Results 81 to 90 of about 226,967 (304)

MITF maintains genome stability in nonmelanocyte lineages

open access: yesMolecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir   +13 more
wiley   +1 more source

The E3 Ubiquitin Ligase Mind Bomb 1 Controls Adenovirus Genome Release at the Nuclear Pore Complex

open access: yesCell Reports, 2019
Summary: Adenoviruses (AdVs) cause respiratory, ocular, and gastrointestinal tract infection and inflammation in immunocompetent people and life-threatening disease upon immunosuppression.
Michael Bauer   +8 more
doaj   +1 more source

DCAF26, an adaptor protein of Cul4-based E3, is essential for DNA methylation in Neurospora crassa. [PDF]

open access: yesPLoS Genetics, 2010
DNA methylation is involved in gene silencing and genome stability in organisms from fungi to mammals. Genetic studies in Neurospora crassa previously showed that the CUL4-DDB1 E3 ubiquitin ligase regulates DNA methylation via histone H3K9 trimethylation.
Hui Xu   +8 more
doaj   +1 more source

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

"Cullin 4 makes its mark on chromatin"

open access: yesCell Division, 2006
Cullin 4 (Cul4), a member of the evolutionally conserved cullin protein family, serves as a scaffold to assemble multisubunit ubiquitin E3 ligase complexes.
Wang Hengbin, Dai Qian
doaj   +1 more source

Differential recruitment of DNA Ligase I and III to DNA repair sites. [PDF]

open access: yes, 2006
DNA ligation is an essential step in DNA replication, repair and recombination. Mammalian cells contain three DNA Ligases that are not interchangeable although they use the same catalytic reaction mechanism.
Rothbauer, Ulrich   +7 more
core   +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

Pol I DNA polymerases stimulate DNA end-joining by Escherichia coli DNA ligase

open access: yes, 2018
© 2018 Klenow and Klentaq are the large fragment domains of the Pol I DNA polymerases from Escherichia coli and Thermus aquaticus, respectively. Herein, we show that both polymerases can significantly stimulate complementary intermolecular end-joining ...
Vince J. LiCata   +4 more
core   +1 more source

Screening and epitope characterization of Nidogen‐2‐specific nanobodies

open access: yesFEBS Open Bio, EarlyView.
Camel immunization and phage display were employed to generate high‐affinity VHH nanobodies against Nidogen‐2. After library construction, biopanning, ELISA screening, sequencing, and recombinant expression, selected nanobodies were purified and characterized, leading to the preliminary exploration of a nanobody‐based sandwich ELISA for specific ...
Jianchuan Wen   +9 more
wiley   +1 more source

POLQ mediated end-joining promotes DNA damage tolerance in neuroblastoma

open access: yesTranslational Oncology
Segmental chromosomal alterations, including 11q deletion and 17q gain, are the strongest predictors of pediatric neuroblastoma relapse. These alterations result from unbalanced translocations linked to erroneous DNA repair.
Sahiti Chukkapalli   +7 more
doaj   +1 more source

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