Results 131 to 140 of about 3,076,380 (339)
A Bifunctional T3SS‐Effector Simultaneously Cleaves Host MAP Kinase and Inhibits PPM1A Phosphatase
Pathogenic bacteria exploit the metalloprotease effector NleD to subvert host defenses. Structural, biochemical, and infection analyses reveal a bifunctional mechanism by which NleD binds and inhibits the host phosphatase PPM1A while preserving its proteolytic activity against MAPKs.
Yaakov Socol +18 more
wiley +1 more source
Glycine and GABA mediate inhibitory neurotransmission in the spinal cord and central nervous system. The general concept of neurotransmission is now challenged by the contribution of both phasic activation of postsynaptic glycine and GABAA receptors ...
Emilie Muller +3 more
doaj +1 more source
How Neuromorphic Microstructures Control In Vitro Early‐Stage Neuronal Outgrowth
Biomimetic approach to neuronal interaction with neuromorphic microstructures. ABSTRACT Neuromorphic biomaterials represent a novel class of materials designed to replicate the architecture and functionality of neuronal structures, offering new opportunities in tissue engineering and bioelectronics.
Claudia Latte Bovio +5 more
wiley +1 more source
We present a dual‐organ, biomarker‐integrated ovaryendometrium organ‐on‐a‐chip that recapitulates 3D tissue complexity, menstrual cycle dynamics, and hormonal crosstalk. This platform enables real‐time, cell‐typespecific fluorescent readouts of reproductive toxicity using ANGPTL4 and SERPINB2 as early‐response reporters.
Soo‐Rim Kim +6 more
wiley +1 more source
Functional Interactions of Alcohol-sensitive Sites in the \u3cem\u3eN\u3c/em\u3e-Methyl-d-aspartate Receptor M3 and M4 Domains [PDF]
The N-methyl-d-aspartate receptor is an important mediator of the behavioral effects of ethanol in the central nervous system. Previous studies have demonstrated sites in the third and fourth membrane-associated (M) domains of the N-methyl-d-aspartate ...
Dwyer, Donard S. +5 more
core +1 more source
SETDB1 is progressively downregulated in ALD, correlating with disease severity. SETDB1 deficiency impairs LAP by disrupting Rubicon membrane localization, leading to defective lipid droplet clearance. Concurrently, loss of SETDB1 reduces nuclear LC3B, causing R‐loop accumulation and cGAS‐STING‐driven inflammation. Lipidated LC3B mediates LAP‐dependent
Yi Zhang +17 more
wiley +1 more source
Endocytic Control of Cell‐Autonomous and Non‐Cell‐Autonomous Functions of p53
NUMB Ex3‐containing isoforms localize to the plasma membrane, where they recruit p53 through SNX9 and direct it to multivesicular bodies and exosomes. Exported p53 is taken up by neighboring cells and activates nuclear programs, revealing an intercellular, exosome‐based pathway that might help establish a tumor‐suppressive microenvironment.
Roberta Cacciatore +20 more
wiley +1 more source
Adrenergic pathways in glycine-mediated feeding behavior: Evidence from layer chickens
Glycinergic and adrenergic systems are integral to the regulation of meal consumption in avian species; however, the interactions between these systems have not been previously documented. This investigation was conducted to explore the interplay between
Hamed Zarei +2 more
doaj +1 more source
Zinc Exposure Causes Disulfidptosis to Induce Miscarriage by Up‐Regulating GATA1/METTL1/SLC7A11 Axis
Zn exposure up‐regulates GATA1, promoting GATA1‐mediated METTL1 and SLC7A11 transcription. It also enhances METTL1‐mediated m7G modification on SLC7A11 mRNA, increasing SLC7A11 mRNA stability. Ultimately, Zn exposure up‐regulates SLC7A11 at both transcriptional and post‐transcriptional levels, causing disulfidptosis. Knockdown of murine Slc7a11, Gata1,
Wenxin Huang +16 more
wiley +1 more source
Molecular Requirements for Ethanol Differential Allosteric Modulation of Ligand-Gated Ion Channels Based on Selective G Beta Gamma Modulation [PDF]
It is now believed that the allosteric modulation produced by ethanol in glycine receptors (GlyRs) depends on alcohol binding to discrete sites within the protein structure.
Aguayo, Luis G +6 more
core +1 more source

