PMID- 10648599
OWN - NLM
STAT- MEDLINE
DCOM- 20000215
LR  - 20190508
IS  - 0270-7306 (Print)
IS  - 0270-7306 (Linking)
VI  - 20
IP  - 4
DP  - 2000 Feb
TI  - Extracellular signal-regulated kinase binds to TFII-I and regulates its
      activation of the c-fos promoter.
PG  - 1140-8
AB  - We have previously shown that TFII-I enhances transcriptional activation of the
      c-fos promoter through interactions with upstream elements in a signal-dependent 
      manner. Here we demonstrate that activated Ras and RhoA synergize with TFII-I for
      c-fos promoter activation, whereas dominant-negative Ras and RhoA inhibit these
      effects of TFII-I. The Mek1 inhibitor, PD98059 abrogates the enhancement of the
      c-fos promoter by TFII-I, indicating that TFII-I function is dependent on an
      active mitogen-activated protein (MAP) kinase pathway. Analysis of the TFII-I
      protein sequence revealed that TFII-I contains a consensus MAP kinase interaction
      domain (D box). Consistent with this, we have found that TFII-I forms an in vivo 
      complex with extracellular signal-related kinase (ERK). Point mutations within
      the consensus MAP kinase binding motif of TFII-I inhibit its ability to bind ERK 
      and its ability to enhance the c-fos promoter. Therefore, the D box of TFII-I is 
      required for its activity on the c-fos promoter. Moreover, the interaction
      between TFII-I and ERK can be regulated. Serum stimulation enhances complex
      formation between TFII-I and ERK, and dominant-negative Ras abrogates this
      interaction. In addition, TFII-I can be phosphorylated in vitro by ERK and
      mutation of consensus MAP kinase substrate sites at serines 627 and 633 impairs
      the phosphorylation of TFII-I by ERK and its activity on the c-fos promoter.
      These results suggest that ERK regulates the activity of TFII-I by direct
      phosphorylation.
FAU - Kim, D W
AU  - Kim DW
AD  - Department of Cellular and Molecular Physiology, Tufts University School of
      Medicine, Boston, Massachusetts 02111, USA.
FAU - Cochran, B H
AU  - Cochran BH
LA  - eng
GR  - R01 GM051551/GM/NIGMS NIH HHS/United States
GR  - R01-GM51551/GM/NIGMS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (DNA Primers)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Transcription Factors)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.6.5.2 (ras Proteins)
RN  - EC 3.6.5.2 (rho GTP-Binding Proteins)
SB  - IM
MH  - 3T3 Cells
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - DNA Primers/genetics
MH  - DNA-Binding Proteins/genetics/*metabolism
MH  - Gene Expression Regulation
MH  - *Genes, fos
MH  - Humans
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/genetics/*metabolism
MH  - Molecular Sequence Data
MH  - Phosphorylation
MH  - Promoter Regions, Genetic
MH  - Recombinant Proteins/genetics/metabolism
MH  - Sequence Homology, Amino Acid
MH  - Signal Transduction
MH  - Transcription Factors/genetics/*metabolism
MH  - ras Proteins/metabolism
MH  - rho GTP-Binding Proteins/metabolism
PMC - PMC85232
EDAT- 2000/01/29 09:00
MHDA- 2000/02/19 09:00
CRDT- 2000/01/29 09:00
PHST- 2000/01/29 09:00 [pubmed]
PHST- 2000/02/19 09:00 [medline]
PHST- 2000/01/29 09:00 [entrez]
AID - 10.1128/mcb.20.4.1140-1148.2000 [doi]
PST - ppublish
SO  - Mol Cell Biol. 2000 Feb;20(4):1140-8. doi: 10.1128/mcb.20.4.1140-1148.2000.