We are analyzing https://link.springer.com/article/10.1007/s10555-024-10209-3.

Title:
Multifaceted role of the DNA replication protein MCM10 in maintaining genome stability and its implication in human diseases | Cancer and Metastasis Reviews
Description:
MCM10 plays a vital role in genome duplication and is crucial for DNA replication initiation, elongation, and termination. It coordinates several proteins to assemble at the fork, form a functional replisome, trigger origin unwinding, and stabilize the replication bubble. MCM10 overexpression is associated with increased aggressiveness in breast, cervical, and several other cancers. Disruption of MCM10 leads to altered replication timing associated with initiation site gains and losses accompanied by genome instability. Knockdown of MCM10 affects the proliferation and migration of cancer cells, manifested by DNA damage and replication fork arrest, and has recently been shown to be associated with clinical conditions like CNKD and RCM. Loss of MCM10 function is associated with impaired telomerase activity, leading to the accumulation of abnormal replication forks and compromised telomere length. MCM10 interacts with histones, aids in nucleosome assembly, binds BRCA2 to maintain genome integrity during DNA damage, prevents lesion skipping, and inhibits PRIMPOL-mediated repriming. It also interacts with the fork reversal enzyme SMARCAL1 and inhibits fork regression. Additionally, MCM10 undergoes several post-translational modifications and contributes to transcriptional silencing by interacting with the SIR proteins. This review explores the mechanism associated with MCM10’s multifaceted role in DNA replication initiation, chromatin organization, transcriptional silencing, replication stress, fork stability, telomere length maintenance, and DNA damage response. Finally, we discuss the role of MCM10 in the early detection of cancer, its prognostic significance, and its potential use in therapeutics for cancer treatment.
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Keywords {🔍}

pubmed, article, google, scholar, cas, mcm, replication, dna, central, cell, cancer, journal, molecular, human, biology, research, helicase, cells, origin, maintenance, wang, zhang, protein, nature, genes, initiation, fork, complex, prognostic, bielinsky, httpsdoiorg, role, stress, minichromosome, httpsdoiorgs, chen, required, instability, cmg, genetics, sciences, origins, eukaryotic, damage, biological, chemistry, proteins, replisome, genome, assembly,

Topics {✒️}

month download article/chapter bi-allelic mcm10 variants suppress primpol-mediated repriming beta-catenin/lef-1 pathway inhibits primpol-mediated repriming single-stranded dna gate nuclease-resistant nuclear structures single-stranded gap formation anti-parasitic agent suramin dna double-strand breaks shankar prasad das potent strand-annealing activity pre-replicative complex formation cell cycle-dependent proteolysis jayaprakash sasikumar orc/cdc6/mcm2-7 complex dna polymerase alpha-primase accepted manuscript version chromosomal dna replication intra-s-phase checkpoint full article pdf cervical cancer aggressiveness mcm double-hexamer assembly double-hexameric mcm2-7 complex dna replication timing initiation protein cdc23 cell-cycle-regulated interaction dna-binding properties increased aggressiveness dna replication initiation cdc45-mcm2-7-gins complex cell-cycle progression efficient dna replication altered replication timing stimulates origin binding immune checkpoints cdc45-mcm2-7-gins cnkd replication timing regulation natural killer cells oncogenic chromosomal translocations repair pathway promotes cell proliferation chromosomal replication origins eukaryotic dna replication dna damage response human dna replication replication fork dna dna polymerase-alpha privacy choices/manage cookies disrupt cmg-replisome function

Questions {❓}

Dimerization of Firing Factors for Replication Origin Activation in Eukaryotes: A Crucial Process for Simultaneous Assembly of Bidirectional Replication Forks?

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         description:MCM10 plays a vital role in genome duplication and is crucial for DNA replication initiation, elongation, and termination. It coordinates several proteins to assemble at the fork, form a functional replisome, trigger origin unwinding, and stabilize the replication bubble. MCM10 overexpression is associated with increased aggressiveness in breast, cervical, and several other cancers. Disruption of MCM10 leads to altered replication timing associated with initiation site gains and losses accompanied by genome instability. Knockdown of MCM10 affects the proliferation and migration of cancer cells, manifested by DNA damage and replication fork arrest, and has recently been shown to be associated with clinical conditions like CNKD and RCM. Loss of MCM10 function is associated with impaired telomerase activity, leading to the accumulation of abnormal replication forks and compromised telomere length. MCM10 interacts with histones, aids in nucleosome assembly, binds BRCA2 to maintain genome integrity during DNA damage, prevents lesion skipping, and inhibits PRIMPOL-mediated repriming. It also interacts with the fork reversal enzyme SMARCAL1 and inhibits fork regression. Additionally, MCM10 undergoes several post-translational modifications and contributes to transcriptional silencing by interacting with the SIR proteins. This review explores the mechanism associated with MCM10’s multifaceted role in DNA replication initiation, chromatin organization, transcriptional silencing, replication stress, fork stability, telomere length maintenance, and DNA damage response. Finally, we discuss the role of MCM10 in the early detection of cancer, its prognostic significance, and its potential use in therapeutics for cancer treatment.
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         Chromosomal instability
         Replication stress
         Replication initiation
         Cancer aggressiveness
         Replication timing
         Cancer Research
         Oncology
         Biomedicine
         general
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