Results 61 to 70 of about 197,763 (291)

Bax ablation rescues chondrocytes.

open access: yes, 2012
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

Microglial Deubiquitinase OTUD7B Stabilizes STAT3 to Promote Neuroinflammation and Cognitive Decline in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
. 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.

open access: yes, 2013
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

open access: yesAdvanced Science, EarlyView.
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]

open access: yes, 2015
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

BAX - BEAT [PDF]

open access: yes
OnLine Card Catalogue drawer 0027 (BAX - BEAT).
Craft, Edward
core   +5 more sources

Astrocytic LMP2 Coordinates NF‐κB and TGF‐β1/Smad3 Signaling to Drive Neuroinflammation after Cerebral Ischemia/Reperfusion

open access: yesAdvanced Science, EarlyView.
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

A Metal‐Phenolic Nanocluster Orchestrates Mito‐Ca2+ Metabolic Autonomy for Tumor Ca2+ Interference Therapy

open access: yesAdvanced Science, EarlyView.
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

DHODH Drives Sunitinib Resistance Via a Non‐Enzymatic Mechanism by Inhibiting TRIM28 Ubiquitination and Consequent VEGFA Activation in RCC

open access: yesAdvanced Science, EarlyView.
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

open access: yesAdvanced Science, EarlyView.
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

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