Results 61 to 70 of about 197,763 (291)
Bax ablation rescues chondrocytes.
Proliferative HCS chondrocytic cells treated with Dexa (25 µM) for 72 hrs were analyzed for the expression of the (A) Bax and (B) Bcl-2 proteins. (C) Bax ablation protected proliferative chondrocytes from Dexa-induced apoptosis.
Lars Sävendahl (114293) +4 more
core +1 more source
. ABSTRACT Neuroinflammation driven by microglial activation is a defining feature of Alzheimer's disease (AD), yet the molecular mechanisms sustaining this proinflammatory state remain unclear. Here, we identify the deubiquitinase OTUD7B as a critical regulator of microglial activation and AD pathology.
Luyao Li +15 more
wiley +1 more source
Immunohistochemical localization for Bax.
There was few specific expression of Bax in normal tissue (B). Protein expression of Bax was significantly increased in the epithelial cell, intestine glands and in the inflammatory cells infiltrating in the tissue of model animals (C). Treatment of SASP
Jian Ming Wang (344506), Xin Liu (43569)
core +1 more source
Selenium Nanoparticles Selectively Target KRAS G13D to Inhibit Colorectal Cancer
The mechanisms of SeNPs therapy in cancer treatment, encompass three parallel actions: (1) seleno‐amino acids, key metabolites, upregulate GPX2 expression, thereby inhibiting tumor metastasis via the GPX2‐HIF1α‐VEGF signaling pathway; (2) selenite (SeO32−), an inorganic metabolite, forms hydrogen bonds with amino acid residues 13–17 of the KRAS G13D ...
Xiaoting Liu +13 more
wiley +1 more source
Bax regulates neuronal Ca2+ homeostasis [PDF]
Excessive Ca(2+) entry during glutamate receptor overactivation ("excitotoxicity") induces acute or delayed neuronal death. We report here that deficiency in bax exerted broad neuroprotection against excitotoxic injury and oxygen/glucose deprivation in ...
Heiko Duessmann (7897355) +10 more
core +3 more sources
ABSTRACT Astrocyte reactivity critically shapes neuroinflammatory outcomes after ischemic stroke, yet the upstream regulators governing astrocyte state transitions remain incompletely defined. Here, we identify the immunoproteasome subunit low molecular weight protein 2 (LMP2) as an important modulator of astrocyte functional remodeling following ...
Yanguang Mao +7 more
wiley +1 more source
Tumor Ca2+ interference therapy suffers from self‐protective Ca2+ metabolic autoregulation. In this scenario, a versatile metal‐phenolic nanocluster (TCMH) is engineered to modulate mitochondrial calcium uniporter (MCU) ‐mediated mito‐Ca2+ metabolic autonomy.
Ronglong Chen +13 more
wiley +1 more source
This non‑enzymatic function of DHODH drives sunitinib resistance by competing with TRIM37 to block TRIM28 ubiquitination, thereby stabilizing TRIM28 and activating VEGFA transcription. Disrupting the DHODH–TRIM28 interaction with lisaftoclax restores drug sensitivity.
Shijie Qian +10 more
wiley +1 more source
Matrix Stiffness Induces Endothelial Network Senescence
Using a 3D human in vitro model that decouples mechanical stress from inflammatory or biochemical signals, matrix stiffening induces a senescence phenotype in endothelial networks. This mechano‐induced senescence activates Notch signaling, and pharmacologic Notch inhibition attenuates this stiffness‐induced senescence.
Jiyeon Song +6 more
wiley +1 more source

