Wang S, et al. (2012) Activation of AMP-activated protein kinase α2 by nicotine instigates formation of abdominal aortic aneurysms in mice in vivo. Nat Med 18, 902-10 22561688

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S80-p - ACC1 (human) ▲

Modsite: LHIRSSMsGLHLVKQ SwissProt Entrez-Gene Orthologous residues ACC1 (human): S80‑p, ACC1 iso2 (human): S22‑p, ACC1 iso4 (human): S117‑p, ACC1 (mouse): S79‑p, ACC1 iso2 (mouse): S117‑p, ACC1 (rat): S79‑p, ACC1 iso2 (rat): S79‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  aorta, blood, VSMC-aorta Cellular systems studied:  primary cultured cells, tissue Species studied:  human Enzymes shown to modify site in vitro:  Type Enzyme KINASE AMPKA2 (human) Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes angiotensin_2 increase nicotine increase

T172-p - AMPKA2 (human) ▲

Modsite: SDGEFLRtSCGSPNY SwissProt Entrez-Gene Orthologous residues AMPKA2 (human): T172‑p, AMPKA2 (mouse): T172‑p, AMPKA2 (rat): T172‑p, AMPKA2 (pig): T172‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  aorta, blood, VSMC-aorta Cellular systems studied:  primary cultured cells, tissue Species studied:  human Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes angiotensin_2 increase nicotine increase Downstream Regulation Effect of modification (function):  intracellular localization, phosphorylation

S219-p - AP-2 alpha (human) ▲

Modsite: CSVPGRLsLLSSTSK SwissProt Entrez-Gene Orthologous residues AP‑2 alpha (human): S219‑p, AP‑2 alpha iso2 (human): S213‑p, AP‑2 alpha (mouse): S219‑p, AP‑2 alpha (rat): S219‑p Characterization Methods used to characterize site in vivo:  [32P] ATP in vitro, mutation of modification site, western blotting Relevant cell lines - cell types - tissues:  293 (epithelial), VSMC-aorta Cellular systems studied:  cell lines, primary cultured cells Species studied:  human Enzymes shown to modify site in vitro:  Type Enzyme KINASE AMPKA2 (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE AMPKA2 (human) activation of upstream enzyme, microscopy-colocalization, siRNA inhibition of enzyme, modification site within consensus motif, transfection of wild-type enzyme, pharmacological inhibitor of upstream enzyme, transfection of dominant-negative enzyme, co-immunoprecipitation, genetic knockout/knockin of upstream enzyme, pharmacological activator of upstream enzyme, phospho-antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes nicotine increase angiotensin_2 increase compound_C angiotensin_2, nicotine inhibit treatment-induced increase siRNA decrease siRNA for AMPKA2 decreases phosphorylation Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  transcription, induced Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Induces