Curated Information
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Home > Curated Information Page > PubMed Id: 25257795
Zhang J, et al. (2015) PDGFR-β-activated ACK1-AKT Signaling Promotes Glioma Tumorigenesis. Int J Cancer 136, 1769-80 25257795
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
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Y635-p - Ack (human)
Modsite: PLPPPPAyDDVAQDE SwissProt Entrez-Gene
Orthologous residues
Ack (human): Y635‑p, Ack iso3 (human): Y713‑p, Ack (mouse): Y650‑p, Ack iso2 (mouse): Y635‑p, Ack (rat): Y635‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  brain cancer, glioblastoma, glioma
Relevant cell lines - cell types - tissues:  glial-brain, U-251 MG (glial), U87MG (glial)
Cellular systems studied:  cell lines, tissue
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE PDGFRB (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PDGFRB (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
PDGF increase
AG1295 PDGF inhibit treatment-induced increase
PDK1 (human) increase shRNA decreases
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced, molecular association, regulation
Effect of modification (process):  carcinogenesis, induced, cell growth, induced, signaling pathway regulation, transcription, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
Akt1 (human) Induces co-immunoprecipitation, pull-down assay
Comments:  PDGF-induced PDGFRB-ACK1-AKT signaling
Associated Diseases
Diseases Alterations Comments
glioblastoma multiforme increased

Y176-p - Akt1 (human)
Modsite: EKATGRYyAMKILKK SwissProt Entrez-Gene
Orthologous residues
Akt1 (human): Y176‑p, Akt1 iso2 (human): Y114‑p, Akt1 (mouse): Y176‑p, Akt1 (rat): Y176‑p, Akt1 (fruit fly): Y292‑p, Akt1 (cow): Y176‑p
Characterization
Methods used to characterize site in vivo mutation of modification site
Disease tissue studied:  brain cancer, glioblastoma, glioma
Relevant cell lines - cell types - tissues:  U87MG (glial)
Cellular systems studied:  cell lines

S473-p - Akt1 (human)
Modsite: RPHFPQFsysAsGtA SwissProt Entrez-Gene
Orthologous residues
Akt1 (human): S473‑p, Akt1 iso2 (human): S411‑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 phospho-antibody, western blotting
Disease tissue studied:  brain cancer, glioblastoma, glioma
Relevant cell lines - cell types - tissues:  glial-brain, U-251 MG (glial), U87MG (glial)
Cellular systems studied:  cell lines, tissue
Species studied:  human
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
PDGF increase
AG1295 PDGF inhibit treatment-induced increase
PDGF Ack (human) augment treatment-induced increase shRNA decrease, Y635F-mutant decreases, Y325A-mutant decreases
EGF, PDGF Akt1 (human) inhibit treatment-induced increase Akt1-Y176F mutant
EGF increase
PDGF PDK1 (human) augment treatment-induced increase shRNA inhibits

Y751-p - PDGFRB (human)
Modsite: SKDESVDyVPMLDMK SwissProt Entrez-Gene
Orthologous residues
PDGFRB (human): Y751‑p, PDGFRB (mouse): Y750‑p, PDGFRB (rat): Y750‑p