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Titolo:
RETINOIC ACID POSTTRANSCRIPTIONALLY UP-REGULATES PROTEOLIPID PROTEIN GENE-EXPRESSION IN C6 GLIOMA-CELLS
Autore:
LOPEZBARAHONA M; MINANO M; MIRA E; IGLESIAS T; STUNNENBERG HG; RODRIGUEZPENA A; BERNAL J; MUNOZ A;
Indirizzi:
CSIC,INST INVEST BIOMED,ARTURO DUPERIER 4 E-28029 MADRID SPAIN CSIC,INST INVEST BIOMED,ARTURO DUPERIER 4 E-28029 MADRID SPAIN ANTIBIOT FARMA SA,DEPT INVEST E-28026 MADRID SPAIN EUROPEAN MOLEC BIOL LAB W-6900 HEIDELBERG GERMANY
Titolo Testata:
The Journal of biological chemistry
fascicolo: 34, volume: 268, anno: 1993,
pagine: 25617 - 25623
SICI:
0021-9258(1993)268:34<25617:RAPUPP>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
THYROID-HORMONE RECEPTOR; MYELIN-DEFICIENT RAT; MESSENGER-RNAS; RESPONSE ELEMENT; TRANSCRIPTIONAL REGULATION; DEVELOPMENTAL EXPRESSION; BASIC-PROTEIN; BETA-GENE; PLP GENE; BRAIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
M. Lopezbarahona et al., "RETINOIC ACID POSTTRANSCRIPTIONALLY UP-REGULATES PROTEOLIPID PROTEIN GENE-EXPRESSION IN C6 GLIOMA-CELLS", The Journal of biological chemistry, 268(34), 1993, pp. 25617-25623

Abstract

The proteolipid protein (PLP) gene codes for the major central nervous system myelin protein. We have studied the effects of different agents on the expression of the PLP gene in C6 glioma cells. Retinoic acid(RA), but not dexamethasone, estradiol, insulin, growth hormone, or vitamin D3, had a drastic effect, increasing 10-20-fold the level of PLP mRNA. Concomitantly, RA also induced the appearance of the corresponding immunoreactive protein. The increase in PLP RNA level showed a slow kinetics and was blocked by cycloheximide, suggesting a posttranscriptional regulation by RA. Nuclear run-on assays confirmed that the rate of PLP gene transcription was unchanged by RA. In contrast, we found that retinoic acid augmented PLP mRNA stability, causing a substantial increase in its half-life. RA action was independent of cell density, serum, or PDGF but was partially inhibited by bFGF. On the other hand, thyroid hormone caused a moderate increase in PLP mRNA levels in C6 cells but only when the low numbers of thyroid receptors in these cells were increased by retrovirally mediated expression of an exogenousc-erbA/TRalpha-1 gene. Our results indicate that RA specifically up-regulates PLP expression in glioma C6 cells at a posttranscriptional level by increasing PLP RNA half-life.

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Documento generato il 01/10/20 alle ore 02:36:34