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

Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

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.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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...
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...
Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012 for this...

You might also read

Related Articles

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

Sort by
Same author

Therapeutic targeting of Myc-reprogrammed cancer cell metabolism.

Cold Spring Harbor symposia on quantitative biology·2011
Same author

The immunoglobulin heavy chain gene 3' enhancers induce Bcl2 deregulation and lymphomagenesis in murine B cells.

Leukemia·2011
Same author

The interplay between MYC and HIF in the Warburg effect.

Ernst Schering Foundation symposium proceedings·2008
Same author

Functional long-range interactions of the IgH 3' enhancers with the bcl-2 promoter region in t(14;18) lymphoma cells.

Oncogene·2008
Same author

Activation of the c-myc p1 promoter in Burkitt's lymphoma by the hs3 immunoglobulin heavy-chain gene enhancer.

Leukemia·2007
Same author

The immunoglobulin heavy-chain gene 3' enhancers deregulate bcl-2 promoter usage in t(14;18) lymphoma cells.

Oncogene·2006
Same journal

SRD5A3-mediated aberrant N-glycosylation of SCARA5 promotes ferroptosis in lung adenocarcinoma.

Oncogene·2026
Same journal

Aberrant splicing in human cancer shows possible functional impact on transcription factors.

Oncogene·2026
Same journal

The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.

Oncogene·2026
Same journal

Correction: Neuropilin-1 promotes human glioma progression through potentiating the activity of the HGF/SF autocrine pathway.

Oncogene·2026
Same journal

Amphiregulin-mediated EGFR activation drives both intrinsic and acquired resistance to KRAS G12C inhibitors in KRAS G12C-mutant non-small cell lung cancer.

Oncogene·2026
Same journal

Histone lactylation-driven IGF2BP3 promotes intrahepatic cholangiocarcinoma progression via SPP1/CD44-dependent macrophage polarization.

Oncogene·2026
See all related articles

Related Experiment Video

Updated: Jul 2, 2026

Molecular Imaging to Target Transplanted Muscle Progenitor Cells
09:24

Molecular Imaging to Target Transplanted Muscle Progenitor Cells

Published on: March 27, 2013

Translocations involving c-myc and c-myc function.

L M Boxer1, C V Dang

  • 1Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, California CA 94305, USA.

Oncogene
|October 19, 2001
PubMed
Summary
This summary is machine-generated.

The c-MYC oncogene drives cancer by disrupting normal cell processes. While not essential for cell proliferation, c-MYC integrates and accelerates cellular metabolism and growth.

More Related Videos

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells
09:39

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells

Published on: July 29, 2016

Structure-function Studies in Mouse Embryonic Stem Cells Using Recombinase-mediated Cassette Exchange
15:13

Structure-function Studies in Mouse Embryonic Stem Cells Using Recombinase-mediated Cassette Exchange

Published on: April 27, 2017

Related Experiment Videos

Last Updated: Jul 2, 2026

Molecular Imaging to Target Transplanted Muscle Progenitor Cells
09:24

Molecular Imaging to Target Transplanted Muscle Progenitor Cells

Published on: March 27, 2013

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells
09:39

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells

Published on: July 29, 2016

Structure-function Studies in Mouse Embryonic Stem Cells Using Recombinase-mediated Cassette Exchange
15:13

Structure-function Studies in Mouse Embryonic Stem Cells Using Recombinase-mediated Cassette Exchange

Published on: April 27, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • c-MYC is a classic oncogene activated by chromosomal translocations.
  • Unlike normal cells, c-MYC expression is frequently deregulated in human cancers.

Purpose of the Study:

  • To review the activation mechanisms of the c-MYC gene.
  • To elucidate the multifaceted functions of the c-Myc protein in cellular processes.

Main Methods:

  • Literature review of studies on c-MYC gene activation.
  • Analysis of research on c-Myc protein functions in cell growth, proliferation, apoptosis, and metabolism.

Main Results:

  • c-MYC deregulation is a hallmark of many human cancers.
  • c-Myc functions as an oncogenic transcription factor impacting cell growth, proliferation, apoptosis, and metabolism.
  • Complete c-MYC removal slows cell growth and proliferation.

Conclusions:

  • c-MYC acts as a key integrator and accelerator of cellular metabolism and proliferation.
  • Understanding c-MYC's role is crucial for cancer research and therapeutic strategies.