PMID- 12112017
OWN - NLM
STAT- MEDLINE
DCOM- 20021217
LR  - 20181130
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 86
IP  - 1
DP  - 2002
TI  - Retinoid X receptors and retinoid response in neuroblastoma cells.
PG  - 67-78
AB  - Retinoic acid (RA) modulates differentiation and apoptosis of neural cells via RA 
      receptors (RARs) and retinoid X receptors (RXRs). Neuroblastoma cells are 
      potentially useful models for elucidating the molecular mechanisms of RA in 
      neural cells, and responses to different isomers of RA have been interpreted in 
      terms of differential homo- and heterodimerization of RXRs. The aim of this study 
      was to identify the RXR types expressed in neuroblast and substrate-adherent 
      neuroblastoma cells, and to study the participation of these RXRs in RAR 
      heterodimers. RXRbeta was the predominant RXR type in N-type SH SY 5Y cells and 
      S-type SH EP cells. Gel shift and supershift assays demonstrated that RARbeta and 
      RARgamma predominantly heterodimerize with RXRbeta. In SH SY 5Y cells, 
      RARgamma/RXRbeta was the predominant heterodimer binding to the DR5 RARE in the 
      absence of 9-cis RA (9C), whereas the balance shifted in favor of RARbeta/RXRbeta 
      in the presence of ligand. There was a marked difference between the N- and 
      S-type neuroblastoma cells in retinoid receptor-DNA interactions, and this may 
      underlie the differential effects of retinoids in these neuroblastoma cell types. 
      There was no evidence to indicate that 9C functions via RXR homodimers in either 
      SH SY 5Y or SH EP neuroblastoma cells. The results of this study suggest that 
      interactions between retinoid receptors and other nuclear proteins may be 
      critical determinants of retinoid responses in neural cells.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Rana, Birju
AU  - Rana B
AD  - Department of Endocrinology, Medical Molecular Biology Group, Medical School, 
      University of Newcastle, Newcastle upon Tyne NE2 4HH, UK.
FAU - Veal, Gareth J
AU  - Veal GJ
FAU - Pearson, Andrew D J
AU  - Pearson AD
FAU - Redfern, Christopher P F
AU  - Redfern CP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 0 (Transcription Factors)
RN  - 1UA8E65KDZ (Alitretinoin)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Alitretinoin
MH  - Dimerization
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Neuroblastoma/*genetics/*metabolism
MH  - Receptors, Retinoic Acid/chemistry/*metabolism
MH  - Retinoid X Receptors
MH  - Retinoids/*pharmacology
MH  - Signal Transduction/*drug effects
MH  - Transcription Factors/chemistry/*metabolism
MH  - Tretinoin/pharmacology
MH  - Tumor Cells, Cultured
EDAT- 2002/07/12 10:00
MHDA- 2002/12/18 04:00
CRDT- 2002/07/12 10:00
PHST- 2002/07/12 10:00 [pubmed]
PHST- 2002/12/18 04:00 [medline]
PHST- 2002/07/12 10:00 [entrez]
AID - 10.1002/jcb.10192 [doi]
PST - ppublish
SO  - J Cell Biochem. 2002;86(1):67-78. doi: 10.1002/jcb.10192.