EGF-induced apoptosis in A431 cells is dependent on STAT1, but not on STAT3.

No abstract is available for this paper.

• Publication year

  2007

• Venue

  European Journal of Cell Biology

• Publication date

  2007-10-19

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.EJCB.2007.05.009PMID 17646016
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Opposing actions of STAT-1 and STAT-3

  2005cited by this paper
• Monolayer versus aggregate balance in survival process for EGF‐induced apoptosis in A431 carcinoma cells: Implication of ROS‐P38 MAPK‐integrin α2β1 pathway

  2004cited by this paper
• STAT-1 Interacts with p53 to Enhance DNA Damage-induced Apoptosis*

  2004cited by this paper
• Epidermal growth factor receptor: mechanisms of activation and signalling.

  2003cited by this paper
• Inhibition of NF- (cid:1) B Sensitizes A431 Cells to Epidermal Growth Factor-induced Apoptosis, whereas Its Activation by Ectopic Expression of RelA Confers Resistance*

  2003cited by this paper
• [EGF-induced signal transduction in clonal cells of epidermoid carcinoma A431].

  2003cited by this paper
• [EGF-induced signal transduction in clonal cells of epidermoid carcinoma A431].

  2003cited by this paper
• Signaling through the JAK/STAT pathway, recent advances and future challenges.

  2002cited by this paper
• RNA interference by expression of short-interfering RNAs and hairpin RNAs in mammalian cells

  2002cited by this paper
• The role of STATs in apoptosis.

  2002cited by this paper
• Constitutive activation of Stat3 by the Src and JAK tyrosine kinases participates in growth regulation of human breast carcinoma cells

  2001cited by this paper
• Progression of esophageal carcinoma by loss of EGF-STAT1 pathway.

  2001cited by this paper
• Activation of STAT proteins and growth control

  2001cited by this paper
• Reversible G1 Arrest Induced by Inhibition of the Epidermal Growth Factor Receptor Tyrosine Kinase Requires Up-regulation of p27KIP1 Independent of MAPK Activity*

  2000cited by this paper
• Interruption of NFκb–stat1 signaling mediates EGF‐induced cell‐cycle arrest

  2000cited by this paper
• Interruption of NFkappaB-STAT1 signaling mediates EGF-induced cell-cycle arrest.

  2000cited by this paper
• Up-regulation of alpha 2 beta 1 integrin cell-surface expression protects A431 cells from epidermal growth factor-induced apoptosis.

  2000cited by this paper
• Up‐regulation of α2β1 integrin cell‐surface expresssion protects A431 cells from epidermal growth factor–induced apoptosis

  2000cited by this paper
• Cell signaling by receptor tyrosine kinases.

  2000cited by this paper
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  1999cited by this paper
• ErbB Receptor-induced Activation of Stat Transcription Factors Is Mediated by Src Tyrosine Kinases*

  1999cited by this paper
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  1999cited by this paper
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  1998cited by this paper
• Antisense oligonucleotide of WAF1 gene prevents EGF-induced cell-cycle arrest in A431 cells

  1998cited by this paper
• Involvement of MAP kinase-independent protein kinase C signaling pathway in the EGF-induced p21(WAF1/Cip1) expression and growth inhibition of A431 cells.

  1998cited by this paper
• Requirement of Stat3 but not Stat1 activation for epidermal growth factor receptor- mediated cell growth In vitro.

  1998cited by this paper
• Epidermal growth factor-induced growth inhibition requires Stat1 activation.

  1998cited by this paper
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  1997cited by this paper
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  1997cited by this paper
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  1997cited by this paper
• Activation of the STAT signaling pathway can cause expression of caspase 1 and apoptosis

  1997cited by this paper
• Defective TNF-α-Induced Apoptosis in STAT1-Null Cells Due to Low Constitutive Levels of Caspases

  1997cited by this paper
• Epidermal growth factor-induced apoptosis in A431 cells can be reversed by reducing the tyrosine kinase activity.

  1996cited by this paper
• Growth inhibitory concentrations of EGF induce p21 (WAF1/Cip1) and alter cell cycle control in squamous carcinoma cells.

  1996cited by this paper
• Cell Growth Arrest and Induction of Cyclin-Dependent Kinase Inhibitor p21WAF1/CIP1 Mediated by STAT1

  1996cited by this paper
• Prolonged induction of p21Cip1/WAF1/CDK2/PCNA complex by epidermal growth factor receptor activation mediates ligand-induced A431 cell growth inhibition

  1995cited by this paper
• Prevalence of aberrant expression of the epidermal growth factor receptor in human cancers.

  1991cited by this paper
• Ligand-induced activation of A431 cell epidermal growth factor receptors occurs primarily by an autocrine pathway that acts upon receptors on the surface rather than intracellularly.

  1991cited by this paper
• Functional state of the epidermal growth factor-receptor complexes during their internalization in A-431 cells

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• [Cell strains of A431 epidermoid carcinoma with altered epidermal growth factor reception].

  1989cited by this paper
• Recycling of epidermal growth factor-receptor complexes in A431 cells.

  1989cited by this paper
• EGF induces cell cycle arrest of A431 human epidermoid carcinoma cells

  1986cited by this paper
• Variant of A431 cells isolated by ricin A-conjugated monoclonal antibody directed to EGF receptor: Phosphorylation of EGF receptor and phosphatidylinositol

  1985cited by this paper
• Down-regulation of the epidermal growth factor receptor in KB cells is due to receptor internalization and subsequent degradation in lysosomes.

  1984cited by this paper
• Growth inhibition of human tumor cells in athymic mice by anti-epidermal growth factor receptor monoclonal antibodies.

  1984cited by this paper
• Altered epidermal growth factor (EGF)-stimulated protein kinase activity in variant A431 cells with altered growth responses to EGF.

  1982cited by this paper
• Increased phosphotyrosine content and inhibition of proliferation in EGF-treated A431 cells

  1981cited by this paper

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  2019cites this paper
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  2018cites this paper
• Identifying the signaling mechanisms of EGFR-mediated apoptosis.

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  2015cites this paper
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  2013cites this paper
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