Results 21 to 30 of about 8,832 (194)

A YAP/TAZ–CDC6 Axis Initiates and Maintains Malignant Transformation [PDF]

open access: yesCancer Science, Volume 117, Issue 2, Page 353-363, February 2026.
This study demonstrates that constitutive activation of YAP or TAZ is sufficient to induce and maintain malignant transformation in fibroblasts, identifying them as essential oncogenic drivers. Transcriptomic and functional analyses revealed CDC6 as a critical downstream effector of YAP/TAZ, with elevated expression linked to tumorigenesis across ...
David Nduru   +5 more
wiley   +2 more sources

CDKs Give Cdc6 a License to Drive into S Phase [PDF]

open access: yesCell, 2005
The accumulation of Cdc6 promotes the initiation of DNA replication. In this issue of Cell, Mailand and Diffley (2005) show that phosphorylation of Cdc6 by cyclin-dependent kinases prevents its destruction by the anaphase promoting complex (APC). This simple mechanism explains how the APC simultaneously spares Cdc6 while targeting for destruction ...
Ayad, Nagi G.   +2 more
openaire   +3 more sources

Putrescine functions as a metabolic checkpoint in replication stress-induced senescence [PDF]

open access: yesCellular and Molecular Life Sciences
Cellular senescence represents a fundamental biological response to replication stress and other genotoxic insults, acting as both a barrier to malignant transformation and a driver of age-related tissue dysfunction.
Theodora Vasilogiannakopoulou   +8 more
doaj   +2 more sources

License to Replicate: Mechanisms of Licensing Eukaryotic Origins for DNA Replication [PDF]

open access: yesBioEssays, Volume 48, Issue 1, January 2026.
Origin licensing constitutes the first step in initiating eukaryotic genome replication. Licensed origins are marked by an MCM double hexamer complex. This article reviews the molecular mechanisms of MCM double hexamer loading in yeast and higher eukaryotes, based on insights gained from biochemical reconstitution and structural analyses.
Victoria Frisbie, Franziska Bleichert
wiley   +2 more sources

Estrogen-induced upregulation and 3′-UTR shortening of CDC6 [PDF]

open access: yesNucleic Acids Research, 2012
3'-Untranslated region (UTR) shortening of mRNAs via alternative polyadenylation (APA) has important ramifications for gene expression. By using proximal APA sites and switching to shorter 3'-UTRs, proliferating cells avoid miRNA-mediated repression. Such APA and 3'-UTR shortening events may explain the basis of some of the proto-oncogene activation ...
Begum H. Akman   +2 more
openaire   +4 more sources

RPL28 mediates sorafenib resistance in hepatocellular carcinoma by downregulating CDC6 expression [PDF]

open access: yesFrontiers in Oncology
AimSorafenib is a milestone targeted therapy for advanced hepatocellular carcinoma (HCC), yet resistance to this agent severely limits its clinical efficacy. The molecular mechanisms underlying sorafenib resistance are incompletely understood.
Yi Shi   +5 more
doaj   +2 more sources

DNA replication licensing factor Cdc6 and Plk4 kinase antagonistically regulate centrosome duplication via Sas-6

open access: yesNature Communications, 2017
Centrosome duplication is synchronized with cell cycle events but how this is regulated at a molecular level is unclear. Here, the authors show that the DNA replication licensing factor Cdc6 restrains centrosome duplication via binding and inhibiting Sas-
Xiaowei Xu   +9 more
doaj   +2 more sources

CDC6 as early biomarker for myocardial infarction with acute cellular senescence and repair mechanisms [PDF]

open access: yesScientific Reports
We aimed to the exploration of genes related to the cell cycle and the mechanisms of cardiac cell repair and senescence post-MI. The sequencing dataset of myocardial infarction in mice (GSE161427) was downloaded from the Gene Expression Omnibus (GEO ...
Yun Wen   +5 more
doaj   +2 more sources

Unidirectional MCM translocation away from ORC drives origin licensing [PDF]

open access: yesNature Communications
The MCM motor of the eukaryotic replicative helicase is loaded as a double hexamer onto DNA by the Origin Recognition Complex (ORC), Cdc6, and Cdt1. ATP binding supports formation of the ORC-Cdc6-Cdt1-MCM (OCCM) helicase-recruitment complex where ORC ...
Agata Butryn   +2 more
doaj   +2 more sources

CDC6, a key replication licensing factor, is overexpressed and confers poor prognosis in diffuse large B-cell lymphoma

open access: yesBMC Cancer, 2023
Background Cell division cycle 6 (CDC6) is a key licensing factor in the assembly of pre-replicative complexes at origins of replication. The role of CDC6 in the pathogenesis of in diffuse larger B-cell lymphoma (DLBCL) remains unknown.
Mingfang Shen   +7 more
doaj   +1 more source

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