期刊
BIOMEDICINES
卷 6, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines6010035
关键词
VHL; Hypoxia; ccRCC
资金
- DoD BCRP Breakthrough Fellowship Award [W81XWH-17-1-0016]
- National Cancer Institute [R01CA211732, R21CA223675]
- DoD [W81XWH-15-1-0599]
- Komen Career Catalyst Awardee
- Mary Kay Foundation Awardee
Von Hippel-Lindau (VHL) is an important tumor suppressor that is lost in the majority of clear cell carcinoma of renal cancer (ccRCC). Its regulatory pathway involves the activity of E3 ligase, which targets hypoxia inducible factor alpha (including HIF1 alpha and HIF2 alpha) for proteasome degradation. In recent years, emerging literature suggests that VHL also possesses other HIF-independent functions. This review will focus on VHL-mediated signaling pathways involving the latest identified substrates/binding partners, including N-Myc downstream-regulated gene 3 (NDRG3), AKT, and G9a, etc., and their physiological roles in hypoxia signaling and cancer. We will also discuss the crosstalk between VHL and NF-kappa B signaling. Lastly, we will review the latest findings on targeting VHL signaling in cancer.
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