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

4.7K
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...
4.7K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

8.0K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
8.0K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

7.0K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.9K
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...
3.9K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

2.9K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.9K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

4.2K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.2K

You might also read

Related Articles

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

Sort by
Same author

Rational Engineering of Self-Supported Catalysts for High-Performance Electrochemical Oxygen Evolution and Ethylene Glycol Oxidation.

Chemistry of materials : a publication of the American Chemical Society·2026
Same author

Retraction.

Science signaling·2026
Same author

Self-Nitriding Nanostructured Transition Metal Nitrides in Architected-Carbon Matrices: Unveiling Mechanisms and Advancing Performance in Lithium-Sulfur Pouch Cells.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Dysregulated Protease Homeostasis Defines Primary FSGS.

Kidney360·2026
Same author

The mTOR signaling pathway regulates key steps of mammary gland organoid genesis in a temporal manner.

Scientific reports·2026
Same author

Targeting the UFL1-AKT cascade suppresses triple-negative breast cancer progression.

Nature communications·2026

Related Experiment Video

Updated: Oct 12, 2025

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

9.0K

TBX2 controls a proproliferative gene expression program in melanoma.

Sizhu Lu1, Pakavarin Louphrasitthiphol1,2, Nishit Goradia3

  • 1Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.

Genes & Development
|November 25, 2021
PubMed
Summary
This summary is machine-generated.

This study reveals TBX2

Keywords:
DNA bindingDNA binding specificityTBX2cell cycleproliferationsenescence

More Related Videos

Author Spotlight: Assessing the Potential of Circulating Tumor Cells in Leptomeningeal Disease Research
06:25

Author Spotlight: Assessing the Potential of Circulating Tumor Cells in Leptomeningeal Disease Research

Published on: March 29, 2024

1.1K
A Melanoma Patient-Derived Xenograft Model
07:07

A Melanoma Patient-Derived Xenograft Model

Published on: May 20, 2019

12.6K

Related Experiment Videos

Last Updated: Oct 12, 2025

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

9.0K
Author Spotlight: Assessing the Potential of Circulating Tumor Cells in Leptomeningeal Disease Research
06:25

Author Spotlight: Assessing the Potential of Circulating Tumor Cells in Leptomeningeal Disease Research

Published on: March 29, 2024

1.1K
A Melanoma Patient-Derived Xenograft Model
07:07

A Melanoma Patient-Derived Xenograft Model

Published on: May 20, 2019

12.6K

Area of Science:

  • Cellular senescence
  • Cancer biology
  • Molecular mechanisms of aging

Background:

  • Cellular senescence is crucial for development, aging, and cancer prevention, but its regulation is not fully understood.
  • TBX2, an anti-senescence transcription repressor, is involved in development and cancer, yet its targets and partners remain unclear.
  • Understanding TBX2's role is vital for cancer research and therapeutic development.

Purpose of the Study:

  • To elucidate the regulatory network of TBX2 in promoting proliferation and overcoming senescence.
  • To identify TBX2 target genes and cooperating factors in melanoma.
  • To investigate the link between PI3K signaling, TBX2, and cancer cell proliferation.

Main Methods:

  • Utilized melanoma as a model system.
  • Investigated TBX2's downstream signaling pathways, including PI3K.
  • Analyzed TBX2 binding sites and interactions with transcription factors using in vivo and biochemical methods.
  • Examined the role of E2F1 as a TBX2 target gene.

Main Results:

  • TBX2 functions downstream of PI3K signaling.
  • TBX2 directly binds to and regulates the expression of E2F1, a cell cycle regulator.
  • TBX2 preferentially binds to E-boxes (CACGTG) over its canonical T-element motif in vivo.
  • TBX2 interacts with BCOR/PRC1.1 complex components, recruiting them to the E2F1 locus.

Conclusions:

  • PI3K signaling modulates TBX2 activity to drive proliferation in cancer.
  • TBX2 utilizes E-boxes for binding and recruits cofactors like BCOR/PRC1.1 to regulate target genes such as E2F1.
  • These findings offer critical insights into TBX2-mediated senescence bypass and cancer progression.