PMID- 1328864
OWN - NLM
STAT- MEDLINE
DCOM- 19921116
LR  - 20210804
IS  - 0270-7306 (Print)
IS  - 1098-5549 (Electronic)
IS  - 0270-7306 (Linking)
VI  - 12
IP  - 11
DP  - 1992 Nov
TI  - Terminal differentiation in keratinocytes involves positive as well as negative 
      regulation by retinoic acid receptors and retinoid X receptors at retinoid 
      response elements.
PG  - 4862-71
AB  - Terminal differentiation of epidermal keratinocytes is inhibited by 1 microM 
      retinoic acid, a concentration which induces differentiation in a number of cell 
      types, including F9 teratocarcinoma cells. The molecular basis for these opposing 
      retinoid responses is unknown, although retinoic acid receptors (RARs) and 
      retinoid X receptors (RXRs) have been detected in both cell types. When F9 cells 
      are stably transfected with a truncated RAR alpha lacking the E/F domain 
      necessary for ligand binding and RAR/RXR dimerization, action at retinoid 
      response elements is suppressed and cells produce a retinoic acid-resistant 
      phenotype; i.e., they are blocked in differentiation (A. S. Espeseth, S. P. 
      Murphy, and E. Linney, Genes Dev. 3:1647-1656, 1989). If retinoid receptors 
      influence epidermal differentiation only in a negative fashion, then suppression 
      of transactivation at retinoid response elements would be expected to enhance, 
      rather than block, keratinocyte differentiation. In this study, we show that 
      surprisingly, even though constitutive expression of an analogous truncated RAR 
      gamma in keratinocytes specifically suppressed transactivation at retinoid 
      response elements, keratinocytes were blocked, rather than enhanced, in their 
      ability to undergo morphological and biochemical features of differentiation. 
      These findings demonstrate a direct and hitherto unrecognized role for RARs and 
      RXRs in positively as well as negatively regulating epidermal differentiation. 
      Additionally, our studies extend those of Espeseth et al. (Genes Dev. 
      3:1647-1656, 1989), indicating a novel RAR function independent of the E/F 
      domain.
FAU - Aneskievich, B J
AU  - Aneskievich BJ
AD  - Department of Molecular Genetics and Cell Biology, Howard Hughes Medical 
      Institute, University of Chicago, Illinois 60637.
FAU - Fuchs, E
AU  - Fuchs E
LA  - eng
GR  - AR31737/AR/NIAMS 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  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (Carrier Proteins)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 0 (Retinol-Binding Proteins)
RN  - 5688UTC01R (Tretinoin)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Base Sequence
MH  - Carrier Proteins/*metabolism
MH  - Cell Differentiation/physiology
MH  - DNA
MH  - Humans
MH  - Keratinocytes/*cytology
MH  - Molecular Sequence Data
MH  - Promoter Regions, Genetic
MH  - Proto-Oncogene Proteins c-jun/metabolism
MH  - Receptors, Retinoic Acid
MH  - Receptors, Thyroid Hormone/metabolism
MH  - Retinol-Binding Proteins/*metabolism
MH  - Tretinoin/*metabolism
MH  - Tumor Cells, Cultured
PMC - PMC360419
EDAT- 1992/11/01 00:00
MHDA- 1992/11/01 00:01
PMCR- 1992/11/01
CRDT- 1992/11/01 00:00
PHST- 1992/11/01 00:00 [pubmed]
PHST- 1992/11/01 00:01 [medline]
PHST- 1992/11/01 00:00 [entrez]
PHST- 1992/11/01 00:00 [pmc-release]
AID - 10.1128/mcb.12.11.4862-4871.1992 [doi]
PST - ppublish
SO  - Mol Cell Biol. 1992 Nov;12(11):4862-71. doi: 10.1128/mcb.12.11.4862-4871.1992.