Results 171 to 180 of about 774,543 (406)

Aberrant expression of nuclear prothymosin α contributes to epithelial‐mesenchymal transition in lung cancer

open access: yesMolecular Oncology, EarlyView.
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen   +12 more
wiley   +1 more source

Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence

open access: yesMolecular Oncology, EarlyView.
The individual functions of three isoforms exchanging ADP and ATP (ADP/ATP translocases; ANTs) on the mitochondrial membrane remain unclear. We developed a method for quantitatively differentiating highly similar human ANT1, ANT2, and ANT3 using parallel reaction monitoring. This method allowed us to assess changes in translocase levels during cellular
Zuzana Liblova   +18 more
wiley   +1 more source

Early metastasis is characterized by Gr1+ cell dysregulation and is inhibited by immunomodulatory nanoparticles

open access: yesMolecular Oncology, EarlyView.
Breast cancer metastasis is associated with myeloid cell dysregulation and the lung‐specific accumulation of tumor‐supportive Gr1+ cells. Gr1+ cells support metastasis, in part, through a CHI3L1‐mediated mechanism, which can be targeted and inhibited with cargo‐free, polymeric nanoparticles.
Jeffrey A. Ma   +9 more
wiley   +1 more source

Detecting homologous recombination deficiency for breast cancer through integrative analysis of genomic data

open access: yesMolecular Oncology, EarlyView.
This study develops a semi‐supervised classifier integrating multi‐genomic data (1404 training/5893 validation samples) to improve homologous recombination deficiency (HRD) detection in breast cancer. Our method demonstrates prognostic value and predicts chemotherapy/PARP inhibitor sensitivity in HRD+ tumours.
Rong Zhu   +12 more
wiley   +1 more source

Whole body deletion of Gpr68 does not change hematopoietic stem cell function

open access: yesStem Cell Research, 2020
G protein-coupled receptor 68 (GPR68) responds to extracellular protons, thus called the proton-sensing G protein-coupled receptor (GPCR), leading to activation of the phospholipase C-β (PLCβ)/calcium (Ca2+) pathway or the adenylyl cyclase (AC)/cyclic ...
Xiaofei He   +7 more
doaj  

Rapid endocytosis of a G protein-coupled receptor: substance P evoked internalization of its receptor in the rat striatum in vivo. [PDF]

open access: green, 1995
Patrick W. Mantyh   +8 more
openalex   +1 more source

Loss of proton‐sensing GPR4 reduces tumor progression in mouse models of colon cancer

open access: yesMolecular Oncology, EarlyView.
G protein‐coupled receptor 4 (GPR4) is a pH‐sensing receptor activated by acidic pH. GPR4 expression is increased in patients with inflammatory bowel disease who are at high risk of developing colorectal cancer. In mouse models, loss of GPR4 attenuated tumor progression. This correlated with increased IL2 and natural killer cell activity.
Leonie Perren   +16 more
wiley   +1 more source

Identification and characterization of a G protein-coupled receptor homolog encoded by murine cytomegalovirus [PDF]

open access: bronze, 1997
Nicholas Davis‐Poynter   +6 more
openalex   +1 more source

TRPM8 levels determine tumor vulnerability to channel agonists

open access: yesMolecular Oncology, EarlyView.
TRPM8 is a Ca2+ permissive channel. Regardless of the amount of its transcript, high levels of TRPM8 protein mark different tumors, including prostate, breast, colorectal, and lung carcinomas. Targeting TRPM8 with channel agonists stimulates inward calcium currents followed by emptying of cytosolic Ca2+ stores in cancer cells.
Alessandro Alaimo   +18 more
wiley   +1 more source

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