Results 81 to 90 of about 710,489 (317)

DNA unwinding mechanism of a eukaryotic replicative CMG helicase

open access: yesNature Communications, 2020
The DNA duplex is known to be split apart in a steric exclusion manner during replication, but the specific mechanism has remained unclear. Here the authors present a cryo-EM structure of a eukaryotic replicative CMG helicase on forked DNA, revealing the
Zuanning Yuan   +5 more
doaj   +1 more source

ABL kinase‐dependent phosphorylation of SH proteins promotes their direct interaction with CRK family SH2 domains

open access: yesFEBS Letters, EarlyView.
CT10 regulator of kinase (CRK) and CRK‐Like (CRKL) are signaling adaptors driving cell adhesion, motility, differentiation, and proliferation. SH2‐domain containing (SH) proteins are enriched in YXXP motifs which when phosphorylated create preferred binding sites for CRK family SH2 domains.
Phoebe M. Cousens   +8 more
wiley   +1 more source

Depletion of Uhrf1 inhibits chromosomal DNA replication in Xenopus egg extracts [PDF]

open access: yes, 2013
UHRF1 (ubiquitin-like, containing PHD and RING finger domains 1) has a well-established role in epigenetic regulation through the recognition of various histone marks and interaction with chromatin-modifying proteins.
Taylor, Elaine   +3 more
core  

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

open access: yesMolecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce   +11 more
wiley   +1 more source

TRAIL‐PEG‐Apt‐PLGA nanosystem as an aptamer‐targeted drug delivery system potential for triple‐negative breast cancer therapy using in vivo mouse model

open access: yesMolecular Oncology, EarlyView.
Aptamers are used both therapeutically and as targeting agents in cancer treatment. We developed an aptamer‐targeted PLGA–TRAIL nanosystem that exhibited superior therapeutic efficacy in NOD/SCID breast cancer models. This nanosystem represents a novel biotechnological drug candidate for suppressing resistance development in breast cancer.
Gulen Melike Demirbolat   +8 more
wiley   +1 more source

Ciz1 cooperates with cyclin-A-CDK2 to activate mammalian DNA replication in vitro [PDF]

open access: yes, 2010
Initiation of mammalian DNA replication can be reconstituted from isolated G1-phase nuclei and cell extracts, supplemented with cyclin-dependent protein kinases (CDKs).
Sercombe, Heather E   +3 more
core  

Mathematical modelling of whole chromosome replication [PDF]

open access: yes, 2010
All chromosomes must be completely replicated prior to cell division, a requirement that demands the activation of a sufficient number of appropriately distributed DNA replication origins.
de Moura, Alessandro P.S.   +4 more
core   +1 more source

Dimethyl fumarate combined with cisplatin at subcytotoxic doses sensitizes cervical cancer toward ferroptosis and apoptosis through GSH restriction and p53 (re)activation

open access: yesMolecular Oncology, EarlyView.
Dimethyl fumarate (DMF) reduces growth of HPV‐positive cervical cancer spheroids and induces ferroptosis in cervical cancer cells via blocking SLC7A11/Glutathione (GSH) axis. Combination of subcytotoxic doses of DMF and cisplatin (CDDP) further suppresses spheroid growth and drives cell death in 2D culture models.
Carolina Punziano   +6 more
wiley   +1 more source

GEMC1, a novel factor required for chromosomal DNA replication

open access: yes, 2009
In eukaryotic cells DNA replication begins from multiple origins. During the process of initiation, the DNA replication fork is established at each origin. In lower eukaryotes many factors required for chromosomal DNA replication have been identified.
Balestrini, A.
core  

Molecular Architecture of the DNA Replication Origin Activation Checkpoint [PDF]

open access: yes, 2010
Perturbation of DNA replication initiation arrests human cells in G1, pointing towards an origin activation checkpoint. We used RNAi against Cdc7 kinase to inhibit replication initiation and dissect this checkpoint in fibroblasts.
Claire Mulvey   +13 more
core   +1 more source

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