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Lack of effect of cyclic adenosine monophosphate modulation during prematuration in vitro on development to the blastocyst stage and expression of specific genes associated with lineage commitment.
JDS Commun
January 2025
Department of Animal Sciences and D.H. Barron Reproductive and Perinatal Biology Research Program, University of Florida, Gainesville, FL 32611-0910.
Pharmacological elevation of cyclic AMP (cAMP) of cultured cumulus-oocyte complexes (COC) before or coincident with initiation of maturation has been reported to improve outcomes for various systems for in vitro production of embryos. Here it was hypothesized that artificial elevation of cAMP in the oocyte for a 2-h period of prematuration would improve developmental competence of matured oocytes and result in increased blastocyst yield and altered expression of genes important for embryonic differentiation. Treated COC were cultured for 2 h with dibutyryl cAMP (dbcAMP), a membrane-permeable form of cAMP, and 3-isobutyl-1-methylxanthine (IBMX), which inhibits phosphodiesterases that convert cAMP to ATP.
View Article and Find Full Text PDFDiscovery of an Orally Bioavailable STING Inhibitor with In Vivo Anti-Inflammatory Activity in Mice with STING-Mediated Inflammation.
J Med Chem
January 2025
State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.
The cyclic GMP-AMP synthase (cGAS)-stimulator of the interferon genes (STING) pathway plays a key role in triggering interferon and inflammatory responses against microbial invasion or tumor. However, aberrant activation of the cGAS-STING pathway is associated with a variety of inflammatory and autoimmune diseases, and thus inhibition of STING is regarded as a potential new approach to treating these diseases. Herein, we report a series of novel indolyl-urea derivatives as STING inhibitors.
View Article and Find Full Text PDFCell-free assays reveal that the HIV-1 capsid protects reverse transcripts from cGAS immune sensing.
PLoS Pathog
January 2025
Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, United States of America.
Retroviruses can be detected by the innate immune sensor cyclic GMP-AMP synthase (cGAS), which recognizes reverse-transcribed DNA and activates an antiviral response. However, the extent to which HIV-1 shields its genome from cGAS recognition remains unclear. To study this process in mechanistic detail, we reconstituted reverse transcription, genome release, and innate immune sensing of HIV-1 in a cell-free system.
View Article and Find Full Text PDFStructural and evolutionary insights into the functioning of glycoprotein hormones and their receptors.
Andrology
January 2025
Department of Biochemistry and Molecular Biophysics, Columbia University, New York, New York, USA.
The neuroendocrine system that comprises the glycoprotein hormones (GpHs) and their receptors is essential for reproduction and metabolism. Each GpH hormone is an αβ heterodimer of cystine-knot proteins and its cognate receptor is a G-protein coupled receptor (GPCR) distinguished by a large leucine-rich-repeat (LRR) extracellular domain that binds the hormone and a class A GPCR transmembrane domain that signals through an associating heterotrimeric G protein. Hence, the receptors are called LRR-containing GPCRs-LGRs.
View Article and Find Full Text PDFPlatinum drugs upregulate CXCR4 and PD-L1 expression via ROS-dependent pathways, with implications for novel combined treatment in gastric cancer.
J Pathol Clin Res
January 2025
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, PR China.
CXC chemokine receptor 4 (CXCR4) and programmed cell death-ligand 1 (PD-L1) are two critical molecules involved in the tumor immune microenvironment. However, the impact of platinum drugs, such as cisplatin, on CXCR4 or PD-L1 expression and the underlying mechanisms in gastric cancer (GC) remain unknown. Moreover, the correlation between their expression levels in GC remains elusive.
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