PMID- 10455134
OWN - NLM
STAT- MEDLINE
DCOM- 19990930
LR  - 20191210
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 35
DP  - 1999 Aug 27
TI  - AML1 (CBFalpha2) cooperates with B cell-specific activating protein (BSAP/PAX5)
      in activation of the B cell-specific BLK gene promoter.
PG  - 24671-6
AB  - AML1 plays a critical role during hematopoiesis and chromosomal translocations
      involving AML1 are commonly associated with different forms of leukemia,
      including pre-B acute lymphoblastic leukemia. To understand the function of AML1 
      during B cell differentiation, we analyzed regulatory regions of B cell-specific 
      genes for potential AML1-binding sites and have identified a putative
      AML1-binding site in the promoter of the B cell-specific tyrosine kinase gene,
      blk. Gel mobility shift assays and transient transfection assays demonstrate that
      AML1 binds specifically to this site in the blk promoter and this binding site is
      important for blk promoter activity. Furthermore, in vitro binding analysis
      revealed that the AML1 runt DNA-binding domain physically interacts with the
      paired DNA-binding domain of BSAP, a B cell-specific transcription factor. BSAP
      has been shown previously to be important for B cell-specific regulation of the
      blk gene. Physical interaction of AML1 with BSAP correlates with functional
      cooperativity in transfection studies where AML1 and BSAP synergistically
      activate blk promoter transcription by more than 50-fold. These results
      demonstrate physical and functional interactions between AML1 and BSAP and
      suggest that AML1 is an important factor for regulating a critical B
      cell-specific gene, blk.
FAU - Libermann, T A
AU  - Libermann TA
AD  - New England Baptist Bone and Joint Institute, Beth Israel Deaconess Medical
      Center, Harvard Medical School, Boston, Massachusetts 02115, USA.
FAU - Pan, Z
AU  - Pan Z
FAU - Akbarali, Y
AU  - Akbarali Y
FAU - Hetherington, C J
AU  - Hetherington CJ
FAU - Boltax, J
AU  - Boltax J
FAU - Yergeau, D A
AU  - Yergeau DA
FAU - Zhang, D E
AU  - Zhang DE
LA  - eng
GR  - AI39613/AI/NIAID NIH HHS/United States
GR  - CA/AI59589/CA/NCI NIH HHS/United States
GR  - CA72009/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Bik protein, mouse)
RN  - 0 (Carrier Proteins)
RN  - 0 (Core Binding Factor Alpha 2 Subunit)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (PAX5 Transcription Factor)
RN  - 0 (PAX5 protein, human)
RN  - 0 (Pax5 protein, mouse)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RUNX1 protein, human)
RN  - 0 (Runx1 protein, mouse)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - Animals
MH  - Apoptosis Regulatory Proteins
MH  - B-Lymphocytes/*metabolism
MH  - Base Sequence
MH  - Binding Sites
MH  - Carrier Proteins/*genetics
MH  - Cell Line
MH  - Core Binding Factor Alpha 2 Subunit
MH  - DNA-Binding Proteins/*metabolism
MH  - Gene Expression Regulation
MH  - Genes, Reporter
MH  - Humans
MH  - Mice
MH  - *Mitochondrial Proteins
MH  - Molecular Sequence Data
MH  - Mutation
MH  - Nuclear Proteins/*metabolism
MH  - PAX5 Transcription Factor
MH  - Promoter Regions, Genetic
MH  - Protein Binding
MH  - *Proto-Oncogene Proteins
MH  - Transcription Factors/*metabolism
MH  - Transcriptional Activation
EDAT- 1999/08/24 00:00
MHDA- 1999/08/24 00:01
CRDT- 1999/08/24 00:00
PHST- 1999/08/24 00:00 [pubmed]
PHST- 1999/08/24 00:01 [medline]
PHST- 1999/08/24 00:00 [entrez]
AID - 10.1074/jbc.274.35.24671 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Aug 27;274(35):24671-6. doi: 10.1074/jbc.274.35.24671.