TRIP13 protects pancreatic cancer cells against intrinsic and therapy-induced DNA replication stress.

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Tác giả: Jay R Anand, Jessica Bowser, Channing J Der, Gaith N Droby, Sayali Joseph, Jeffrey A Klomp, Urvi Patel, Jeremy E Purvis, Cyrus Vaziri, Samuel C Wolff, Xingyuan Zhang

Ngôn ngữ: eng

Ký hiệu phân loại: 617.51 *Head

Thông tin xuất bản: United States : bioRxiv : the preprint server for biology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 471081

Oncogene activation in normal untransformed cells induces DNA replication stress and creates a dependency on DNA Damage Response (DDR) mechanisms for cell survival. Different oncogenic stimuli signal via distinct mechanisms in every cancer setting. The DDR is also pathologically re-programmed and deployed in diverse ways in different cancers. Because mutant KRAS is the driver oncogene in 90% of Pancreatic Ductal Adenocarcinomas (PDAC), here we have investigated DDR mechanisms by which KRAS-induced DNA replication stress is tolerated in normal human pancreatic epithelial cells (HPNE). Using a candidate screening approach, we identify TRIP13 as a KRAS
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