Results 131 to 140 of about 595,354 (350)
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
Division of Metabolic Engineering [PDF]
この論文は国立情報学研究所の学術雑誌公開支援事業により電子化されまし
中村 憲夫 +6 more
core +1 more source
AZD9291 has shown promise in targeted cancer therapy but is limited by resistance. In this study, we employed metabolic labeling and LC–MS/MS to profile time‐resolved nascent protein perturbations, allowing dynamic tracking of drug‐responsive proteins. We demonstrated that increased NNMT expression is associated with drug resistance, highlighting NNMT ...
Zhanwu Hou +5 more
wiley +1 more source
Metabolic engineering of plant alkaloid biosynthesis [PDF]
Fumihiko Sato +7 more
openalex +1 more source
Division of Metabolic Engineering [PDF]
この論文は国立情報学研究所の学術雑誌公開支援事業により電子化されまし
宮代 博継 +4 more
core +1 more source
A‐to‐I editing of miRNAs, particularly miR‐200b‐3p, contributes to HGSOC progression by enhancing cancer cell proliferation, migration and 3D growth. The edited form is linked to poorer patient survival and the identification of novel molecular targets.
Magdalena Niemira +14 more
wiley +1 more source
YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy +9 more
wiley +1 more source
Emerging role of ARHGAP29 in melanoma cell phenotype switching
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster +3 more
wiley +1 more source
New Directions in Carbohydrate Engineering: A Metabolic Substrate-Based Approach to Modify the Cell Surface Display of Sialic Acids [PDF]
Kevin J. Yarema
openalex +1 more source
Metabolic engineering of [PDF]
Xueming Zhao +5 more
openaire +2 more sources

