Results 181 to 190 of about 56,064 (322)

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

Mobility to and from, around and about Brussels

open access: yesBrussels Studies, 2009
Michel Hubert   +2 more
doaj   +1 more source

Large differences between UK black carbon emission factors. [PDF]

open access: yesCarbon Balance Manag
Brighty A, Staffell I, ApSimon H.
europepmc   +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

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