Results 231 to 240 of about 2,088,899 (353)

Raphin‐1 mediates the survival and sensitivity to radiation of pediatric‐type diffuse high‐grade glioma via phosphorylated eukaryotic initiation factor 2α‐dependent and ‐independent processes

open access: yesMolecular Oncology, EarlyView.
Raphin‐1 reduces the survival of PED‐DHGG cells and enhances their radiation sensitivity through both PeIF2α‐dependent and PeIF2α‐independent mechanisms. Raphin‐1 sustains elevated levels of PeIF2α, contributing to its PeIF2α‐dependent effects. Additionally, raphin‐1 interacts with CReP to mediate a separate radiosensitizing pathway that operates ...
Karin Eytan   +4 more
wiley   +1 more source

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

Mutants in the symmetric semigroups [PDF]

open access: yesCzechoslovak Mathematical Journal, 1971
openaire   +2 more sources

Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs

open access: yesMolecular Oncology, EarlyView.
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

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