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Anaphase Promoting Complex00:50

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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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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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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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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Related Experiment Video

Updated: May 5, 2026

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
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Cullin 5 destabilizes Cas to inhibit Src-dependent cell transformation.

Anjali Teckchandani1, George S Laszlo, Sergi Simó

  • 1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, Seattle, WA 98109, USA.

Journal of Cell Science
|November 29, 2013
PubMed
Summary

Cullin-5-RING-E3-ubiquitin-ligase complexes (Cul5-CRLs) prevent mammary epithelial cell transformation by regulating Src-Cas signaling. Loss of Cul5 promotes cell growth and migration, mediated by the Src-Cas pathway and SOCS6.

Keywords:
CasCul5Cullin 5MigrationSrcTransformationUbiquitin

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Protein ubiquitylation and degradation irreversibly terminate signaling pathways.
  • Mammary epithelial cell transformation can be driven by aberrant signaling pathways.

Purpose of the Study:

  • To investigate the role of cullin-5-RING-E3-ubiquitin-ligase complexes (Cul5-CRLs) in preventing epithelial cell transformation.
  • To elucidate the mechanism by which Cul5-CRLs regulate the Src-Cas signaling pathway.

Main Methods:

  • Studied mammary epithelial cells with and without Cul5.
  • Utilized genetic manipulation (knockdown) and protein degradation assays.
  • Investigated the interaction between Src, p130Cas, and SOCS6.

Main Results:

  • Loss of Cul5 leads to growth-factor-independent growth, migration, and colony dysmorphogenesis dependent on Src.
  • Cul5 and Src cooperate to promote the degradation of Src substrate p130Cas via SOCS6 and the proteasome.
  • Cas is essential for Cul5-deficient cell transformation, while SOCS6 regulates membrane ruffling.

Conclusions:

  • Endogenous Cul5 suppresses epithelial cell transformation by inhibiting Src-Cas signaling.
  • The Cul5-CRL-SOCS6-Cas axis is a critical regulator of mammary epithelial cell homeostasis and transformation.