The bromodomain protein Brd4 is a positive regulatory component of P-TEFb and stimulates RNA polymerase II-dependent transcription.

By M. Jang, K. Mochizuki, Meisheng Zhou, Ho Jeong, J. Brady, K. Ozato. Molecules and Cells, 2005

1,277 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/6629bc1462cc46c437e93e4e8d517d5e29630e4d

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Citations in the corpus

BRD4 and Cancer: going beyond transcriptional regulation (2018, background): “Interaction with BRD4 prevents P-TEFb binding to the inhibitory ribonucleoprotein complex 7SK/ HEXIM that sequesters P-TEFb in its inactive form [43, 45].”
Histone Marks in the 'Driver's Seat': Functional Roles in Steering the Transcription Cycle. (2017, background): “Importantly, BRD4 can interact with P-TEFb to facilitate Pol II pause release from promoter proximal regions [46,47].”
The mechanisms behind the therapeutic activity of BET bromodomain inhibition (2014, background): “Brd4 has been shown to regulate multiple steps of HIV transcription (Jang et al., 2005; Yang et al., 2005), and a series of recent studies have shown that BET inhibitors can trigger HIV transcription in latently infected cells, thus activating viral replication (Banerjee et al., 2012; Boehm et al.,…”
Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “JQ-1 binds the first bromodomain of the BET protein BRD4, which is a key tethering factor that interacts with cyclin T1 and cdk9 to form a core positive transcription elongation factor b (P-TEFb) (Jang et al., 2005).”
Bimolecular fluorescence complementation (BiFC) analysis as a probe of protein interactions in living cells. (2008, background): “BiFC complexes have been visualized in all major subcellular compartments of mammalian cells, including numerous subnuclear structures (23,30,31,37,38,45,47,51,54,85, 93,101,128), lysosomes (30), the plasma membrane (35,39,49,62,66,73,95,126), lamellipodia (21), golgi (78), the endoplasmic reticulum”
Super-enhancers in the control of cell identity and disease. (2013, positive): “Brd4, a member of the bromodomain protein family, binds to Mediator and acetylated histones, and is involved in regulation of transcriptional elongation by RNA polymerase II (Jang et al., 2005; Jiang et al., 1998).”
Remodeling of the enhancer landscape during macrophage activation is coupled to enhancer transcription (2013, background): “cofactor Mediator and positive transcription elongation factor b (P-TEFb) (Jang et al., 2005; Yang et al., 2005).”
Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers (2013, background): “BRD4 is known to interact with Mediator and P-TEFb and to be involved in the control of transcriptional elongation by RNAPol II (Conaway and Conaway, 2011; Dawson et al., 2011; Jang et al., 2005; Krueger et al., 2010; Rahman et al., 2011; Yang et al., 2005).”
Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia (2011, background): “Abundant anti-apoptotic BCL-2 is a molecular target in leukaemias with t(4;11) translocation.”