Results 221 to 230 of about 4,346,916 (366)

Feasibility study of very high aprotinin dosage in polytrauma patients [PDF]

open access: yes, 1987
Clasen, C.   +4 more
core  

Redox regulation meets metabolism: targeting PRDX2 to prevent hepatocellular carcinoma

open access: yesMolecular Oncology, EarlyView.
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

TAK1 inhibition effectively suppresses NLRP3 inflammasome-mediated inflammation and osteoclastic bone resorption in rheumatoid arthritis

open access: gold, 2020
Hirofumi Tenshin   +13 more
openalex   +1 more source

Combining antibody conjugates with cytotoxic and immune‐stimulating payloads maximizes anti‐cancer activity

open access: yesMolecular Oncology, EarlyView.
Methods to improve antibody–drug conjugate (ADC) treatment durability in cancer therapy are needed. We utilized ADCs and immune‐stimulating antibody conjugates (ISACs), which are made from two non‐competitive antibodies, to enhance the entry of toxic payloads into cancer cells and deliver immunostimulatory agents into immune cells.
Tiexin Wang   +3 more
wiley   +1 more source

Dammarenediol II enhances etoposide‐induced apoptosis by targeting O‐GlcNAc transferase and Akt/GSK3β/mTOR signaling in liver cancer

open access: yesMolecular Oncology, EarlyView.
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

Home - About - Disclaimer - Privacy