A
Anupong Tangpeerachaikul
Researcher at Harvard University
Publications - 3
Citations - 425
Anupong Tangpeerachaikul is an academic researcher from Harvard University. The author has contributed to research in topics: Cyclin-dependent kinase 8 & Cyclin-dependent kinase. The author has an hindex of 3, co-authored 3 publications receiving 320 citations.
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Journal ArticleDOI
Mediator kinase inhibition further activates super-enhancer-associated genes in AML
Henry E. Pelish,Brian B. Liau,Ioana Nitulescu,Anupong Tangpeerachaikul,Zachary C. Poss,Diogo H. Da Silva,Brittany T. Caruso,Alexander Arefolov,Olugbeminiyi O Fadeyi,Amanda L. Christie,Karrie Du,Deepti Banka,E.V. Schneider,Anja Jestel,Ge Zou,Chong Si,Christopher C. Ebmeier,Roderick T. Bronson,Andrei V. Krivtsov,Andrew G. Myers,Nancy E. Kohl,Andrew L. Kung,Scott A. Armstrong,Madeleine E. Lemieux,Dylan J. Taatjes,Matthew D. Shair +25 more
TL;DR: It is shown that the Mediator-associated kinases cyclin-dependent kinase 8 (CDK8) and CDK19 restrain increased activation of key SE-associated genes in acute myeloid leukaemia (AML) cells.
Journal ArticleDOI
Identification of Mediator Kinase Substrates in Human Cells using Cortistatin A and Quantitative Phosphoproteomics
Zachary C. Poss,Christopher C. Ebmeier,Aaron T. Odell,Anupong Tangpeerachaikul,Thomas Lee,Henry E. Pelish,Matthew D. Shair,Robin D. Dowell,William M. Old,Dylan J. Taatjes +9 more
TL;DR: Quantitative proteome analyses revealed that CA selectively affected pathways implicated in inflammation, growth, and metabolic regulation, and increased turnover of Mediator kinase targets was not generally observed.
Proceedings ArticleDOI
Abstract 1468: NUV-655 (NVL-655) is a selective, brain-penetrant ALK inhibitor with antitumor activity against the lorlatinib-resistant G1202R/L1196M compound mutation
Henry E. Pelish,Anupong Tangpeerachaikul,Nancy E. Kohl,James R. Porter,Matthew D. Shair,Joshua C. Horan +5 more
TL;DR: Pelish et al. as mentioned in this paper designed a novel ALK inhibitor NUV-655 (NVL-655) for broader coverage of ALK resistance mutations, activity in the CNS, and selectivity over structurally related tropomyosin receptor kinase B (TRKB).