Results 191 to 200 of about 2,836,933 (367)

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

Erythrokeratoderma Variabilis Caused by p.Gly45Glu in Connexin 31: Importance of the First Extracellular Loop Glycine Residue for Gap Junction Function

open access: gold, 2015
Takuya Takeichi   +8 more
openalex   +2 more sources

Developing evidence‐based, cost‐effective P4 cancer medicine for driving innovation in prevention, therapeutics, patient care and reducing healthcare inequalities

open access: yesMolecular Oncology, EarlyView.
The cancer problem is increasing globally with projections up to the year 2050 showing unfavourable outcomes in terms of incidence and cancer‐related deaths. The main challenges are prevention, improved therapeutics resulting in increased cure rates and enhanced health‐related quality of life.
Ulrik Ringborg   +43 more
wiley   +1 more source

Cell surface interactome analysis identifies TSPAN4 as a negative regulator of PD‐L1 in melanoma

open access: yesMolecular Oncology, EarlyView.
Using cell surface proximity biotinylation, we identified tetraspanin TSPAN4 within the PD‐L1 interactome of melanoma cells. TSPAN4 negatively regulates PD‐L1 expression and lateral mobility by limiting its interaction with CMTM6 and promoting PD‐L1 degradation.
Guus A. Franken   +7 more
wiley   +1 more source

Correlation analysis of gap junction lattice images

open access: bronze, 1990
Gina E. Sosinsky   +3 more
openalex   +1 more source

PARP inhibition and pharmacological ascorbate demonstrate synergy in castration‐resistant prostate cancer

open access: yesMolecular Oncology, EarlyView.
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon   +13 more
wiley   +1 more source

In situ structure of a gap junction-stomatin complex. [PDF]

open access: yesSci Adv
Rosenkranz N   +11 more
europepmc   +1 more source

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