Results 171 to 180 of about 643,488 (262)
The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII‐δ
UCHL1 is highly upregulated in mice and patients with AF. UCHL1 directly binds to and removes K48‐linked polyubiquitin chains from CaMKII‐δ at K251 and enhances CaMKII‐δ stability, which activates RyR2, disrupts Ca2+ handling, and promotes AF. These findings establish UCHL1 as a critical regulator of CaMKII‐δ stability and AF‐related Ca2+ handling ...
Hai‐Lian Bi +6 more
wiley +1 more source
The Philosophy of Hughlings Jackson [PDF]
George K, York, David A, Steinberg
openaire +2 more sources
ABSTRACT Beta‐amyloid peptide (Aβ)‐induced suppression of hippocampal GABAergic interneuron activity drives hyperexcitability, amyloid pathology, and cognitive impairment in Alzheimer's disease (AD), suggesting that enhancing hippocampal inhibition may be protective.
Rahmi Lee +3 more
wiley +1 more source
Neuronal activation leads to astrocytic transient volume changes, activating transient receptor potential ankyrin 1 (TRPA1) channels, leading to Ca2+ influx. Activation of TRPA1 causes the release of D‐serine through BEST1. Finally, the augmented extracellular levels of D‐serine boost neuronal activity by binding GluN1‐containing NMDARs, leading to CBV
Kayoung Han +11 more
wiley +1 more source
STING/Type I Interferon Pathway Activation Confers Multimodal Therapeutic Benefits in Osteomyelitis
STING/type I interferon signaling counteracts osteomyelitis through coordinated control of pain, bone destruction, and abscess formation. It inhibits pathogen‐induced nociceptor activation, restrains osteoclast‐mediated bone resorption, and suppresses IL‐1β‐driven neutrophil recruitment.
Yang Chen +19 more
wiley +1 more source
Cannabinoid CB1 Receptor in Nociceptors Mediates Postoperative Analgesia via ASIC3 Inhibition
CB1R and ASIC3 are co‐expressed in CGRP+ nociceptors of mouse DRG. Plantar incision triggers an upregulation of ASIC3 and activation of ASIC3+ neurons, driving mechanical allodynia. CB1R activation suppresses ASIC3 function and downstream ERK1/2 phosphorylation, thereby braking nociceptive signaling and accelerating pain resolution.
Kangtai Xu +13 more
wiley +1 more source

