Mutant IDH impairs chromatin binding by PDGFB to promote chromosome instability.

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Tác giả: Dong-Joo Choi, Rachel N Curry, Benjamin Deneen, Leyla Fahim, Marco Gallo, Akdes Serin Harmanci, Arif Harmanci, Peihao He, Yeunjung Ko, Wookbong Kwon, Jason Lee, Brittney Lozzi, Jin Ma, Joshua Marcus, Malcolm F McDonald, Carrie Mohila, Asha Multani, Isabella O'Reilly, Noah Powell, Ganesh Rao, Anna Rosenbaum, Debo Sardar, Su Wang

Ngôn ngữ: eng

Ký hiệu phân loại: 785.13 *Trios

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

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 682585

Non-canonical roles for growth factors in the nucleus have been previously described, but their mechanism of action and biological roles remain enigmatic. Platelet-derived growth factor B (PDGFB) can drive formation of low-grade glioma and here we show that it localizes to the nucleus of human glioma cells where it binds chromatin to preserve genome stability and cell lineage. Failure of PDGFB to localize to the nucleus leads to chromosomal abnormalities, aberrant heterochromatin architecture and accelerated tumorigenesis. Furthermore, nuclear localization of PDGFB is reliant upon the expression levels and mutation status of isocitrate dehydrogenase (IDH). Unexpectedly, we identified macrophages as the predominant source of PDGFB in human, finding that immune-derived PDGFB can localize to the nucleus of glioma cells. Collectively, these studies show that immune derived PDGFB enters the nucleus of glioma cells to maintain genomic stability, while identifying a new mechanism by which IDH mutations promote gliomagenesis.
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