N
Nicholas B. La Thangue
Researcher at University of Oxford
Publications - 109
Citations - 12618
Nicholas B. La Thangue is an academic researcher from University of Oxford. The author has contributed to research in topics: Transcription factor & E2F. The author has an hindex of 49, co-authored 105 publications receiving 11482 citations. Previous affiliations of Nicholas B. La Thangue include University of Glasgow & National Institute for Medical Research.
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Journal ArticleDOI
Selective inhibition of BET bromodomains.
Panagis Filippakopoulos,Jun Qi,Sarah Picaud,Yao Shen,William B. Smith,Oleg Fedorov,Elizabeth M. Morse,T. Keates,Tyler T. Hickman,I. Felletar,Martin Philpott,Shonagh Munro,Michael R. McKeown,Yuchuan Wang,Amanda L. Christie,Nathan West,Michael J. Cameron,Brian E. Schwartz,Tom D. Heightman,Nicholas B. La Thangue,Christopher A. French,Olaf Wiest,Andrew L. Kung,Stefan Knapp,Stefan Knapp,James E. Bradner +25 more
TL;DR: A cell-permeable small molecule (JQ1) that binds competitively to acetyl-lysine recognition motifs, or bromodomains is reported, establishing proof-of-concept for targeting protein–protein interactions of epigenetic ‘readers’, and providing a versatile chemical scaffold for the development of chemical probes more broadly throughout the b romodomain family.
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p300/CBP proteins: HATs for transcriptional bridges and scaffolds
H M Chan,Nicholas B. La Thangue +1 more
TL;DR: p300/CBP transcriptional co-activator proteins play a central role in co-ordinating and integrating multiple signal-dependent events with the transcription apparatus, allowing the appropriate level of gene activity to occur in response to diverse physiological cues.
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Arginine methylation regulates the p53 response
Martin Jansson,Stephen T. Durant,Er Chieh Cho,Sharon Sheahan,Mariola J. Edelmann,Benedikt M. Kessler,Nicholas B. La Thangue +6 more
TL;DR: It is shown that the protein arginine methyltransferase (PRMT) 5, as a co-factor in a DNA damage responsive co-activator complex that interacts with p53, is responsible for methylating p53 and that PRMT5 depletion triggers p53-dependent apoptosis.
Journal ArticleDOI
HDAC inhibitors in cancer biology: emerging mechanisms and clinical applications
Omar Khan,Nicholas B. La Thangue +1 more
TL;DR: Developments in the understanding of molecular events that underlie the anti‐cancer effects of HDAC inhibitors are discussed and this information is related to the emerging clinical picture for the application of these inhibitors in the treatment of cancer.
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Chk2 activates E2F-1 in response to DNA damage
TL;DR: It is reported that checkpoint kinase 2 (Chk2) regulates E2F-1 activity in response to the DNA-damaging agent etoposide, resulting in apoptosis and a role for E2f-1 in checkpoint control and a plausible explanation for the tumour suppressor activity of E2 F-1.