Curated Information
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Home > Curated Information Page > PubMed Id: 27650555
Dai X, et al. (2016) Phosphorylation of CHOP (C/EBP Homologous Protein) by the AMP-Activated Protein Kinase Alpha 1 in Macrophages Promotes CHOP Degradation and Reduces Injury-Induced Neointimal Disruption In Vivo. Circ Res 119, 1089-1100 27650555
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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S30-p - DDIT3 (human)
Modsite: EDLQEVLssDENGGT SwissProt Entrez-Gene
Orthologous residues
DDIT3 (human): S30‑p, DDIT3 (mouse): S30‑p, DDIT3 (rat): S30‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  macrophage-bone marrow, RAW 264.7 (macrophage)
Cellular systems studied:  cell lines, primary cells
Species studied:  mouse
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA1 (human) genetic knockout/knockin of upstream enzyme, modification site within consensus motif, co-immunoprecipitation, pharmacological activator of upstream enzyme, phospho-antibody, microscopy-colocalization
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
acadesine increase
A79662 increase
compound_C decrease
Downstream Regulation
Effect of modification (function):  protein degradation, ubiquitination