HPV18 E7 inhibitors encompass a group of compounds that can either directly or indirectly hinder the function of the HPV18 E7 protein within cellular pathways. These inhibitors target specific biochemical and cellular processes that are exploited by HPV18 E7 to promote its oncogenic activities. For instance, compounds like retinoic acid, curcumin, and resveratrol indirectly inhibit HPV18 E7 by modulating the expression and stability of key proteins, such as Rb and p53, which are central to E7-mediated cell cycle progression and survival regulation. By doing so, these chemicals interfere with the intricate web of molecular interactions that E7 relies on for its activity.
Additionally, HPV18 E7 inhibitors like cisplatin and AZD8055 disrupt critical signaling pathways, such as the PI3K/Akt and mTORC1 pathways, which E7 hijacks to support its pro-survival and proliferative functions. Furthermore, JAK inhibitors, bortezomib, SB203580, and sorafenib indirectly hinder E7 by interfering with the JAK/STAT, proteasome, p38 MAPK, and RAF/MEK/ERK pathways, respectively, which are associated with E7-mediated immune evasion, inflammation, and cell proliferation. Collectively, the chemical class of HPV18 E7 inhibitors presents a spectrum of compounds with diverse mechanisms of action, all aimed at disrupting the cellular processes and pathways that enable HPV18 E7 to exert its oncogenic effects.
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