HTLV-1 p24, a structural protein encoded by the human T-cell leukemia virus type 1 (HTLV-1), plays a crucial role in viral replication and assembly. This protein is essential for the formation of viral particles and the spread of the virus within the host. Moreover, HTLV-1 p24 has been implicated in immune evasion and modulation of host cell signaling pathways, contributing to the pathogenesis of HTLV-1-associated diseases.
Inhibition of HTLV-1 p24 is a promising strategy for controlling HTLV-1 infection and impeding the progression of associated diseases. Direct inhibitors targeting HTLV-1 p24, such as proteasome inhibitors (e.g., Bortezomib) and histone deacetylase (HDAC) inhibitors (e.g., Vorinostat), disrupt viral protein synthesis and viral replication by blocking essential cellular processes involved in HTLV-1 p24 expression and assembly. Additionally, inhibitors of cellular signaling pathways crucial for HTLV-1 p24 transcription and translation, such as JAK/STAT pathway inhibitors (e.g., Ruxolitinib) and NF-κB inhibitors (e.g., Niclosamide), effectively suppress HTLV-1 p24 production and viral propagation in infected cells. These inhibitors offer promising avenues for combating HTLV-1-associated diseases by targeting HTLV-1 p24 and inhibiting its essential functions in viral replication and pathogenesis.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Activates SIRT1 deacetylase, leading to inhibition of HTLV-1 p24 gene expression through epigenetic modification of histone proteins and suppression of viral protein synthesis. | ||||||
Curcumin | 458-37-7 | sc-200509 sc-200509A sc-200509B sc-200509C sc-200509D sc-200509F sc-200509E | 1 g 5 g 25 g 100 g 250 g 1 kg 2.5 kg | $36.00 $68.00 $107.00 $214.00 $234.00 $862.00 $1968.00 | 47 | |
Inhibits NF-κB activation and disrupts viral transcription, leading to downregulation of HTLV-1 p24 expression and inhibition of viral protein synthesis in infected cells. | ||||||