Results 11 to 20 of about 1,425,864 (268)

Rethinking origin licensing [PDF]

open access: yeseLife, 2017
Human cells that lack a subunit in their origin recognition complex are viable, which suggests the existence of alternative mechanisms to initiate DNA replication.
Stephen P Bell
doaj   +6 more sources

Mobile origin-licensing factors confer resistance to conflicts with RNA polymerase

open access: yesCell Reports, 2022
Summary: Fundamental to our understanding of chromosome duplication is the idea that replication origins function both as sites where MCM helicases are loaded during the G1 phase and where synthesis begins in S phase.
Karl E Duderstadt   +2 more
exaly   +4 more sources

AlphaFold-guided phylogenetic analyses suggest surprising heterogeneity in metazoan replication origin licensing mechanisms [PDF]

open access: yesEMBO Journal
DNA replication initiation is a tightly regulated process that requires the coordinated assembly of replication machineries throughout the genome. During the first step of initiation, origin licensing, the MCM replicative helicase motor is loaded onto ...
Franziska Bleichert
exaly   +3 more sources

Rapid DNA replication origin licensing protects stem cell pluripotency [PDF]

open access: yeseLife, 2017
Complete and robust human genome duplication requires loading minichromosome maintenance (MCM) helicase complexes at many DNA replication origins, an essential process termed origin licensing. Licensing is restricted to G1 phase of the cell cycle, but G1
Jacob Peter Matson   +10 more
doaj   +4 more sources

Efficiency and equity in origin licensing to ensure complete DNA replication [PDF]

open access: yesBiochemical Society Transactions, 2021
The cell division cycle must be strictly regulated during both development and adult maintenance, and efficient and well-controlled DNA replication is a key event in the cell cycle. DNA replication origins are prepared in G1 phase of the cell cycle in a process known as origin licensing which is essential for DNA replication initiation in the ...
Liu Mei, Jeanette Gowen Cook
exaly   +4 more sources

A mechanism of origin licensing control through autoinhibition of S. cerevisiae ORC·DNA·Cdc6 [PDF]

open access: yesNature Communications, 2022
Cryo-EM structures of S. cerevisiae ORC bound to DNA and Cdc6 reveal an autoinhibited conformation and suggest a mechanism of origin licensing control in response to CDK phosphorylation.
Jan Marten Schmidt   +5 more
doaj   +2 more sources

Nucleosome-directed replication origin licensing independent of a consensus DNA sequence [PDF]

open access: yesNature Communications, 2022
Most eukaryotes do not use a consensus DNA sequence as binding sites for the origin recognition complex (ORC) to initiate DNA replication, however budding yeast do. Here the authors show S. cerevisiae ORC can bind nucleosomes near nucleosome-free regions
Sai Li   +5 more
doaj   +2 more sources

Human CST suppresses origin licensing and promotes AND-1/Ctf4 chromatin association [PDF]

open access: yesLife Science Alliance, 2019
This study suggests a novel role of the telomere-associated human CST complex in suppressing origin licensing, through interactions with MCM, while promoting the recruitment of AND-1 and DNA polymerase alpha for replisome formation. Human CTC1-STN1-TEN1 (
Yilin Wang   +4 more
doaj   +2 more sources

Cdc6 is sequentially regulated by PP2A-Cdc55, Cdc14, and Sic1 for origin licensing in S. cerevisiae [PDF]

open access: yeseLife, 2022
Cdc6, a subunit of the pre-replicative complex (pre-RC), contains multiple regulatory cyclin-dependent kinase (Cdk1) consensus sites, SP or TP motifs. In Saccharomyces cerevisiae, Cdk1 phosphorylates Cdc6-T7 to recruit Cks1, the Cdk1 phospho-adaptor in S
Jasmin Philip   +7 more
doaj   +2 more sources

Aneuploidy alleviates the cell proliferation defect caused by mutations affecting origin licensing in Saccharomyces cerevisiae. [PDF]

open access: yesPLoS Genetics
Although aneuploidy is generally detrimental to the survival and growth of normal cells, it can be beneficial under certain stress conditions, such as those caused by harmful mutations.
Christophe de La Roche Saint-André
doaj   +2 more sources

Home - About - Disclaimer - Privacy