Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways.

The Journal of clinical investigation·2009
Same author

Cripto-1 overexpression is involved in the tumorigenesis of nasopharyngeal carcinoma.

BMC cancer·2009
Same author

Range of motion and orientation of the lumbar facet joints in vivo.

Spine·2009
Same author

[Silencing of COX-2 in nasopharyngeal carcinoma cells with a shRNAmir lentivirus vector].

Nan fang yi ke da xue xue bao = Journal of Southern Medical University·2009
Same author

The risk of melamine-induced nephrolithiasis in young children starts at a lower intake level than recommended by the WHO.

Pediatric nephrology (Berlin, Germany)·2009
Same author

Adult scoliosis in patients over sixty-five years of age: outcomes of operative versus nonoperative treatment at a minimum two-year follow-up.

Spine·2009

Related Experiment Video

Updated: Jun 8, 2026

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates
08:19

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates

Published on: April 22, 2019

Increased Cul1 expression promotes melanoma cell proliferation through regulating p27 expression.

Guangdi Chen1, Gang Li

  • 1Department of Dermatology and Skin Science, Jack Bell Research Centre, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, British Columbia, BC V6H 3Z6, Canada.

International Journal of Oncology
|September 30, 2010
PubMed
Summary

Cullin1 (Cul1) protein regulates melanoma cell growth by controlling cell cycle progression. This study shows Cul1 degradation of p27 enhances melanoma cell proliferation, explaining its increased expression in early melanoma.

Related Experiment Videos

Last Updated: Jun 8, 2026

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates
08:19

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates

Published on: April 22, 2019

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cullin1 (Cul1) is a scaffold protein in SCF (Skp1/Cullin/Rbx1/F-box protein) ubiquitin ligase complexes.
  • Aberrant Cul1 expression is linked to SCF E3 ligase dysfunction.
  • Increased Cul1 expression is observed in early-stage melanoma.

Purpose of the Study:

  • To investigate the specific role of Cul1 in melanoma development and progression.
  • To elucidate the molecular mechanisms by which Cul1 influences melanoma cell growth and cell cycle.
  • To understand the significance of elevated Cul1 levels in early melanoma.

Main Methods:

  • Gene silencing (knockdown) and overexpression of Cul1 in melanoma cells.
  • Cell proliferation and growth assays.
  • Cell cycle progression analysis.
  • Western blotting to assess protein levels, including p27 degradation via SCFSkp2 complex.

Main Results:

  • Knockdown of Cul1 significantly inhibited melanoma cell growth.
  • Overexpression of Cul1 promoted melanoma cell proliferation and accelerated cell cycle progression.
  • Cul1 was found to regulate melanoma cell growth and cell cycle by mediating the degradation of the cell cycle inhibitor p27 through the SCFSkp2 complex.

Conclusions:

  • Cul1 plays a critical role in promoting melanoma cell proliferation by regulating cell cycle progression.
  • The degradation of p27 by the SCFSkp2-Cul1 complex is a key mechanism underlying Cul1's function in melanoma.
  • This study enhances the understanding of Cul1's involvement in early melanoma development and its potential as a therapeutic target.