Results 241 to 250 of about 1,594,666 (333)

β‐TrCP overexpression enhances cisplatin sensitivity by depleting BRCA1

open access: yesMolecular Oncology, EarlyView.
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

Unveiling unique protein and phosphorylation signatures in lung adenocarcinomas with and without ALK, EGFR, and KRAS genetic alterations

open access: yesMolecular Oncology, EarlyView.
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

Olaparib synergy screen reveals Exemestane induces replication stress in triple‐negative breast cancer

open access: yesMolecular Oncology, EarlyView.
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

Dynamic coupling of fast channel gating with slow ATP-turnover underpins protein transport through the Sec translocon. [PDF]

open access: yesEMBO J
Crossley JA   +7 more
europepmc   +1 more source

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