Results 191 to 200 of about 1,305,585 (286)
UFM1 at the endoplasmic reticulum: linking ER stress, ribosome quality control, and ER-phagy. [PDF]
Komatsu M, Mao G.
europepmc +1 more source
ER stress and β cell death — therapeutic approach to combat ER stress
Takashi, Hara, Fumihiko, Urano
openaire +3 more sources
Redox regulation meets metabolism: targeting PRDX2 to prevent hepatocellular carcinoma
PRDX2 acts as a central redox hub linking metabolic dysfunction‐associated steatohepatitis (MASH) to hepatocellular carcinoma (HCC). In normal hepatocytes, PRDX2 maintains redox balance and metabolic homeostasis under oxidative stress. In contrast, during malignant transformation, PRDX2 promotes oncogenic signaling, stemness, and tumor initiation ...
Naroa Goikoetxea‐Usandizaga +2 more
wiley +1 more source
Integrin-specific signaling drives ER stress-dependent atherogenic endothelial activation. [PDF]
Ben Dhaou C +13 more
europepmc +1 more source
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee +8 more
wiley +1 more source
NUSAP1 Drives Endometrial Carcinoma via IP3R Phosphorylation, Calcium Dyshomeostasis, and ER-Stress-Mediated Apoptosis. [PDF]
Xiao H +5 more
europepmc +1 more source
Aptamers are used both therapeutically and as targeting agents in cancer treatment. We developed an aptamer‐targeted PLGA–TRAIL nanosystem that exhibited superior therapeutic efficacy in NOD/SCID breast cancer models. This nanosystem represents a novel biotechnological drug candidate for suppressing resistance development in breast cancer.
Gulen Melike Demirbolat +8 more
wiley +1 more source
Loss of BAP31 Is Detrimentally Aging Photoreceptors Through ER Stress-Mediated Retinal Degeneration. [PDF]
Gao F +6 more
europepmc +1 more source
Targeting p38α in cancer: challenges, opportunities, and emerging strategies
p38α normally regulates cellular stress responses and homeostasis and suppresses malignant transformation. In cancer, however, p38α is co‐opted to drive context‐dependent proliferation and dissemination. p38α also supports key functions in cells of the tumor microenvironment, including fibroblasts, myeloid cells, and T lymphocytes.
Angel R. Nebreda
wiley +1 more source
ER stress tolerance is regulated by copper-dependent PERK kinase activity. [PDF]
Bond Newton SE +9 more
europepmc +1 more source

