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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...

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Related Experiment Video

Updated: May 7, 2026

Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts
11:19

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Published on: October 9, 2016

The STAT3-DNMT1 connection.

N Shaun B Thomas1

  • 1Department of Haematological Medicine; Rayne Institute; King's College London; London, UK.

JAK-STAT
|September 24, 2013
PubMed
Summary
This summary is machine-generated.

Acetylation of STAT3 protein controls DNA methylation, impacting gene activity. This mechanism influences genes like estrogen receptor alpha (ESR1), crucial in breast cancer progression.

Keywords:
DNA methylationDNMT1STAT3acetylationcancerepigeneticstranscription

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Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Biology

Background:

  • Gene activity is controlled by transcriptional and epigenetic regulation.
  • Previous work indicated Signal Transducer and Activator of Transcription 3 (STAT3) binds DNA methyltransferase 1 (DNMT1), suggesting a role in epigenetic gene silencing.
  • The precise mechanism linking STAT3, DNMT1, and gene regulation remained unclear.

Purpose of the Study:

  • To elucidate the mechanism by which STAT3 influences epigenetic gene silencing.
  • To investigate the role of STAT3 acetylation in regulating DNMT1 binding and DNA methylation.
  • To examine the impact of this mechanism on the expression of key genes, such as estrogen receptor alpha (ESR1), in breast cancer.

Main Methods:

  • Investigated the interaction between acetylated STAT3 and DNMT1.
  • Assessed CpG DNA methylation patterns in target gene promoters.
  • Analyzed the expression of genes including ESR1 in breast cancer cells.

Main Results:

  • Demonstrated that acetylation of STAT3 directly regulates the binding of DNMT1.
  • Showed that this interaction leads to specific CpG DNA methylation.
  • Identified altered regulation of several genes, including ESR1, mediated by this pathway in breast cancer cells.

Conclusions:

  • STAT3 acetylation is a critical regulator of DNMT1 binding and subsequent DNA methylation.
  • This epigenetic mechanism plays a significant role in controlling gene expression, notably affecting ESR1 in breast cancer.
  • Findings provide a deeper understanding of epigenetic regulation in cancer and potential therapeutic targets.