PMID- 19321449
OWN - NLM
STAT- MEDLINE
DCOM- 20090707
LR  - 20240317
IS  - 0021-9258 (Print)
IS  - 1083-351X (Electronic)
IS  - 0021-9258 (Linking)
VI  - 284
IP  - 21
DP  - 2009 May 22
TI  - TIF1beta/KAP-1 is a coactivator of the orphan nuclear receptor NGFI-B/Nur77.
PG  - 14147-56
LID - 10.1074/jbc.M809023200 [doi]
AB  - In efforts to define mechanisms of transcriptional activation by the orphan 
      nuclear receptor NGFI-B (Nur77), we identified TIF1beta by mass spectrometry 
      within a nuclear protein complex containing NGFI-B. TIF1beta, also known as KAP-1 
      (KRAB domain-associated protein) or KRIP-1, acts as a transcriptional corepressor 
      for many transcription factors, in particular for the Kruppel-associated box 
      domain-containing zinc finger transcription factors. TIF1beta is also an 
      intrinsic component of two chromatin remodeling and histone deacetylase 
      complexes, the N-CoR1 and nucleosome remodeling and deacetylation complexes. In 
      contrast to these activities, we report that TIF1beta is a coactivator of NGFI-B 
      and that it is as potent as the SRC coactivators in this context. Using pull-down 
      assays and immunoprecipitation, we showed that TIF1beta interacts directly with 
      NGFI-B and with other Nur family members. NGFI-B is an important mediator of 
      hypothalamic corticotropin-releasing hormone (CRH) activation of 
      proopiomelanocortin (POMC) transcription, and TIF1beta enhances transcription 
      mediated through the NGFI-B target, the Nur response element (NurRE). The NurRE 
      binds Nur factor dimers and is responsive to signaling pathways. In keeping with 
      the role of NGFI-B as mediator of CRH signaling, we found that TIF1beta is 
      recruited to the POMC promoter following CRH stimulation and that TIF1beta 
      potentiates CRH and protein kinase A signaling through the NurRE; it acts 
      synergistically with the SRC2 coactivator. However, the actions of TIF1beta and 
      SRC2 were mapped to different NGFI-B AF-1 subdomains. Taken together, these 
      results indicate that TIF1beta is an important coactivator of NGFI-B-dependent 
      transcription.
FAU - Rambaud, Juliette
AU  - Rambaud J
AD  - Laboratory of Molecular Genetics, Institut de Recherches Cliniques de Montreal, 
      Montreal, Quebec H2W 1R7, Canada.
FAU - Desroches, Julien
AU  - Desroches J
FAU - Balsalobre, Aurelio
AU  - Balsalobre A
FAU - Drouin, Jacques
AU  - Drouin J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090325
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Cell Extracts)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (NR4A1 protein, human)
RN  - 0 (NR4A2 protein, human)
RN  - 0 (Nuclear Receptor Coactivator 2)
RN  - 0 (Nuclear Receptor Subfamily 4, Group A, Member 1)
RN  - 0 (Nuclear Receptor Subfamily 4, Group A, Member 2)
RN  - 0 (Receptors, Steroid)
RN  - 0 (Repressor Proteins)
RN  - 0 (Transcription Factors)
RN  - 66796-54-1 (Pro-Opiomelanocortin)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
RN  - EC 2.3.2.27 (TRIM28 protein, human)
RN  - EC 2.3.2.27 (Tripartite Motif-Containing Protein 28)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
SB  - IM
MH  - Cell Extracts
MH  - Cell Line
MH  - Cell Nucleus/metabolism
MH  - Corticotropin-Releasing Hormone/metabolism
MH  - Cyclic AMP-Dependent Protein Kinases/metabolism
MH  - DNA-Binding Proteins/chemistry/*metabolism
MH  - Humans
MH  - Molecular Weight
MH  - Nuclear Receptor Coactivator 2/metabolism
MH  - Nuclear Receptor Subfamily 4, Group A, Member 1
MH  - Nuclear Receptor Subfamily 4, Group A, Member 2
MH  - Pro-Opiomelanocortin/genetics
MH  - Protein Binding
MH  - Protein Structure, Tertiary
MH  - Receptors, Steroid/*metabolism
MH  - Repressor Proteins/chemistry/*metabolism
MH  - Response Elements/genetics
MH  - Signal Transduction
MH  - Transcription Factors/metabolism
MH  - Transcription, Genetic
MH  - Tripartite Motif-Containing Protein 28
PMC - PMC2682863
EDAT- 2009/03/27 09:00
MHDA- 2009/07/08 09:00
PMCR- 2010/05/22
CRDT- 2009/03/27 09:00
PHST- 2009/03/27 09:00 [entrez]
PHST- 2009/03/27 09:00 [pubmed]
PHST- 2009/07/08 09:00 [medline]
PHST- 2010/05/22 00:00 [pmc-release]
AID - S0021-9258(20)58123-4 [pii]
AID - 14147 [pii]
AID - 10.1074/jbc.M809023200 [doi]
PST - ppublish
SO  - J Biol Chem. 2009 May 22;284(21):14147-56. doi: 10.1074/jbc.M809023200. Epub 2009 
      Mar 25.