Results 271 to 280 of about 8,918,962 (325)
β‐TrCP overexpression enhances cisplatin sensitivity by depleting BRCA1
Low levels of β‐TrCP (Panel A) allow the accumulation of BRCA1 and CtIP, which facilitate the repair of cisplatin‐induced DNA damage via homologous recombination (HR) and promote tumor cell survival. In contrast, high β‐TrCP expression (Panel B) leads to BRCA1 and CtIP degradation, impairing HR repair, resulting in persistent DNA damage and apoptosis ...
Rocío Jiménez‐Guerrero+8 more
wiley +1 more source
Stemness properties, including quiescence, self‐renewal, and chemoresistance, are closely associated with leukemia relapse. Here, we demonstrate that DNA damage‐inducible transcript 4 (DDIT4) is induced in the hypoxic bone marrow niche and is essential for maintaining the stemness of AML1‐ETO9a leukemia cells.
Yishuang Li+12 more
wiley +1 more source
A comparative analysis of non-invasive respiratory support modalities in the treatment of acute hypercapnic respiratory failure: a network meta-analysis. [PDF]
Yan L, Wu G.
europepmc +1 more source
Proteomic and phosphoproteomic analyses were performed on lung adenocarcinoma (LUAD) tumors with EGFR, KRAS, or EML4–ALK alterations and wild‐type cases. Distinct protein expression and phosphorylation patterns were identified, especially in EGFR‐mutated tumors. Key altered pathways included vesicle transport and RNA splicing.
Fanni Bugyi+12 more
wiley +1 more source
Securing face images in UAV networks using chaos and DNA cryptography approach. [PDF]
Inam S+4 more
europepmc +1 more source
Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs
In HGSOC with normal KRAS expression, high PTP4A3 expression regulates autophagy activation. Conversely, in HGSOC with high KRAS expression, KRAS dictates autophagy control, and PTP4A3 is not required. When high PTP4A3 expression is inhibited, HGSOC cells are preferentially sensitised towards DNA‐damaging agents.
Ana López‐Garza+3 more
wiley +1 more source
Screening 166 FDA‐approved anticancer drugs identifies the aromatase inhibitor Exemestane as a synergistic partner of PARP inhibitor Olaparib in BRCA‐proficient triple‐negative breast cancer. Exemestane induces ROS‐mediated replication stress, enhancing DNA damage and apoptosis alongside Olaparib.
Nur Aininie Yusoh+5 more
wiley +1 more source