Please use this identifier to cite or link to this item: https://doi.org/10.1182/blood-2008-01-134122
Title: PEBP2-2/CBF-2 dependent phosphorylation of RUNX1 and p300 by HIPK2: Implications for leukemogenesis
Authors: Wee, H.-J.
Voon, D.C.-C.
Bae, S.-C.
Ito, Y. 
Issue Date: 1-Nov-2008
Citation: Wee, H.-J., Voon, D.C.-C., Bae, S.-C., Ito, Y. (2008-11-01). PEBP2-2/CBF-2 dependent phosphorylation of RUNX1 and p300 by HIPK2: Implications for leukemogenesis. Blood 112 (9) : 3777-3787. ScholarBank@NUS Repository. https://doi.org/10.1182/blood-2008-01-134122
Abstract: The heterodimeric transcription factor RUNX1/PEBP2-β (also known as AML1/CBF-β) is essential for definitive hematopoiesis. Here, we show that interaction with PEBP2-β leads to the phosphorylation of RUNX1, which in turn induces p300 phosphorylation. This is mediated by homeodomain interacting kinase 2 (HIPK2), targeting Ser249, Ser273, and Thr 276 in RUNX1, in a mannerthat is also dependent on the RUNX1 PY motif. Importantly, we observed the in vitro disruption of this phosphorylation cascade by multiple leukemogenic genetic defects targeting RUNX1/CBFB. In particular, the oncogenic protein PEBP2-β-SMMHC prevents RUNX1/p300 phosphorylation by sequestering HIPK2 to mlslocalized RUNX1/β-SMMHC complexes. Therefore, phosphorylation of RUNX1 appears a critical step In Its association with and phosphorylation of p300, and Its disruption may be a common theme In RUASX1-associated leukemogenesls. © 2008 by The American Society of Hematology.
Source Title: Blood
URI: http://scholarbank.nus.edu.sg/handle/10635/132801
ISSN: 00064971
DOI: 10.1182/blood-2008-01-134122
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

38
checked on Nov 11, 2018

WEB OF SCIENCETM
Citations

36
checked on Oct 17, 2018

Page view(s)

13
checked on Oct 4, 2018

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.