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CDC7-DBF4 kinase (DDK) has a primary role in the replication checkpoint to promote single-stranded DNA accumulation at stalled forks, which is required to initiate a robust checkpoint response and cell cycle arrest to maintain genome integrity.
Higher expression of CDC7 in odontogenic keratocyst (OKC) and radicular cyst was shown in comparison to dentigerous cyst, while radicular cyst and OKC groups showed no difference in CDC7 expression.
Results suggest a new role of Claspin in initiation of DNA replication during normal S phase through the recruitment of Cdc7 that facilitates phosphorylation of Mcm proteins.
Increased Cdc7-dependent replication initiation is a hallmark of p53 gain-of function mutations in lung adenocarcinoma.
Both CDC7 and DBF4 promoters bind E2F, suggesting that increased E2F activity in RB1 mutant cancers promotes increased DDK expression. Surprisingly, increased DDK expression levels are also correlated with both increased chemoresistance and genome-wide mutation frequencies.
p53-dependent control of CDC7 levels is essential for blocking G1/S cell-cycle transition upon genotoxic stress.
we propose that phosphorylation of TOP2A by CDC7/DBF4 in early S-phase prevents its localization and/or activity at centromeres, and inhibition of TOP2A function could be relevant to prevent premature separation of centromeric DNA.
The data support a model where Cdc7 (de)phosphorylation is the molecular switch for the activation and inactivation of DNA replication in mitosis, directly connecting Cdc7 and PP1a/Cdk1 to the regulation of once-per-cell cycle DNA replication in mammalian cells.
Our data show that Cdc7 is highly expressed in colorectal cancer
The presence of the index SNP rs1192415 (TGFBR3-CDC7) was associated with visual field progression in POAG (primary open-angle glaucoma) patients.
MiR-630 promoted apoptosis by downregulation of CDC7.
The state of DUE-B phosphorylation is maintained by the equilibrium between Cdc7-dependent phosphorylation and PP2A-dependent dephosphorylation.
The interaction between Claspin and Cdc7 is not dependent on Cdc7 kinase activity, but Claspin interaction with the DNA helicase subunit Mcm2 is lost upon Cdc7 inhibition.
huCdc7 may play an important role in the development and progression of colorectal cancer.
Cdcy is universally up-regulated in oral squamous cell carcinoma is an independent prognostic marker, contributing to resistance to DNA damaging agents.
The results suggest that CDC7 expression level can be specific prognostic factors for Diffuse large B-cell lymphoma patients
Significantly higher levels of apoptosis were detected in siCDC7-transfected cells.
Cdc7 phosphorylates and interacts with Tob to inhibit the Cul4-DDB1(Cdt2)-dependent Tob degradation.
cell death process induced by Cdc7 depletion
bipartite interaction between Cdc7 and Dbf4/ASK subunits facilitates ATP binding and substrate recognition by the Cdc7 kinase.
Cdc7 physically and functionally interacts with Nkx2.5 to regulate Myocd promoter activity
Cdc7 mediates SMC differentiation through a mechanism distinct from cell proliferation.
MCM4 phosphorylation by Cdc7 kinase facilitates its interaction with Cdc45 on chromatin
This gene encodes a cell division cycle protein with kinase activity that is critical for the G1/S transition. The yeast homolog is also essential for initiation of DNA replication as cell division occurs. Overexpression of this gene product may be associated with neoplastic transformation for some tumors. Multiple alternatively spliced transcript variants that encode the same protein have been detected.
cell division cycle 7-related protein kinase
, CDC7 (cell division cycle 7, S. cerevisiae, homolog)-like 1
, CDC7-related kinase
, cell division cycle 7 homolog
, cell division cycle 7-like protein 1
, cell division cycle 7-like 1