Mithramycin is a gene-selective Sp1 inhibitor that identifies a biological intersection between cancer and neurodegeneration

Oncogenic transformation of postmitotic neurons triggers cell death, but the identity of genes critical for degeneration remain unclear. The antitumor antibiotic mithramycin prolongs survival of mouse models of Huntington's disease in vivo and inhibits oxidative stress-induced death in cortical...

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التفاصيل البيبلوغرافية
المؤلف الرئيسي:	Sleiman, Sama F. (author)
مؤلفون آخرون:	Langley, Brett C. (author), Berlin, Jill (author), Xia, Li (author), Payappilly, Jimmy B. (author), Kharel, Madan K. (author), Guo, Hengchang (author), Thonpson, Leslie Michels (author), Mahishi, Lata (author), Ahuja, Preeti (author), Maclellan, W. Robb (author), Geschwind, Daniel H. (author), Coppola, Giovanni (author), Rohr, Jurgen (author), Ratan, Rajiv R. (author)
التنسيق:	article
منشور في:	2011
الوصول للمادة أونلاين:	http://hdl.handle.net/10725/6141 https://doi.org/10.1523/JNEUROSCI.0710-11.2011 http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php http://www.jneurosci.org/content/31/18/6858.short
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Mithramycin is a gene-selective Sp1 inhibitor that identifies a biological intersection between cancer and neurodegeneration

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