ArticleNucleic acids research2006
Nitric oxide activation of Erk1/2 regulates the stability and translation of mRNA transcripts containing CU-rich elements.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- The 3'‑untranslated region of XB130 regulates its mRNA stability and translational efficiency in non‑small cell lung cancer cells.Oncology letters · 2023Article
- Arginine regulates HSPA5/BiP translation through ribosome pausing in triple-negative breast cancer cells.British journal of cancer · 2023Article
- Nitric Oxide Exerts Basal and Insulin-Dependent Anorexigenic Actions in POMC Hypothalamic Neurons.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Global Characteristics of CSIG-Associated Gene Expression Changes in Human HEK293 Cells and the Implications for CSIG Regulating Cell Proliferation and Senescence.Frontiers in endocrinology · 2015Article
- Massively parallel functional annotation of 3' untranslated regions.Nature biotechnology · 2014Article
- Role of transcription factor Sp1 and RNA binding protein HuR in the downregulation of Dr+ Escherichia coli receptor protein decay accelerating factor (DAF or CD55) by nitric oxide.The FEBS journal · 2013Article
- Exogenous, but not Endogenous Nitric Oxide Inhibits Adhesion Molecule Expression in Human Endothelial Cells.Frontiers in physiology · 2012Article
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6 authors at 1 institution in 1 country.
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Abstract
Nitric oxide (NO*) can stabilize mRNA by activating p38 mitogen-activated protein kinase (MAPK). Here, transcript stabilization by NO* was investigated in human THP-1 cells using microarrays. After LPS pre-stimulation, cells were treated with actinomycin D and then exposed to NO* without or with the p38 MAPK inhibitor SB202190 (SB). The decay of 220 mRNAs was affected; most were stabilized by NO*. Unexpectedly, SB often enhanced rather than antagonized transcript stability. NO* activated p38 MAPK and Erk1/2; SB blocked p38 MAPK, but further activated Erk1/2. RT-PCR confirmed that NO* and SB could additively stabilize certain mRNA transcripts, an effect abolished by Erk1/2 inhibition. In affected genes, these responses were associated with CU-rich elements (CURE) in 3'-untranslated regions (3'-UTR). NO* stabilized the mRNA of a CURE-containing reporter gene, while repressing translation. Dominant-negative Mek1, an Erk1/2 inhibitor, abolished this effect. NO* similarly stabilized, but blocked translation of MAP3K7IP2, a natural CURE-containing gene. NO* increased hnRNP translocation to the cytoplasm and binding to CURE. Over-expression of hnRNP K, like NO*, repressed translation of CURE-containing mRNA. These findings define a sequence-specific mechanism of NO*-triggered gene regulation that stabilizes mRNA, but represses translation.
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