Mechanisms of adrenocorticotropin-induced activation of erk 1/2 map kinase in the human H295R adrenal cell line [PDF]
PhDThe role of ACTH in stimulating or inhibiting growth of adrenal cells has been a subject of some controversy. Reports that ACTH may stimulate Erk/MAP kinase in Y1 cells have suggested a role for cAMP in this process.
Janes, Mandy Elaine
core +4 more sources
Chemically engineering ligand selectivity at the free fatty acid receptor 2 based on pharmacological variation between species orthologs [PDF]
When it is difficult to develop selective ligands within a family of related G-protein-coupled receptors (GPCRs), chemically engineered receptors activated solely by synthetic ligands (RASSLs) are useful alternatives for probing receptor function. In the
Christiansen, Elisabeth +16 more
core +1 more source
MagmaFlow: A desktop platform for artificial intelligence‐driven expression analysis
MagmaFlow is a free, no‐code platform for gene expression analysis. It generates interactive volcano plots, links genes to literature, pathways, and diseases, prioritizes candidates using millions of publications, identifies affected biological processes, builds network diagrams, and exports publication‐ready figures and reports for macOS and Windows ...
Carlos E. Buss +7 more
wiley +1 more source
Enhancing the fight against malaria : from genome to structure and activity of a G-protein coupled receptor from the mosquito, Anopheles Gambiae [PDF]
Includes abstract.Includes bibliographical references (leaves 183-184).G-proton coupled receptors (GPCRs) are excellent drug targets that occupy a central position in the physiology of insects and are involved in transmission of signal from the ...
Mugumbate, Grace Chitima
core +1 more source
Enhanced expression of G-protein coupled estrogen receptor (GPER/GPR30) in lung cancer
Background G-protein-coupled estrogen receptor (GPER/GPR30) was reported to bind 17β-estradiol (E2), tamoxifen, and ICI 182,780 (fulvestrant) and promotes activation of epidermal growth factor receptor (EGFR)-mediated signaling in breast, endometrial and
Jala Venkatakrishna Rao +3 more
doaj +1 more source
Frizzled Proteins are bona fide G Protein-Coupled Receptors [PDF]
Receptors of the Frizzled family initiate Wnt ligand-dependent signaling controlling multiple steps in organism development and highly conserved in evolution. Misactivation of the Wnt/Frizzled signaling is cancerogenic.
Silke Buestorf, Vladimir L. Katanaev
core
Three‐dimensional bioprinting transforms breast cancer modeling from simple constructs into spatially organized, multicellular, perfused, and patient‐derived platforms. This review shows how bioinks, cellular composition, architecture, and flow govern tumor behavior and drug response, while revealing why complexity alone is insufficient without ...
Mustafa Nakipoglu +7 more
wiley +1 more source
Anti‐PD‐1/PD‐L1 blockade has revolutionized cancer immunotherapy, but is ineffective against endocrine‐treated (i.e., Tamoxifen), relapsed ER+ breast cancer (BC) patients. This study provides insight into the sub‐optimal response of ER+BCs to anti‐PD‐1/PD‐L1 blockade – highlighting the induction of STING and the CEACAM1/TIM3 axis after chronic ...
Marvin Angelo E Aberin +20 more
wiley +1 more source
Congenital hypogonadotropic hypogonadism due to GnRH receptor mutations in three brothers reveal sites affecting conformation and coupling [PDF]
Congenital hypogonadotropic hypogonadism (CHH) is characterized by low gonadotropins and failure to progress normally through puberty. Mutations in the gene encoding the GnRH receptor (GNRHR1) result in CHH when present as compound heterozygous or ...
Newton, Claire +23 more
core +2 more sources
GPER as a Receptor for Endocrine-Disrupting Chemicals (EDCs)
Endocrine-disrupting chemicals (EDCs) are exogenous chemicals that interfere with endogenous hormonal systems at various levels, resulting in adverse health effects. EDCs belong to diverse chemical families and can accumulate in the environment, diet and
Séverine Périan, Jean-Marc Vanacker
doaj +1 more source

