ArticleCellular and molecular gastroenterology and hepatology2020
Tetranucleotide Microsatellite Mutational Behavior Assessed in Real Time: Implications for Future Microsatellite Panels.
Article in Cellular and molecular gastroenterology and hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Genetic or pharmacological disruption of the MSH3 Y245/K246 IDL binding pocket slows CAG repeat expansion.NAR molecular medicine · 2026Article
- Prevalence of germline MSH3 polymorphisms in ulcerative colitis and early-onset colorectal cancer patients that potentiates inflammation-to-cancer transformation.Human molecular genetics · 2026Article
- Inflammation Drives Phosphorylation and Acetylation of MutS Homolog 3 and Interaction with Cytosolic HDAC6.Journal of Cancer · 2026Article
- Double-Strand Breaks Induce Nuclear-Cytosolic Shuttling of Polymorphic DNA Mismatch Repair Protein MutS Homolog 3 and Binding to NEMO/IKKγ in Colon Cancer Cells.Gastro hep advances · 2025Article
- THE JEREMIAH METZGER LECTURE: ENVIRONMENTAL INFLUENCES ON COLORECTAL CANCER.Transactions of the American Clinical and Climatological Association · 2024Article
- Article
- Drugging DNA Damage Repair Pathways for Trinucleotide Repeat Expansion Diseases.Journal of Huntington's disease · 2021Review
- The Human DNA Mismatch Repair Protein MSH3 Contains Nuclear Localization and Export Signals That Enable Nuclear-Cytosolic Shuttling in Response to Inflammation.Molecular and cellular biology · 2020Article
- Immunological Features with DNA Microsatellite Alterations in Patients with Colorectal Cancer.Journal of cancer immunology · 2020Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsFifty percent of colorectal cancers show elevated microsatellite alterations at selected tetranucleotide repeats (EMAST) and are associated with inflammation, metastasis, and poor patient outcome. EMAST results from interleukin 6-induced nuclear-to-cytosolic displacement of the DNA mismatch repair protein Mutated S Homolog 3, allowing frameshifts of dinucleotide and tetranucleotide but not mononucleotide microsatellites. Unlike mononucleotide frameshifts that universally shorten in length, we previously observed expansion and contraction frameshifts at tetranucleotide sequences. Here, we developed cell models to assess tetranucleotide frameshifts in real time.
methodsWe constructed plasmids containing native (AAAG)
resultsFrameshift mutation rates were 31.6 to 71.1 × 10
conclusionsTetranucleotide frameshifts show a deletion bias and undergo more than 1 deletion event via intermediates, with insertions converted into deletions. Tetranucleotide markers added to traditional microsatellite instability panels will be able to determine both EMAST and classic microsatellite instability, but needs to be assessed by multiple markers to account for mutational behavior and intermediates.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.