PMID- 8417360
OWN - NLM
STAT- MEDLINE
DCOM- 19930127
LR  - 20210526
IS  - 0270-7306 (Print)
IS  - 1098-5549 (Electronic)
IS  - 0270-7306 (Linking)
VI  - 13
IP  - 1
DP  - 1993 Jan
TI  - GATA and Ets cis-acting sequences mediate megakaryocyte-specific expression.
PG  - 668-76
AB  - The human glycoprotein IIB (GPIIB) gene is expressed only in megakaryocytes, and 
      its promoter displays cell type specificity. We show that this specificity 
      involved two cis-acting sequences. The first one, located at -55, contains a GATA 
      binding site. Point mutations that abolish protein binding on this site decrease 
      the activity of the GPIIB promoter but do not affect its tissue specificity. The 
      second one, located at -40, contains an Ets consensus sequence, and we show that 
      Ets-1 or Ets-2 protein can interact with this -40 GPIIB sequence. Point mutations 
      that impair Ets binding decrease the activity of the GPIIB promoter to the same 
      extent as do mutations that abolish GATA binding. A GPIIB 40-bp DNA fragment 
      containing the GATA and Ets binding sites can confer activity to a heterologous 
      promoter in megakaryocytic cells. This activity is independent of the GPIIB DNA 
      fragment orientation, and mutations on each binding site result in decreased 
      activity. Using cotransfection assays, we show that c-Ets-1 and human GATA1 can 
      transactive the GPIIB promoter in HeLa cells and can act additively. Northern 
      (RNA) blot analysis indicates that the ets-1 mRNA level is increased during 
      megakaryocyte-induced differentiation of erythrocytic/megakaryocytic cell lines. 
      Gel retardation assays show that the same GATA-Ets association is found in the 
      human GPIIB enhancer and the rat platelet factor 4 promoter, the other two 
      characterized regulatory regions of megakaryocyte-specific genes. These results 
      indicate that GATA and Ets cis-acting sequences are an important determinant of 
      megakaryocytic specific gene expression.
FAU - Lemarchandel, V
AU  - Lemarchandel V
AD  - INSERM U.91, Hopital Henri-Mondor, Creteil, France.
FAU - Ghysdael, J
AU  - Ghysdael J
FAU - Mignotte, V
AU  - Mignotte V
FAU - Rahuel, C
AU  - Rahuel C
FAU - Romeo, P H
AU  - Romeo PH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (ERF protein, human)
RN  - 0 (ETS1 protein, human)
RN  - 0 (ETS2 protein, human)
RN  - 0 (Ets1 protein, rat)
RN  - 0 (Oligodeoxyribonucleotides)
RN  - 0 (Platelet Membrane Glycoproteins)
RN  - 0 (Proto-Oncogene Protein c-ets-1)
RN  - 0 (Proto-Oncogene Protein c-ets-2)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-ets)
RN  - 0 (RNA, Messenger)
RN  - 0 (Repressor Proteins)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
SB  - IM
GS  - GPIIB
GS  - PF4
GS  - c-ets-1/ge
GS  - c-ets-2/ge
MH  - Base Sequence
MH  - DNA-Binding Proteins/*metabolism
MH  - Enhancer Elements, Genetic
MH  - *Gene Expression Regulation
MH  - HeLa Cells
MH  - Humans
MH  - Megakaryocytes/*physiology
MH  - Molecular Sequence Data
MH  - Oligodeoxyribonucleotides/chemistry
MH  - Platelet Membrane Glycoproteins/*genetics
MH  - *Promoter Regions, Genetic
MH  - Proto-Oncogene Protein c-ets-1
MH  - Proto-Oncogene Protein c-ets-2
MH  - Proto-Oncogene Proteins/metabolism
MH  - Proto-Oncogene Proteins c-ets
MH  - RNA, Messenger/genetics
MH  - *Repressor Proteins
MH  - *Trans-Activators
MH  - Transcription Factors/*metabolism
MH  - Transcriptional Activation
PMC - PMC358945
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
PMCR- 1993/01/01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
PHST- 1993/01/01 00:00 [pmc-release]
AID - 10.1128/mcb.13.1.668-676.1993 [doi]
PST - ppublish
SO  - Mol Cell Biol. 1993 Jan;13(1):668-76. doi: 10.1128/mcb.13.1.668-676.1993.