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      https://www.ias.ac.in/article/fulltext/jbsc/044/06/0147

    • Keywords

       

      AurkB; acetylation; kinase activity; stability; Tip60

    • Abstract

       

      The Aurora kinases represent a group of serine/threonine kinases which are crucial regulators of mitosis. DysregulatedAurora kinase B (AurkB) expression, stemming from genomic amplification, increased gene transcription or overexpressionof its allosteric activators, is capable of initiating and sustaining malignant phenotypes. Although AurkB level in cells iswell-orchestrated, studies that relate to its stability or activity, independent of mitosis, are lacking. We report that AurkBundergoes acetylation in vitro by lysine acetyltransferases (KATs) belonging to different families, namely by p300 andTip60. The haploinsufficient tumor suppressor Tip60 acetylates two highly conserved lysine residues within the kinasedomain of AurkB which not only impinges the protein stability but also its kinase activity. These results signify a probableoutcome on the increase in ‘‘overall activity’’ of AurkB upon Tip60 downregulation, as observed under cancerous conditions.The present work, therefore, uncovers an important functional interplay between AurkB and Tip60, frailty of whichmay be an initial event in carcinogenesis.

    • Author Affiliations

       

      ARNAB BOSE1 SURABHI SUDEVAN1 VINAY J RAO1 HIROKI SHIMA2 ARUN KUMAR TRIVEDI3 KAZUHIKO IGARASHI2 TAPAS K KUNDU1

      1. Transcription and Disease Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, Karnataka, India
      2. Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Aoba-ku, Sendai 980-8575, Japan
      3. Division of Cancer Biology, CSIR-Central Drug Research Institute (CSIR-CDRI), Sector-10, Jankipuram Extension, Lucknow, UP 226031, India
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