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Harvey rat sarcoma protein (H-Ras) is a small GTPase and key member of the Ras subfamily within the Ras superfamily of GTPases[2][3][6]. It acts as a molecular switch in cells, cycling between active (GTP-bound) and inactive (GDP-bound) states to regulate signal transduction from multiple types of cell surface receptors[1][2][3][4]. H-Ras controls essential cellular processes including cell proliferation, differentiation, and survival[2][3][6]. Its gene, HRAS, is a proto-oncogene, and activating mutations convert it into an oncogene associated with uncontrolled cell growth and tumorigenesis—though HRAS mutations are less common in cancers than those in KRAS or NRAS, they are notable in select tumors (e.g., salivary gland, mouth, vulvar carcinoma)[1][4]. HRas is a longstanding but challenging oncology target, due both to its essential role in normal cells and the biochemical difficulty of targeting its function pharmacologically[4][6].
Inhibition of prenylation (farnesyltransferase inhibitors), Direct interference with Ras-GTP interactions, Downregulation of downstream pathways (RAF/MEK/ERK)
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