Results 161 to 170 of about 817,806 (383)

Polyfunctional CD8+CD226+RUNX2hi effector T cells are diminished in advanced stages of chronic lymphocytic leukemia

open access: yesMolecular Oncology, EarlyView.
CD226+CD8+ T cells express elevated levels of RUNX2, exhibit higher proliferation capacity, cytokines and cytolytic molecules expression, and migratory capacity. In contrast, CD226−CD8+ T cells display an exhausted phenotype associated with the increased expression of co‐inhibitory receptors and impaired effector functions.
Maryam Rezaeifar   +4 more
wiley   +1 more source

Inhibition of acyl‐CoA synthetase long‐chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction

open access: yesMolecular Oncology, EarlyView.
Triacsin C inhibition of the acyl‐CoA synthetase long chain (ACSL) family decreases multiple myeloma cell survival, proliferation, mitochondrial respiration, and membrane potential. Made with Biorender.com. Multiple myeloma (MM) is an incurable cancer of plasma cells with a 5‐year survival rate of 59%.
Connor S. Murphy   +12 more
wiley   +1 more source

Towards monitoring conformational changes of the GPCR neurotensin receptor 1 by single-molecule FRET [PDF]

open access: yesarXiv, 2018
Neurotensin receptor 1 (NTSR1) is a G protein-coupled receptor that is important for signaling in the brain and the gut. Its agonist ligand neurotensin (NTS), a 13-amino-acid peptide, binds with nanomolar affinity from the extracellular side to NTSR1 and induces conformational changes that trigger intracellular signaling processes.
arxiv  

Threonine 180 Is Required for G-protein-coupled Receptor Kinase 3- and β-Arrestin 2-mediated Desensitization of the µ-Opioid Receptor in Xenopus Oocytes [PDF]

open access: yes, 2001
To determine the sites in the µ-opioid receptor (MOR) critical for agonist-dependent desensitization, we constructed and coexpressed MORs lacking potential phosphorylation sites along with G-protein activated inwardly rectifying potassium channels ...
Celvert, Jeremy P.   +4 more
core  

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, EarlyView.
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

Cloning, sequencing and tissue distribution of a candidate G protein‐coupled receptor from rat pituitary gland [PDF]

open access: bronze, 1991
Karin A. Eidne   +5 more
openalex   +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

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

Home - About - Disclaimer - Privacy