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

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...
Cancer02:18

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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...
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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

You might also read

Related Articles

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

Sort by
Same author

Reply to 'Single-cell evidence for PANoptosome complexes'.

Nature reviews. Molecular cell biology·2026
Same author

Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.

Nature communications·2026
Same author

The benchmarking and application of tag-degraders in vivo to validate therapeutic targets.

Nature communications·2026
Same author

The transmembrane domain structure of TNFR1 suppresses ligand-independent autoactivation but is not required for TNF-induced signaling.

Science signaling·2026
Same author

Hemidesmosomal Proteins in Oral Cancer Progression: An Immunohistochemical Study of Human and Mouse.

Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology·2026
Same author

The PANoptosis hypothesis examined.

Nature reviews. Molecular cell biology·2026

Related Experiment Video

Updated: Jul 6, 2026

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
11:36

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

Published on: July 25, 2019

Ubiquitylation and cancer development.

Maria Miasari1, Hamsa Puthalakath, John Silke

  • 1Department of Biochemistry, La Trobe University, Victoria 3086, Australia.

Current Cancer Drug Targets
|March 14, 2008
PubMed
Summary

Cancer cells

Area of Science:

  • Cellular Biology
  • Oncology
  • Biochemistry

Background:

  • Ubiquitylation is a critical cellular process.
  • Cancer cells exhibit heightened dependence on ubiquitylation compared to normal cells.
  • Proteasome inhibitors (PI) are effective cancer therapeutics with good in vivo tolerance.

Purpose of the Study:

  • To review existing models explaining cancer cell sensitivity to proteasome inhibitors.
  • To propose a novel hypothesis regarding cancer cell reliance on the proteasome.
  • To explore the role of endoplasmic reticulum (ER) stress in proteasome inhibitor sensitivity.

Main Methods:

  • Literature review of existing studies on proteasome inhibitors and cancer cell death.
  • Analysis of proposed mechanisms involving p53 and Bcl-2 Homology (BH3) proteins.

More Related Videos

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model
09:00

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model

Published on: April 17, 2026

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates
09:47

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates

Published on: May 10, 2022

Related Experiment Videos

Last Updated: Jul 6, 2026

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
11:36

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

Published on: July 25, 2019

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model
09:00

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model

Published on: April 17, 2026

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates
09:47

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates

Published on: May 10, 2022

  • Evaluation of the hypothesis linking abnormal tumor physiology, ER strain, and proteasome dependence.

    • Main Results:

    • Current models inadequately explain the differential sensitivity of cancer cells to PIs.
    • Multiple Myeloma serves as a model where high antibody production leads to ER strain and proteasome dependence.
    • Tumor cells experiencing ER stress or equivalent conditions may be particularly vulnerable to PIs.

    Conclusions:

    • Cancer cell sensitivity to proteasome inhibitors may stem from their abnormal physiology and increased reliance on the proteasome.
    • Endoplasmic reticulum stress is a key factor contributing to this heightened susceptibility.
    • This understanding could guide the development of more targeted proteasome inhibitor therapies.