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: 15128824 
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.
Mattioli I, et al. (2004) Transient and selective NF-kappa B p65 serine 536 phosphorylation induced by T cell costimulation is mediated by I kappa B kinase beta and controls the kinetics of p65 nuclear import. J Immunol 172, 6336-44 15128824
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

S32-p - IkB-alpha (human) ▲
Orthologous residues
IkB‑alpha (human): S32‑p, IkB‑alpha (mouse): S32‑p, IkB‑alpha (rat): S32‑p
Characterization
 Methods used to characterize site in vivo:  [32P] bio-synthetic labeling, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  Jurkat (T lymphocyte)
 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
anti-CD3 increase
anti-CD28 anti-CD3 augment treatment-induced increase
parthenolide anti-CD3 inhibit treatment-induced increase
bisindolylmaleimide anti-CD3 inhibit treatment-induced increase
MG132 anti-CD3 augment treatment-induced increase
anti-CD28 increase
parthenolide anti-CD28 inhibit treatment-induced increase
bisindolylmaleimide anti-CD28 inhibit treatment-induced increase
MG132 anti-CD28 augment treatment-induced increase

S36-p - IkB-alpha (human) ▲
Orthologous residues
IkB‑alpha (human): S36‑p, IkB‑alpha (mouse): S36‑p, IkB‑alpha (rat): S36‑p
Characterization
 Methods used to characterize site in vivo:  [32P] bio-synthetic labeling, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  Jurkat (T lymphocyte)
 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
anti-CD3 increase
anti-CD28 anti-CD3 augment treatment-induced increase
parthenolide anti-CD3 inhibit treatment-induced increase
bisindolylmaleimide anti-CD3 inhibit treatment-induced increase
MG132 anti-CD3 augment treatment-induced increase
anti-CD28 increase
parthenolide anti-CD28 inhibit treatment-induced increase
bisindolylmaleimide anti-CD28 inhibit treatment-induced increase
MG132 anti-CD28 augment treatment-induced increase

S180-p - IKK-alpha (human) ▲
Orthologous residues
IKK‑alpha (human): S180‑p, IKK‑alpha (mouse): S180‑p, IKK‑alpha (rat): S180‑p
Characterization
 Methods used to characterize site in vivo:  [32P] bio-synthetic labeling, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  Jurkat (T lymphocyte)
 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
anti-CD3 increase
anti-CD28 anti-CD3 augment treatment-induced increase
anti-CD28 increase

S181-p - IKK-beta (human) ▲
Orthologous residues
IKK‑beta (human): S181‑p, IKK‑beta (mouse): S181‑p, IKK‑beta (rat): S181‑p
Characterization
 Methods used to characterize site in vivo:  [32P] bio-synthetic labeling, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  Jurkat (T lymphocyte)
 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
anti-CD3 increase
anti-CD28 anti-CD3 augment treatment-induced increase
anti-CD28 increase

S536-p - NFkB-p65 (human) ▲
Orthologous residues
NFkB‑p65 (human): S536‑p, NFkB‑p65 (mouse): S534‑p, NFkB‑p65 (rat): S535‑p
Characterization
 Methods used to characterize site in vivo:  [32P] bio-synthetic labeling, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  Jurkat (T lymphocyte)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE IKK-beta (human) transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anti-CD3 increase
anti-CD28 anti-CD3 augment treatment-induced increase
parthenolide anti-CD3 inhibit treatment-induced increase
bisindolylmaleimide anti-CD3 inhibit treatment-induced increase
MG132 anti-CD3 augment treatment-induced increase
anti-CD28 increase
parthenolide anti-CD28 inhibit treatment-induced increase
bisindolylmaleimide anti-CD28 inhibit treatment-induced increase
MG132 anti-CD28 augment treatment-induced increase
Downstream Regulation
 Effect of modification (function):  intracellular localization, protein stabilization
 Effect of modification (process):  transcription, altered


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.