ArticleOncogene2003
Thiol alkylation inhibits the mitogenic effects of platelet-derived growth factor and renders it proapoptotic via activation of STATs and p53 and induction of expression of caspase1 and p21(waf1/cip1).
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Nitrogen Mustard Alkylates and Cross-Links p53 in Human Keratinocytes.Chemical research in toxicology · 2022Article
- Inhibitory effect of PDGF-BB and serum-stimulated responses in vascular smooth muscle cell proliferation by hinokitiol via up-regulation of p21 and p53.Archives of medical science : AMS · 2018Article
- STAT1 modification improves therapeutic effects of interferons on lung cancer cells.Journal of translational medicine · 2015Article
- Comprehensive metagenomic analysis of glioblastoma reveals absence of known virus despite antiviral-like type I interferon gene response.International journal of cancer · 2014Article
- Individual interferon regulatory factor-3 thiol residues are not critical for its activation following virus infection.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2012Article
- Vanin-1 pantetheinase drives smooth muscle cell activation in post-arterial injury neointimal hyperplasia.PloS one · 2012Article
- Identification of two reactive cysteine residues in the tumor suppressor protein p53 using top-down FTICR mass spectrometry.Journal of the American Society for Mass Spectrometry · 2011Article
- STAT1 and pathogens, not a friendly relationship.Biochimie · 2010Review
- STAT1 pathway mediates amplification of metastatic potential and resistance to therapy.PloS one · 2009Article
- Mutant p53 targeting by the low molecular weight compound STIMA-1.Molecular oncology · 2008Article
- Increased mitochondrial thioredoxin 2 potentiates N-ethylmaleimide-induced cytotoxicity.Chemical research in toxicology · 2008Article
- Reactive oxygen species signaling in vascular smooth muscle cells.Cardiovascular research · 2006Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Thiols provide the major intracellular redox milieu and can undergo reversible oxidation and reduction. To understand the role of thiols in redox signaling events, we have studied the effect of N-ethylmaleimide, a specific thiol alkylating agent, on platelet-derived growth factor-BB (PDGF-BB)-induced mitogenesis in vascular smooth muscle cells (VSMC). Thiol alkylation inhibited PDGF-BB-induced expression of the Fos and Jun family proteins and AP-1 activity in VSMC. Thiol alkylation also inhibited PDGF-BB-induced expression of cyclin A and growth in these cells. In contrast, thiol alkylation enhanced and sustained the effect of PDGF-BB on the activation of the Jak STAT pathway, and this event was correlated with inhibition of protein tyrosine phosphatase lB activity. Thiol alkylation via inducing the expression of p21(waf1/cip1) in a STAT1- and p53-dependent manner antagonized the downregulation of this cell cycle inhibitory molecule by PDGF-BB. The inhibition of AP-1 and activation of STATs, particularly STAT1, by thiol alkylation correlated with increased production of active caspase 1 and apoptosis in VSMC. Together, these findings suggest a role for thiols in mediating mitogenic and/or apoptotic signaling events in VSMC. These results also show that a sustained change in the intracellular thiol redox state can convert a mitogen into a death promoter.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.