Results 111 to 120 of about 2,389,732 (232)

The DNA-binding domain of S. Pombe Mrc1 (Claspin) acts to enhance stalling at replication barriers [PDF]

, 2015
Funding: Marie Curie Cancer Care (J.Z. and J.Z.D.), Biotechnology and Biological Sciences Research Council (J.Z.D.) and Cancer Research UK (E.H.) supported this work.During S-phase replication forks can stall at specific genetic loci.
Dalgaard, J.Z., Emma Louise Godfrey, Zech, Jurgen, Emma Louise Godfrey (774106), Godfrey, E.L., Jacob Zeuthen Dalgaard, Hisao Masai (59105), Edgar Hartsuiker, Zech, J., Juergen Zech (774105), Jacob Zeuthen Dalgaard (774107), Masai, H., Hartsuiker, E., Juergen Zech, Edgar Hartsuiker (254659), Hisao Masai   +15 more
core   +1 more source

Primosomal protein PriC rescues replication initiation stress by bypassing the DnaA-DnaB interaction step for DnaB helicase loading at oriC

eLife
In Escherichia coli, replisome and replication fork assembly is initiated by DnaB helicase loading at the chromosomal origin oriC via its interactions with the DnaA initiator and the DnaC helicase loader.
Ryusei Yoshida, Kazuma Korogi, Qinfei Wu, Shogo Ozaki, Tsutomu Katayama   +4 more
doaj   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

Molecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura, Tadahiro Kuribayashi, Johannes Brägelmann, Sachi Okawa, Masataka Taoka, Shunta Mori, Tomoka Nishimura, Takaaki Tanaka, Go Makimoto, Kiichiro Ninomiya, Kammei Rai, Eiki Ichihara, Ryohei Katayama, Katsuyuki Hotta, Masahiro Tabata, Yosuke Togashi, Yoshinobu Maeda, Martin L. Sos, Katsuyuki Kiura, Kadoaki Ohashi   +19 more
wiley   +1 more source

Decreased MCM2-6 in Drosophila S2 cells does not generate significant DNA damage or cause a marked increase in sensitivity to replication interference. [PDF]

, 2011
A reduction in the level of some MCM proteins in human cancer cells (MCM5 in U20S cells or MCM3 in Hela cells) causes a rapid increase in the level of DNA damage under normal conditions of cell proliferation and a loss of viability when the cells are ...
Cotterill, S., Vincent Coulon, Christelle de Renty, Gostan, T., Isabelle Crevel, Renty, C., De, Gostan, T, Cotterill, S, Renty, C.,, Crevel Isabelle, Gostan Thierry, Crevel, G., Crevel, I., Cotterill Sue, Crevel Gilles, Coulon Vincent, de Renty, C, Crevel, G, Crevel, I, Gilles Crevel, Coulon, V., Thierry Gostan, de Renty Christelle, Sue Cotterill, Coulon, V   +24 more
core   +2 more sources

UV- and MMS-induced mutagenesis of lambdaO(am)8 phage under nonpermissive conditions for phage DNA replication. [PDF]

, 2003
Mutagenesis in Escherichia coli, a subject of many years of study is considered to be related to DNA replication. DNA lesions nonrepaired by the error-free nucleotide excision repair (NER), base excision repair (BER) and recombination repair (RR), stop ...
Felczak, Magdalena, Krwawicz, Joanna, Pietrzykowska, Irena, Czajkowska, Anna   +3 more
core   +1 more source

A back-up mechanism for replication

eLife
A protein called PriC allows DNA replication to proceed in Escherichia coli when the complex that usually initiates this process is compromised.
Godefroid Charbon, Anders Løbner-Olesen
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

Molecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober, Leire Moreno‐Cugnon, Laura Martínez‐Pérez, Amaia Ercilla, Amaia Zabala‐Letona, Adrián Vicente‐Barrueco, Maider Fagoaga‐Eugui, Saioa Garcia‐Longarte, Blanca Calle‐Ciborro, Encarnación Pérez‐Andrés, Onintza Carlevaris, Sara Pozo, Isabel Mendizabal, Ugo Mayor, Arkaitz Carracedo, Violaine Sée, Edurne Berra   +16 more
wiley   +1 more source

Real-time analysis of initiation regulation systems during the progression of the reconstituted chromosomal replication cycle

Scientific Reports
Chromosome replication in Escherichia coli is primarily regulated at the initiation stage, where the DnaA protein activates replication at the chromosomal origin, oriC.
Koki Kanoh, Masayuki Su’etsugu
doaj   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

Molecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder, Klaas de Lint, Hồ Mỹ Phúc Võ, Mariana M. Góis, Rosalie A. Kampen, Marta San Martin Alonso, Ilse Nootenboom, Veronica Garzero, Tiemen J. Wendel, Rob M. F. Wolthuis, Sylvie M. Noordermeer   +10 more
wiley   +1 more source