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Related Concept Videos

Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

Mismatch Repair

Overview
Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Microtubule Instability02:17

Microtubule Instability

Microtubules are hollow cylindrical filaments having a diameter of approximately 25 nm and a length that varies from 200 nm to 25 μm. GTP-bound tubulin subunits form αβ-heterodimers for microtubule assembly. These core building blocks interact longitudinally, polymerizing into protofilaments. The protofilaments then interact with one another through lateral bonding forces to form stable cylindrical microtubules. These cylindrical filaments are dynamic as they undergo repeated assembly and...
Crossing Over01:30

Crossing Over

Crossing over is the exchange of genetic information between homologous chromosomes during prophase I of meiosis I. Genetic recombination gives rise to allelic diversity in the newly formed daughter cells. In humans, crossing over produces genetically distinct haploid egg and sperm cells that undergo fertilization to produce unique offspring. Before cell division starts, the germ cell’s chromosome(s) undergo duplication in the S phase of the cell cycle. As the cells enter prophase I, duplicated...
MicroRNAs01:22

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA ends...

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Related Experiment Video

Updated: May 30, 2026

Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks
12:19

Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks

Published on: November 10, 2016

Causal link between microsatellite instability and hMRE11 dysfunction in human cancers.

Xiling Wu1, Yang Xu, Weihang Chai

  • 1School of Molecular Biosciences, Washington State University, Pullman, WA 99164, USA.

Molecular Cancer Research : MCR
|August 19, 2011
PubMed
Summary

Genomic instability, including microsatellite instability (MSI), is common in cancer. This study explores the complex relationship between DNA mismatch repair deficiency and the hMRE11 gene, suggesting a role beyond simple inactivation.

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Last Updated: May 30, 2026

Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks
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Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • Genomic integrity is crucial for cell survival; genomic instability is a hallmark of cancer.
  • Microsatellite instability (MSI), caused by DNA mismatch repair (MMR) deficiency, is a common sequence variation in tumors.
  • MMR deficiency alone does not initiate cancer; mutations in cell survival and DNA damage response genes are key.

Purpose of the Study:

  • To investigate the molecular mechanisms linking MMR deficiency to alterations in the hMRE11 gene.
  • To clarify the complex involvement of hMRE11 within the MMR pathway.
  • To explore the potential role of hMRE11 in maintaining telomere repeat stability.

Main Methods:

  • Literature review and analysis of existing studies on MSI, MMR deficiency, and hMRE11.
  • Comparative analysis of different microsatellite loci behavior in relation to MMR status.
  • Exploration of proposed models for hMRE11-MMR pathway interactions.

Main Results:

  • The association between shortened hMRE11 poly(T)11 tracts and MMR deficiency is observed, but the underlying molecular basis is unclear.
  • Evidence suggests hMRE11's involvement with the MMR pathway is more intricate than direct inactivation.
  • Microsatellite loci are not uniformly affected by MMR deficiency, indicating complex instability patterns.

Conclusions:

  • The relationship between MMR deficiency and hMRE11 requires further elucidation, likely involving complex interactions rather than simple target gene inactivation.
  • hMRE11 may play a role in genomic stability beyond its direct association with MMR.
  • Further research is needed to fully understand hMRE11's function in cancer development and telomere maintenance.