Curated Information
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Home > Curated Information Page > PubMed Id: 25826088
Huang CC, Wu DW, Lin PL, Lee H (2015) Paxillin promotes colorectal tumor invasion and poor patient outcomes via ERK-mediated stabilization of Bcl-2 protein by phosphorylation at Serine 87. Oncotarget 6, 8698-708 25826088
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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S87-p - Bcl-2 (human)
Modsite: AAAGPALsPVPPVVH SwissProt Entrez-Gene
Orthologous residues
Bcl‑2 (human): S87‑p, Bcl‑2 (mouse): S84‑p, Bcl‑2 (rat): S84‑p
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  HCT116 (intestinal)
Cellular systems studied:  cell lines
Species studied:  human
Comments:  colorectal carcinoma patient samples
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
PXN (human) increase
U0126 PXN (human) inhibit treatment-induced increase
selumetinib PXN (human) inhibit treatment-induced increase
Downstream Regulation
Effect of modification (function):  protein stabilization
Comments:  PXN-mediated cell invasiveness
Associated Diseases
Diseases Alterations Comments
colorectal cancer increased high pBcl-2-S87 had poor outcomes