PMID- 9223286
OWN - NLM
STAT- MEDLINE
DCOM- 19970827
LR  - 20190501
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 94
IP  - 15
DP  - 1997 Jul 22
TI  - Activation of the orphan receptor RIP14 by retinoids.
PG  - 7909-14
AB  - Retinoids are crucial regulators of a wide variety of processes in both 
      developing and adult animals. These effects are thought to be mediated by the 
      retinoic acid (RA) receptors and the retinoid X receptors (RXRs). We have 
      identified an additional retinoid-activated receptor that is neither a retinoic 
      acid receptors nor an RXR. RXR-interacting protein 14 (RIP14), a recently 
      described orphan member of the nuclear receptor superfamily, can be activated by 
      either all-trans-RA (tRA) or the synthetic retinoid TTNPB [[E]-4-[2-(5, 6, 7, 
      8-tetrahydro-5, 5, 8, 8-tetramethyl-2-naphthalenyl)propen-1-yl]benzoic 
      acid].RIP14 binds to DNA as a heterodimer with RXR. In the presence of either tRA 
      or TTNPB, the addition of 9-cis-RA or the RXR-specific agonist LG1069 [4-[1-(3, 
      5, 5, 8, 8-pentamethyl-5, 6, 7, 8-tertrahydro-2-naphthyl)ethenyl]benzoic acid] 
      results in additional activation. Mutations of the ligand-dependent 
      transcriptional activation functions indicate that TTNPB activates the RIP14 
      component of the RIP14-RXR heterodimer, that 9-cis-RA and LG1069 activate RXR, 
      and that tRA activates via both RIP14 and RXR. Despite the very effective 
      activation of RIP14 by tRA or TTNPB, relatively high concentrations of these 
      compounds are required, and no evidence for direct binding of either compound was 
      obtained using several approaches. These results suggest that RIP14 is the 
      receptor for an as-yet-unidentified retinoid metabolite.
FAU - Zavacki, A M
AU  - Zavacki AM
AD  - Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 
      02114, USA.
FAU - Lehmann, J M
AU  - Lehmann JM
FAU - Seol, W
AU  - Seol W
FAU - Willson, T M
AU  - Willson TM
FAU - Kliewer, S A
AU  - Kliewer SA
FAU - Moore, D D
AU  - Moore DD
LA  - eng
GR  - F32 DK09641/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Klf2 protein, mouse)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
RN  - 0C5V0MRU6P (farnesoid X-activated receptor)
SB  - IM
MH  - Animals
MH  - Carrier Proteins/*drug effects/genetics/metabolism
MH  - Cell Line
MH  - DNA-Binding Proteins
MH  - Kruppel-Like Transcription Factors
MH  - Mice
MH  - Mutagenesis
MH  - Rats
MH  - *Receptors, Cytoplasmic and Nuclear
MH  - Receptors, Retinoic Acid/drug effects/metabolism
MH  - Retinoid X Receptors
MH  - Retinoids/*pharmacology
MH  - Sequence Deletion
MH  - *Trans-Activators
MH  - Transcription Factors/drug effects/metabolism
PMC - PMC21528
EDAT- 1997/07/22 00:00
MHDA- 1997/07/22 00:01
PMCR- 1998/01/22
CRDT- 1997/07/22 00:00
PHST- 1997/07/22 00:00 [pubmed]
PHST- 1997/07/22 00:01 [medline]
PHST- 1997/07/22 00:00 [entrez]
PHST- 1998/01/22 00:00 [pmc-release]
AID - 1594 [pii]
AID - 10.1073/pnas.94.15.7909 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):7909-14. doi: 
      10.1073/pnas.94.15.7909.