PMID- 15967409
OWN - NLM
STAT- MEDLINE
DCOM- 20050907
LR  - 20071114
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 333
IP  - 4
DP  - 2005 Aug 12
TI  - The tumor necrosis factor-alpha AU-rich element inhibits the stable association 
      of the 40S ribosomal subunit with RNA transcripts.
PG  - 1100-6
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a potent cytokine that is central to 
      normal immune responses as well as autoimmune inflammatory diseases. The 
      production of TNF-alpha protein is thus tightly regulated at multiple levels. 
      Translational control is one of the means by which TNF-alpha production is 
      repressed in unstimulated cells. To examine the mechanism by which the 
      translation of TNF-alpha mRNA transcripts is repressed, we have used an in vitro 
      translation system. The AU-rich element (ARE) in the 3' UTR of TNF-alpha 
      transcripts was sufficient to confer translational repression. This effect was 
      observed using transcripts containing a 5' m(7)G cap but not uncapped 
      transcripts, and was independent of a poly(A) tail. Sucrose gradient analysis 
      revealed that ARE-containing transcripts were present at relatively lower amounts 
      in 80S-associated fractions and higher amounts in non-ribosome-bound RNA 
      fractions, with no accumulation of 48S-associated transcripts. ARE-mediated 
      translational repression was competitively inhibited by ARE-containing 
      transcripts. These data indicate that a TNF-alpha ARE-binding trans-acting 
      factor(s) inhibits the association of the 43S complex with RNA transcripts.
FAU - Wax, Stephen D
AU  - Wax SD
AD  - Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, 
      Harvard Medical School, Boston, MA, USA.
FAU - Nakamura, Hideki
AU  - Nakamura H
FAU - Anderson, Paul J
AU  - Anderson PJ
LA  - eng
GR  - AI01834/AI/NIAID NIH HHS/United States
GR  - AI133600/AI/NIAID NIH HHS/United States
GR  - AI50167/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Protein Subunits)
RN  - 0 (Repressor Proteins)
RN  - 0 (Ribosomal Proteins)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Base Sequence
MH  - Gene Expression Regulation/*physiology
MH  - Protein Biosynthesis/*physiology
MH  - Protein Subunits
MH  - Repetitive Sequences, Nucleic Acid
MH  - Repressor Proteins/genetics/*metabolism
MH  - Ribosomal Proteins/genetics/*metabolism
MH  - Transcription Factors/genetics/*metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/*metabolism
EDAT- 2005/06/22 09:00
MHDA- 2005/09/08 09:00
CRDT- 2005/06/22 09:00
PHST- 2005/06/01 00:00 [received]
PHST- 2005/06/06 00:00 [accepted]
PHST- 2005/06/22 09:00 [pubmed]
PHST- 2005/09/08 09:00 [medline]
PHST- 2005/06/22 09:00 [entrez]
AID - S0006-291X(05)01222-2 [pii]
AID - 10.1016/j.bbrc.2005.06.018 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2005 Aug 12;333(4):1100-6. doi: 
      10.1016/j.bbrc.2005.06.018.