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Cited by 39

The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.

Cell-specific posttranscriptional regulation of CFTR gene expression via influence of MAPK cascades on 3′UTR part of transcripts

Baudouin-Legros, Maryvonne, Hinzpeter, Alexandre, Jaulmes, Amandine, Brouillard, Franck, Costes, Bruno, Fanen, Pascale, Edelman, Aleksander·2005·American Journal of Physiology-Cell Physiology
DOI 10.1152/ajpcell.00595.2004
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Abstract

Expression of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) gene, which contains the mutations responsible for CF, is regulated by cytokines (TNF-α and IL-1β) in a cell-specific manner. TNF-α decreases CFTR mRNA in human colon cell lines (HT-29), but not in pulmonary cell lines (Calu-3), and IL-1β increases it only in Calu-3 cells. We looked for the cytokine-induced posttranscriptional regulation of CFTR gene expression and studied the modulation of CFTR mRNA stability linked to its 3′ untranslated sequence (3′UTR) in HT-29 and Calu-3 cells. The stability of CFTR mRNA was analyzed by Northern blot after in vitro incubation of total RNAs from CFTR-expressing cells with cytosolic proteins extracted from control or cytokine-treated HT-29 and Calu-3 cells. CFTR mRNA was degraded only by extracts of TNF-α-treated HT-29 cells and not by cytosolic proteins from untreated or IL-1β-treated HT-29 cells. In contrast, extracts of untreated Calu-3 cells enhanced CFTR mRNA degradation, and IL-1β treatment inhibited this; TNF-α had no significant effect. The 3′UTR part of CFTR mRNA was found to be required for this posttranscriptional regulation. The 5′ part of the 3′UTR (the 217 first bases), which contains two AUUUA sequences, was implicated in CFTR mRNA destabilization and the following 136 bases, containing several C-repeats in U-rich environment, in its protection. The proteins, which reacted with the U- and C-repeats of CFTR mRNA 3′UTR, were mainly controlled by stimulation of the p42/p44 and p38 MAP kinase cascades with interaction between these pathways. This posttranscriptional control of gene expression is a common feature of CFTR and many proteins of inflammation.

Overview

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Registry

Crossref · 10.1152/ajpcell.00595.2004

Cites

40 of 40 references verified0 citation errors · 0 not checkable

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Citations

Cites

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Cited by

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Metadata

Authors
Baudouin-Legros, M., Hinzpeter, A., Jaulmes, A., Brouillard, F., Costes, B., Fanen, P., & Edelman, A.
Venue
American Journal of Physiology-Cell Physiology
Publisher
American Physiological Society
Published
2005-11
Volume
289
Issue
5
Pages
C1240-C1250
ISSN
  • 0363-6143
  • 1522-1563
DOI
10.1152/ajpcell.00595.2004
Cited by
39
References
40
Language
en

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Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.