Curated Information
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Home > Curated Information Page > PubMed Id: 30068645
Pan T, et al. (2018) Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Potently Inhibit the Replication of Zika Viruses by Inducing the Degradation of AXL. J Virol 30068645
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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S97-p - CDC37 (human)
Modsite: QLRkEERsWEQkLEE SwissProt Entrez-Gene
Orthologous residues
CDC37 (human): S97‑p, CDC37 (mouse): S98‑p, CDC37 (rat): S98‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  lung cancer, non-small cell lung cancer, non-small cell lung adenocarcinoma
Relevant cell lines - cell types - tissues:  A549 (pulmonary)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKACA (human) siRNA inhibition of enzyme, pharmacological inhibitor of upstream enzyme, phospho-motif antibody
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ibuprofen decrease
Downstream Regulation
Effect of modification (function):  molecular association, regulation, protein stabilization
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
HSP90A (human) Induces co-immunoprecipitation
Comments:  inhibits ubiquitination and degradation of AXL