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REVIEW
Year : 2019  |  Volume : 5  |  Issue : 2  |  Page : 25-32

Phosphorylation of BRCA1-associated protein 1 as an important mechanism in the evasion of tumorigenesis: A perspective


1 Gene Regulation Laboratory, National Institute of Immunology, New Delhi, India
2 Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
3 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
4 Department of Obstetrics and Gynecology, All India Institute of Medical Sciences, New Delhi, India
5 Department of Biotechnology, School of Engineering and Technology, Jaipur National University, Jaipur, Rajasthan, India
6 Biochemistry and Toxicology Laboratory, School of Environmental Sciences, Jawaharlal Nehru University, New Delhi, India

Correspondence Address:
Dr. Deepak Parashar
Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee 53226, Wisconsin
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ctm.ctm_1_19

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The human BRCA1-associated protein 1 (BAP1), a deubiquitinase, is a tumor suppressor protein known to be associated with a multicellular complex containing tumor suppressors, thereby coregulating various cellular processes such as DNA repair, gene transcription, cell cycle progression, and phosphorylation. Mutation and inactivation of BAP1 have long been reported in many malignancies and has been deployed in the prognosis of few malignancies. However, the mechanism of BAP1 regulation and its therapeutic significance have not been thoroughly explored. In addition to deubiquitination, BAP1 also responds to DNA damage and can induce cell death via apoptosis, necrosis, and ferroptosis. The mechanistic insight of BAP1-regulation is a complex subject and its thorough understanding would address the enigma of BAP1 mutation in malignancy. There are various tiers of regulation, though still needs to be explored, of BAP1 activity such as epigenetic regulation and posttranslational modification (PTM). Of various PTMs, posttranslational phosphorylation (PTP) has been poorly understood and meekly addressed in the literature. Here, we aim to provide an updated and integrated understanding of the PTP-mediated BAP1 regulation and its plausible role in cancer prevention. Exploring the functional consequence of BAP1 phosphorylation in its deubiquitinating potential might establish a new paradigm for its regulation in maintaining cellular homeostasis and cancer prevention.


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