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Open AccessReview

P-TEFb as A Promising Therapeutic Target

Department of Medicine, University of California, San Francisco, CA 94143-0703, USA
Academic Editor: Takaomi Sanda
Molecules 2020, 25(4), 838; https://doi.org/10.3390/molecules25040838 (registering DOI)
Received: 5 January 2020 / Revised: 6 February 2020 / Accepted: 7 February 2020 / Published: 14 February 2020
(This article belongs to the Special Issue Transcription Factors as Therapeutic Targets II)
The positive transcription elongation factor b (P-TEFb) was first identified as a general factor that stimulates transcription elongation by RNA polymerase II (RNAPII), but soon afterwards it turned out to be an essential cellular co-factor of human immunodeficiency virus (HIV) transcription mediated by viral Tat proteins. Studies on the mechanisms of Tat-dependent HIV transcription have led to radical advances in our knowledge regarding the mechanism of eukaryotic transcription, including the discoveries that P-TEFb-mediated elongation control of cellular transcription is a main regulatory step of gene expression in eukaryotes, and deregulation of P-TEFb activity plays critical roles in many human diseases and conditions in addition to HIV/AIDS. P-TEFb is now recognized as an attractive and promising therapeutic target for inflammation/autoimmune diseases, cardiac hypertrophy, cancer, infectious diseases, etc. In this review article, I will summarize our knowledge about basic P-TEFb functions, the regulatory mechanism of P-TEFb-dependent transcription, P-TEFb’s involvement in biological processes and diseases, and current approaches to manipulating P-TEFb functions for the treatment of these diseases. View Full-Text
Keywords: P-TEFb; transcription elongation; HIV; cancer; cardiac hypertrophy; RNA polymerase II; infectious diseases; inflammation; autoimmune diseases; inhibitors P-TEFb; transcription elongation; HIV; cancer; cardiac hypertrophy; RNA polymerase II; infectious diseases; inflammation; autoimmune diseases; inhibitors
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Fujinaga, K. P-TEFb as A Promising Therapeutic Target. Molecules 2020, 25, 838.

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