Curated Information
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Home > Curated Information Page > PubMed Id: 27218122
Nakamura M, et al. (2016) Mst1-mediated phosphorylation of Bcl-xL is required for myocardial reperfusion injury. JCI Insight 1 27218122
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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S14-p - Bcl-xL (mouse)
Modsite: ELVVDFLsYKLSQKG SwissProt Entrez-Gene
Orthologous residues
Bcl‑xL (human): S14‑p, Bcl‑xL (mouse): S14‑p, Bcl‑xL (rat): S14‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  heart [Bcl-xL (mouse), genetic knockin]
Cellular systems studied:  tissue
Species studied:  mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ischemia/reperfusion increase

T183-p - MST1 (mouse)
Modsite: DtMAKRNtVIGTPFW SwissProt Entrez-Gene
Orthologous residues
MST1 (human): T183‑p, MST1 iso2 (human): T183‑p, MST1 (mouse): T183‑p, MST1 (rat): T183‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  heart [Bcl-xL (mouse), genetic knockin]
Cellular systems studied:  tissue
Species studied:  mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ischemia/reperfusion increase