Results 51 to 60 of about 341,882 (288)

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites

open access: yesNature Communications, 2017
The choice between homologous recombination and non-homologous end-joining is largely influenced by cell cycle. Here the authors show that APCCdh1 promotes homologous recombination by removing USP1, allowing polyubiquitinated histones to recruit BRCA1.
Kyungsoo Ha   +15 more
doaj   +1 more source

One end to rule them all: Non-homologous end-joining and homologous recombination at DNA double-strand breaks. [PDF]

open access: yes, 2020
Double-strand breaks (DSBs) represent the most severe type of DNA damage since they can lead to genomic rearrangements, events that can initiate and promote tumorigenic processes.
Löbrich, Markus, Ensminger, Michael
core   +1 more source

Turning end-joining upside down in mitosis

open access: yesMolecular & Cellular Oncology, 2021
How cells deal with DNA breaks during mitosis is not well understood. While canonical non-homologous end-joining predominates in interphase, it is inhibited in mitosis to avoid telomere fusions.
Marta Llorens-Agost   +4 more
doaj   +1 more source

The regulation of DNA end resection by chromatin response to DNA double strand breaks

open access: yesFrontiers in Cell and Developmental Biology, 2022
DNA double-strand breaks (DSBs) constantly arise upon exposure to genotoxic agents and during physiological processes. The timely repair of DSBs is important for not only the completion of the cellular functions involving DSBs as intermediates, but also ...
Bo-Ruei Chen   +3 more
doaj   +1 more source

Nuclear pore links Fob1‐dependent rDNA damage relocation to lifespan control

open access: yesFEBS Open Bio, EarlyView.
Damaged rDNA accumulates at a specific perinuclear interface that couples nucleolar escape with nuclear envelope association. Nuclear pores at this site help inhibit Fob1‐induced rDNA instability. This spatial organization of damage handling supports a functional link between nuclear architecture, rDNA stability, and replicative lifespan in yeast.
Yamato Okada   +5 more
wiley   +1 more source

PAXX promotes KU accumulation at DNA breaks and is essential for end-joining in XLF-deficient mice

open access: yesNature Communications, 2017
Non-homologous end-joining is the key pathway for repairing double-stranded DNA breaks in mammalian cells. Here the authors show that PAXX promotes the accumulation of KU at DNA breaks and is essential for end-joining in cells lacking XLF.
Xiangyu Liu   +4 more
doaj   +1 more source

promote alternative non‐homologous end‐joining at uncapped telomeres

open access: yes, 2015
Loss of telomere protection occurs during physiological cell senescence and ageing, due to attrition of telomeric repeats and insufficient retention of the telomere-binding factor TRF2.
Keiji Okamoto   +13 more
core   +1 more source

Promiscuous stimulation of HSP70 ATPase activity by parasite‐derived J‐domains

open access: yesFEBS Open Bio, EarlyView.
The malaria parasite Plasmodium falciparum exports three highly homologous yet functionally divergent J‐domain proteins into human erythrocytes. Here, we show that J‐domains isolated from all three proteins effectively stimulate the ATPase activity of both endogenous host and exported parasite HSP70 chaperones.
Julian Barth   +6 more
wiley   +1 more source

CDK1 phosphorylates WRN at collapsed replication forks

open access: yesNature Communications, 2016
End-resection of double strand DNA breaks is essential for pathway choice between non-homologous end-joining and homologous recombination. Here the authors show that phosphorylation of WRN helicase by CDK1 is essential for resection at replication ...
Valentina Palermo   +8 more
doaj   +1 more source

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