PMID- 10598580
OWN - NLM
STAT- MEDLINE
DCOM- 20000110
LR  - 20071114
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 13
IP  - 12
DP  - 1999 Dec
TI  - c-Jun enhancement of cyclic adenosine 3',5'-monophosphate response
      element-dependent transcription induced by transforming growth factor-beta is
      independent of c-Jun binding to DNA.
PG  - 2039-48
AB  - Transforming growth factor-beta (TGFbeta) enhances transcription from reporter
      genes regulated by a single consensus cAMP-response element (CRE) upon
      transfection into the immortalized human keratinocyte cell line, HaCaT. Whereas
      both CRE-binding protein (CREB) and c-Jun present in extracts of unstimulated
      cells can complex with a CRE in gel-shift experiments, TGFbeta treatment
      increases the amount of c-Jun found in the complex. Overexpression of c-Jun is
      sufficient to increase CRE and GAL4-CREB-dependent transcription and mimics the
      stimulatory effects of TGFbeta on transcription from either reporter gene.
      Surprisingly, although a portion of CREB in unstimulated cells is phosphorylated 
      on the activating serine residue, Ser-133, this level of phospho-CREB is not
      altered by TGFbeta treatment. In fact, the CREB-dependent transcriptional effects
      of TGFbeta or c-Jun do not require phosphorylation of Ser-133, although
      CREB-binding protein (CBP) is required as evidenced by the observation that the
      adenoviral oncoprotein E1A can block the effects of both agents. c-Jun
      enhancement of CRE or GAL4-CREB-dependent transcription neither requires the
      DNA-binding nor N-terminal domains of c-Jun. Collectively, these results are
      consistent with a model in which signaling pathways initiated by TGFbeta can
      stimulate CREB-dependent transcription by increasing the cellular concentration
      of c-Jun, which participates in activation of the CBP-containing transcription
      complex.
FAU - Hu, P P
AU  - Hu PP
AD  - Department of Pharmacology and Cancer Biology, Duke University Medical Center,
      Durham, North Carolina 27710, USA.
FAU - Harvat, B L
AU  - Harvat BL
FAU - Hook, S S
AU  - Hook SS
FAU - Shen, X
AU  - Shen X
FAU - Wang, X F
AU  - Wang XF
FAU - Means, A R
AU  - Means AR
LA  - eng
GR  - DK-45746/DK/NIDDK NIH HHS/United States
GR  - GM-33976/GM/NIGMS NIH HHS/United States
GR  - HD-07503/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Adenovirus E1A Proteins)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (Transforming Growth Factor beta)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Adenovirus E1A Proteins/pharmacology
MH  - Cell Line, Transformed
MH  - Cyclic AMP Response Element-Binding Protein/pharmacology/*physiology
MH  - DNA/*metabolism
MH  - Drug Synergism
MH  - Gene Expression
MH  - Humans
MH  - Keratinocytes/metabolism
MH  - Proto-Oncogene Proteins c-jun/genetics/pharmacology/*physiology
MH  - *Transcription, Genetic
MH  - Transfection
MH  - Transforming Growth Factor beta/*pharmacology
EDAT- 1999/12/22 00:00
MHDA- 1999/12/22 00:01
CRDT- 1999/12/22 00:00
PHST- 1999/12/22 00:00 [pubmed]
PHST- 1999/12/22 00:01 [medline]
PHST- 1999/12/22 00:00 [entrez]
AID - 10.1210/mend.13.12.0405 [doi]
PST - ppublish
SO  - Mol Endocrinol. 1999 Dec;13(12):2039-48. doi: 10.1210/mend.13.12.0405.