Markovsky E, et al. (2018) Phosphorylation state of Ser in α-tubulin is a toggle switch that controls proliferating human breast tumors. Cell Signal 52, 74-82 30176291

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S165-p - TUBA1A (human) ▲

Modsite: sVDyGkkskLEFSIy SwissProt Entrez-Gene Orthologous residues TUBA1A (human): S165‑p, TUBA1A (mouse): S165‑p, TUBA1A (rat): S165‑p, TUBA1A (cow): S165‑p Characterization Methods used to characterize site in vivo:  mutation of modification site Disease tissue studied:  breast cancer, breast adenocarcinoma, breast cancer, triple negative Relevant cell lines - cell types - tissues:  MDA-MB-231 (breast cell), MDA-MB-468 (breast cell) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE PKCA (human) pharmacological inhibitor of upstream enzyme, phospho-motif antibody, modification site within consensus motif Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes bisindolylmaleimide decrease Downstream Regulation Effect of modification (process):  carcinogenesis, inhibited, cell cycle regulation, cell growth, inhibited, cytoskeletal reorganization, transcription, altered Comments:  S165D-high expression of N-cadherin while suppressing E-cadherin protein, whereas for 165N E-cadherin remains high, andN-cadherin is decreased Associated Diseases Diseases Alterations Comments breast adenocarcinoma decreased