Results 131 to 140 of about 777,239 (352)

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

Data from Increased Susceptibility of Nrf2 Knockout Mice to Colitis-Associated Colorectal Cancer

open access: gold, 2023
Tin Oo Khor   +10 more
openalex   +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

Scavenger receptor class B type I knockout mice develop extensive diet-induced coronary artery atherosclerosis in an age-dependent manner.

open access: yesPLoS ONE
ObjectiveHomozygous knockout of scavenger receptor class B type I (SR-B1) in mice with atherogenic mutations (such as knockout of the apolipoprotein E or low density lipoprotein receptor genes) results in spontaneous or diet-induced coronary heart ...
Samuel K Lee   +9 more
doaj   +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

Murine obscurin and Obsl1 have functionally redundant roles in sarcolemmal integrity, sarcoplasmic reticulum organization, and muscle metabolism. [PDF]

open access: yes, 2019
Biological roles of obscurin and its close homolog Obsl1 (obscurin-like 1) have been enigmatic. While obscurin is highly expressed in striated muscles, Obsl1 is found ubiquitously.
Blondelle, Jordan   +13 more
core   +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

Transgenic mice: beyond the knockout

open access: yesAmerican Journal of Physiology-Renal Physiology, 2011
Transgenic mice have had a tremendous impact on biomedical research. Most researchers are familiar with transgenic mice that carry Cre recombinase (Cre) and how they are used to create conditional knockouts. However, some researchers are less familiar with many of the other types of transgenic mice and their applications.
openaire   +3 more sources

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