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Related Concept Videos

Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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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M-Cdk Drives Transition Into Mitosis02:15

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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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M cyclin...
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The Spindle Assembly Checkpoint02:19

The Spindle Assembly Checkpoint

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The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
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PI3K/mTOR/AKT Signaling Pathway

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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Related Experiment Video

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Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
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APC/C CDH1 ubiquitinates STAT3 in mitosis.

Debanjan Bhattacharjee1, Sreeram Kaveti1, Nishant Jain1

  • 1Department of Applied Biology, CSIR-Indian Institute of Chemical Technology, Uppal Road, Hyderabad 500007, Telangana State, India; Academy of Scientific and Innovative Research (AcSIR), CSIR-HRDC Campus, Sector 19, Kamala Nehru Nagar, Ghaziabad 201002, Uttar Pradesh, India.

The International Journal of Biochemistry & Cell Biology
|November 18, 2022
PubMed
Summary
This summary is machine-generated.

Targeting STAT3 ubiquitination, not inhibition, shows promise for cancer therapy. Researchers identified APC/C CDH1 as the E3-ligase responsible for STAT3 ubiquitination during mitosis, suggesting a new therapeutic window.

Keywords:
CDH1MitosisPhosphorylationSTAT3Ubiquitination

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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Signal transducer and activator of transcription 3 (STAT3) is an oncogene implicated in tumor growth and poor prognosis.
  • Small molecule STAT3 inhibitors have shown limited clinical success, prompting interest in alternative strategies like STAT3 degraders.
  • STAT3 degraders leverage ubiquitination to elicit long-lasting anti-tumor responses, making STAT3 ubiquitination a more effective therapeutic strategy than inhibition.

Purpose of the Study:

  • To identify E3-ligases responsible for STAT3 ubiquitination in cancer cells.
  • To understand the cell cycle-dependent regulation of STAT3 ubiquitination.
  • To explore the relationship between STAT3 dephosphorylation and ubiquitination for improved cancer therapy design.

Main Methods:

  • Investigated cell cycle-dependent ubiquitination of STAT3 in HEK293T cells.
  • Examined the link between STAT3 dephosphorylation and ubiquitination.
  • Identified the E3-ligase complex responsible for STAT3 ubiquitination during mitosis.

Main Results:

  • STAT3 ubiquitination is significantly higher during mitosis compared to other cell cycle phases.
  • The anaphase-promoting complex/cyclosome (APC/C) with its coactivator CDH1 was identified as the E3-ligase that binds and ubiquitinates STAT3 in mitosis.
  • Inhibition of phosphatases led to decreased STAT3 ubiquitination, suggesting a role for dephosphorylation in regulating this process.

Conclusions:

  • APC/C CDH1 ubiquitinates STAT3 during mitosis.
  • Mitosis represents a potential therapeutic window for targeting STAT3-activated cancers through E3-ligase-mediated degradation.