Results 101 to 110 of about 1,204,389 (301)

BRIT1/MCPH1 links chromatin remodelling to DNA damage response [PDF]

open access: yes, 2009
To detect and repair damaged DNA, DNA damage response proteins need to overcome the barrier of condensed chromatin to gain access to DNA lesions1. ATP-dependent chromatin remodeling is one of the fundamental mechanisms used by cells to relax chromatin in
AA Goodarzi   +41 more
core   +2 more sources

Potential therapeutic targeting of BKCa channels in glioblastoma treatment

open access: yesMolecular Oncology, EarlyView.
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak   +4 more
wiley   +1 more source

CHROMATIN STRUCTURE AND DNA DAMAGE RESPONSE

open access: yesПаёми Сино, 2017
Genomic integrity is constantly exposed to the products of metabolic activities and environmental processes that can induce DNA damage. A well-organized network of signaling cascade, designated as DNA damage response (DDR), encompasses systems of damage ...
M.A. NORMATOVA
doaj   +1 more source

Absence of ERK5/MAPK7 delays tumorigenesis in Atm-/- mice [PDF]

open access: yes, 2017
Ataxia-telangiectasia mutated (ATM) is a cell cycle checkpoint kinase that upon activation by DNA damage leads to cell cycle arrest and DNA repair or apoptosis.
Angulo Ibáñez, María   +6 more
core   +1 more source

Effective therapeutic targeting of CTNNB1‐mutant hepatoblastoma with WNTinib

open access: yesMolecular Oncology, EarlyView.
WNTinib, a Wnt/CTNNB1 inhibitor, was tested in hepatoblastoma (HB) experimental models. It delayed tumor growth and improved survival in CTNNB1‐mutant in vivo models. In organoids, WNTinib outperformed cisplatin and showed enhanced efficacy in combination therapy, supporting its potential as a targeted treatment for CTNNB1‐mutated HB.
Ugne Balaseviciute   +17 more
wiley   +1 more source

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

open access: yesMolecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller   +17 more
wiley   +1 more source

The Histone-Fold Protein CHRAC14 Influences Chromatin Composition in Response to DNA Damage

open access: yesCell Reports, 2014
Summary: Chromatin reorganization and the incorporation of specific histone modifications during DNA damage response are essential steps for the successful repair of any DNA lesion.
Veena Mathew   +5 more
doaj   +1 more source

Beyond DNA repair: DNA-PK function in cancer. [PDF]

open access: yes, 2014
UNLABELLED: The DNA-dependent protein kinase (DNA-PK) is a pivotal component of the DNA repair machinery that governs the response to DNA damage, serving to maintain genome integrity.
Goodwin, Jonathan F, Knudsen, Karen E
core   +1 more source

ATF4‐mediated stress response as a therapeutic vulnerability in chordoma

open access: yesMolecular Oncology, EarlyView.
We screened 5 chordoma cell lines against 100+ inhibitors of epigenetic and metabolic pathways and kinases and identified halofuginone, a tRNA synthetase inhibitor. Mechanistically halofuginone induces an integrated stress response, with eIF2alpha phosphorylation, activation of ATF4 and its target genes CHOP, ASNS, INHBE leading to cell death ...
Lucia Cottone   +11 more
wiley   +1 more source

The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress [PDF]

open access: yes, 2015
The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/
A Dupre   +70 more
core   +1 more source

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