PMID- 10567378
OWN - NLM
STAT- MEDLINE
DCOM- 19991229
LR  - 20190508
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 48
DP  - 1999 Nov 26
TI  - p300 protein as a coactivator of GATA-5 in the transcription of
      cardiac-restricted atrial natriuretic factor gene.
PG  - 34096-102
AB  - A cellular target of adenovirus E1A oncoprotein, p300 is a transcriptional
      coactivator and a negative regulator of cellular proliferation. A previous study 
      suggests that the p300 family is also involved in cell type-specific
      transcription in cardiac myocytes. However, nothing is known about which cardiac 
      transcription factor(s) interact with and transactivate through these proteins.
      The transcription factors GATA-4/5/6 have been implicated as key regulators of
      cardiogenesis, and they participate in the transcription of many cardiac-specific
      genes. Here we show that E1A represses the GATA-5-dependent transactivation of a 
      promoter derived from the cardiac-restricted atrial natriuretic factor gene. This
      repression is correlated with the interaction of E1A with p300, indicating that
      p300 participates in GATA-5-dependent transactivation. E1A markedly
      down-regulates endogenous atrial natriuretic factor expression, as well as
      disrupts the interaction between p300 and GATA-5. A small fragment of p300
      containing the carboxyl-terminal cysteine/histidine-rich domain, sufficient to
      interact with GATA-5, prevents transcriptional activation by GATA-5 as a
      dominant-negative mutant. Consistent with its role as a coactivator, p300
      markedly potentiates GATA-5-activated transcription. These results implicate p300
      as an important component of myocardial cell differentiation and provide an
      insight into the relationship between mechanisms that mediate cell type-specific 
      transcription and cell cycle regulation during cardiogenesis.
FAU - Kakita, T
AU  - Kakita T
AD  - Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto
      University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
FAU - Hasegawa, K
AU  - Hasegawa K
FAU - Morimoto, T
AU  - Morimoto T
FAU - Kaburagi, S
AU  - Kaburagi S
FAU - Wada, H
AU  - Wada H
FAU - Sasayama, S
AU  - Sasayama S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Adenovirus E1A Proteins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (GATA5 Transcription Factor)
RN  - 0 (Gata5 protein, mouse)
RN  - 0 (Gata5 protein, rat)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
RN  - EC 2.3.1.48 (E1A-Associated p300 Protein)
RN  - EC 2.3.1.48 (Ep300 protein, mouse)
RN  - EC 2.3.1.48 (Ep300 protein, rat)
SB  - IM
MH  - 3T3 Cells
MH  - Adenovirus E1A Proteins/genetics
MH  - Animals
MH  - Animals, Newborn
MH  - Atrial Natriuretic Factor/*genetics/metabolism
MH  - Binding Sites
MH  - COS Cells
MH  - DNA-Binding Proteins/genetics/*metabolism
MH  - E1A-Associated p300 Protein
MH  - GATA5 Transcription Factor
MH  - Gene Expression Regulation
MH  - Mice
MH  - Mutation
MH  - Myocardium/cytology/*metabolism
MH  - Nuclear Proteins/genetics/*metabolism
MH  - Promoter Regions, Genetic/genetics
MH  - Protein Binding
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Trans-Activators/genetics/*metabolism
MH  - Transcription Factors/genetics/*metabolism
MH  - Transcription, Genetic
MH  - Transcriptional Activation
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - 10.1074/jbc.274.48.34096 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Nov 26;274(48):34096-102. doi: 10.1074/jbc.274.48.34096.