Results 91 to 100 of about 463,447 (290)

TRPM4 contributes to cell death in prostate cancer tumor spheroids, and to extravasation and metastasis in a zebrafish xenograft model system

open access: yesMolecular Oncology, Volume 19, Issue 5, Page 1299-1309, May 2025.
Transient receptor potential melastatin‐4 (TRPM4) is overexpressed in prostate cancer (PCa). Knockout of TRPM4 resulted in reduced PCa tumor spheroid size and decreased PCa tumor spheroid outgrowth. In addition, lack of TRPM4 increased cell death in PCa tumor spheroids.
Florian Bochen   +6 more
wiley   +1 more source

Slot Blot Analysis of Intracellular Glyceraldehyde-Derived Advanced Glycation End Products Using a Novel Lysis Buffer and Polyvinylidene Difluoride Membrane

open access: yesBio-Protocol
Advanced glycation end products (AGEs) are formed through the reaction/modification of proteins by saccharides (e.g., glucose and fructose) and their intermediate/non-enzymatic products [e.g., methylglyoxal and glyceraldehyde (GA)]. In 2017, Dr. Takanobu
Takanobu Takata   +2 more
doaj   +1 more source

Cystatin A promotes the antitumor activity of T helper type 1 cells and dendritic cells in murine models of pancreatic cancer

open access: yesMolecular Oncology, Volume 19, Issue 5, Page 1452-1470, May 2025.
Pancreatic ductal adenocarcinoma (PDAC) is a disease with very poor prognosis due to therapeutic limitations. We investigated the antitumor effects of cystatin A (CSTA) in PDAC murine models. We are first to confirm that CSTA enhances T helper type 1‐mediated antitumor effects through promotion of dendritic cells and M1 macrophage activity. CSTA can be
Alessandro Nasti   +8 more
wiley   +1 more source

MET variants with activating N‐lobe mutations identified in hereditary papillary renal cell carcinomas still require ligand stimulation

open access: yesMolecular Oncology, EarlyView.
MET variants in the N‐lobe of the kinase domain, found in hereditary papillary renal cell carcinoma, require ligand stimulation to promote cell transformation, in contrast to other RTK variants. This suggests that HGF expression in the microenvironment is important for tumor growth in such patients. Their sensitivity to MET inhibitors opens the way for
Célia Guérin   +14 more
wiley   +1 more source

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

open access: yesMolecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita   +1 more
wiley   +1 more source

Negative charge and membrane-tethered viral 3B cooperate to recruit viral RNA dependent RNA polymerase 3D pol

open access: yesScientific Reports, 2017
Most single stranded plus RNA viruses hijack phosphatidylinositol 4-kinases (PI4Ks) to generate membranes highly enriched in phosphatidylinositol 4-phosphate (PI4P).
Anna Dubankova   +3 more
doaj   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

open access: yesMolecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi   +5 more
wiley   +1 more source

Endolysosomal targeting of a clinical chlorin photosensitiser for light-triggered delivery of nano-sized medicines

open access: yesScientific Reports, 2017
A major problem with many promising nano-sized biotherapeutics including macromolecules is that owing to their size they are subject to cellular uptake via endocytosis, and become entrapped and then degraded within endolysosomes, which can significantly ...
Elnaz Yaghini   +5 more
doaj   +1 more source

Home - About - Disclaimer - Privacy