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Home > Curated Information Page > PubMed Id: 11839738
Uddin S, et al. (2002) Protein kinase C-delta (PKC-delta ) is activated by type I interferons and mediates phosphorylation of Stat1 on serine 727. J Biol Chem 277, 14408-16 11839738
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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T180-p - P38A (human)
Modsite: RHtDDEMtGyVAtRW SwissProt Entrez-Gene
Orthologous residues
P38A (human): T180‑p, P38A iso2 (human): T180‑p, P38A (mouse): T180‑p, P38A iso3 (mouse): T180‑p, P38A (rat): T180‑p, P38A (salmonid): T181‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  bone cancer, leukemia, T cell leukemia, multiple myeloma
Relevant cell lines - cell types - tissues:  MOLT-4 (T lymphocyte), U266 (plasma cell), 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
IFN-alpha increase
rottlerin IFN-alpha inhibit treatment-induced increase
H-7 IFN-alpha inhibit treatment-induced increase
IFN-beta increase
rottlerin IFN-beta inhibit treatment-induced increase
H-7 IFN-beta inhibit treatment-induced increase

Y182-p - P38A (human)
Modsite: tDDEMtGyVAtRWYR SwissProt Entrez-Gene
Orthologous residues
P38A (human): Y182‑p, P38A iso2 (human): Y182‑p, P38A (mouse): Y182‑p, P38A iso3 (mouse): Y182‑p, P38A (rat): Y182‑p, P38A (salmonid): Y183‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  bone cancer, leukemia, T cell leukemia, multiple myeloma
Relevant cell lines - cell types - tissues:  MOLT-4 (T lymphocyte), U266 (plasma cell), 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
IFN-alpha increase
rottlerin IFN-alpha inhibit treatment-induced increase
H-7 IFN-alpha inhibit treatment-induced increase
IFN-beta increase
rottlerin IFN-beta inhibit treatment-induced increase
H-7 IFN-beta inhibit treatment-induced increase

T507-p - PKCD (human)
Modsite: FGEsRAstFCGtPDy SwissProt Entrez-Gene
Orthologous residues
PKCD (human): T507‑p, PKCD iso2 (human): T538‑p, PKCD (mouse): T505‑p, PKCD iso2 (mouse): T531‑p, PKCD (rat): T505‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  bone cancer, leukemia, T cell leukemia, multiple myeloma
Relevant cell lines - cell types - tissues:  MOLT-4 (T lymphocyte), U266 (plasma cell), 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
IFN-alpha increase
IFN-beta increase

S727-p - STAT1 (human)
Modsite: TDNLLPMsPEEFDEV SwissProt Entrez-Gene
Orthologous residues
STAT1 (human): S727‑p, STAT1 iso2 (human): , STAT1 (mouse): S727‑p, STAT1 (rat): S727‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  bone cancer, leukemia, T cell leukemia, multiple myeloma
Relevant cell lines - cell types - tissues:  MOLT-4 (T lymphocyte), U266 (plasma cell), U2OS (bone cell)
Cellular systems studied:  cell lines
Species studied:  human
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKCD (human) pharmacological inhibitor of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IFN-alpha increase
rottlerin IFN-alpha inhibit treatment-induced increase
H-7 IFN-alpha inhibit treatment-induced increase
IFN-beta increase
rottlerin IFN-beta inhibit treatment-induced increase
H-7 IFN-beta inhibit treatment-induced increase