What is it about?
Siah2 acetylation promotes gastric cancer invasiveness.H. pylori enhances Siah2 acetylation by p300 at the K139 residue.ac-K139Siah2 enhances the degradation of cell adhesion-related proteins test in (TES) and filamin-C (FLN-C) in the infected epithelium. Acetylation enhances Siah2 stability and prevents it from proteasomal degradation and therefore, its targets TES and FLN-C are degraded. TES and FLN-C down regulation is associated with the impairment of actin filament organization, filopodia formation and increased invasiveness of gastric epithelial cancer cells.
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Why is it important?
Acetylation of Siah2 is an important checkpoint that can be useful for therapeutic intervention.
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This page is a summary of: Testin and Filamin-C downregulation by acetylated Siah2 increases invasiveness of Helicobacter pylori -infected gastric cancer cells, The International Journal of Biochemistry & Cell Biology, July 2018, Elsevier,
DOI: 10.1016/j.biocel.2018.07.012.
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