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Loss of Tumor Suppressor Gene Functions

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...

The Retinoblastoma Gene

The Retinoblastoma Gene

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.
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Abnormal Proliferation

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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...

Restarting Stalled Replication Forks

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...

Cancer-Critical Genes II: Tumor Suppressor Genes

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...

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Related Experiment Video

Updated: Jul 26, 2025

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Published on: February 13, 2019

Structure and function of the RAD51B-RAD51C-RAD51D-XRCC2 tumour suppressor.

Luke A Greenhough¹, Chih-Chao Liang¹, Ondrej Belan^1,2,3

¹The Francis Crick Institute, London, UK.

|June 21, 2023

Summary

The RAD51B-RAD51C-RAD51D-XRCC2 complex (BCDX2) orchestrates DNA repair by assembling RAD51 filaments, crucial for replication fork protection and double-strand break repair, thereby preventing cancer.

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Last Updated: Jul 26, 2025

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Published on: February 13, 2019

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication

Published on: August 23, 2024

Area of Science:

Molecular Biology
Structural Biology
Genetics

Background:

Homologous recombination is vital for DNA repair, replication fork stability, and meiosis.
Mutations in recombination genes like BRCA2 and RAD51 paralogues are linked to cancers and Fanconi anaemia.
The precise molecular functions of RAD51 paralogues in DNA repair and cancer prevention remain largely unknown.

Purpose of the Study:

To elucidate the structural and functional roles of the RAD51 paralogue complex (BCDX2) in DNA repair and cancer avoidance.

Main Methods:

Cryo-electron microscopy
AlphaFold2 modelling
Structural proteomics
Biochemical assays
Single-molecule analyses

Main Results:

Determined the structure of the RAD51B-RAD51C-RAD51D-XRCC2 (BCDX2) complex.
RAD51C-RAD51D-XRCC2 mimics RAD51 protomers in a filament, while RAD51B is dynamic.
BCDX2 stimulates RAD51 filament nucleation and extension via coupled ATPase activities of RAD51B and RAD51C.
BCDX2 is essential for orchestrating RAD51 assembly on single-stranded DNA.

Conclusions:

BCDX2 plays a critical role in replication fork protection and double-strand break repair through RAD51 filament formation.
The BCDX2 complex is a key mediator of DNA repair pathways essential for tumour suppression.