regulation
 Comments:  mutation of this site impairs checkpoint recovery

S376-p - 53BP1 (mouse)
Orthologous residues
53BP1 (human): S380‑p, 53BP1 (mouse): S376‑p, 53BP1 (rat): S384‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Comments:  only in mitotically arrested cells
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK1 (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
nocodazole increase
roscovitine nocodazole inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  cell cycle regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
PLK1 (human) Induces pull-down assay


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.