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Hsp90 Inhibitor Can Inhibit UV Carcinogenesis
Santosh K. Katiyar Journal of Investigative Dermatology Volume 135, Issue 4, Pages (April 2015) DOI: /jid Copyright © 2015 The Society for Investigative Dermatology, Inc Terms and Conditions
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Schematic illustration showing the molecular targets of 17-[allylamino]-17-demethoxygeldanamycin (17AAG), an inhibitor of heat-shock protein 90 (Hsp90), in UVR-induced skin carcinogenesis. Skin exposure to UVR induces the activation of multiple signal transduction pathways culminating in activation of transcription factors (AP1, NF-κB, Stat3, and so on) and constitutive expression of genes (e.g., cytokines, COX-2, cyclin D1, Survivin, and so on) essential for squamous cell carcinomas (SCCs) development. The molecular targets in UVR-induced skin carcinogenesis require Hsp90 for their maturity, stability, and activity. 17AAG inhibits UVR-induced SCC via inhibition of Hsp90 ATPase activity essential for the stability of UVR-activated signal transduction pathways. Journal of Investigative Dermatology , DOI: ( /jid ) Copyright © 2015 The Society for Investigative Dermatology, Inc Terms and Conditions
![Schematic illustration showing the molecular targets of 17-[allylamino]-17-demethoxygeldanamycin (17AAG), an inhibitor of heat-shock protein 90 (Hsp90), in UVR-induced skin carcinogenesis. Skin exposure to UVR induces the activation of multiple signal transduction pathways culminating in activation of transcription factors (AP1, NF-κB, Stat3, and so on) and constitutive expression of genes (e.g., cytokines, COX-2, cyclin D1, Survivin, and so on) essential for squamous cell carcinomas (SCCs) development. The molecular targets in UVR-induced skin carcinogenesis require Hsp90 for their maturity, stability, and activity. 17AAG inhibits UVR-induced SCC via inhibition of Hsp90 ATPase activity essential for the stability of UVR-activated signal transduction pathways.](http://slideplayer.com./slide/16546972/96/images/2/Schematic+illustration+showing+the+molecular+targets+of+17-%5Ballylamino%5D-17-demethoxygeldanamycin+%2817AAG%29%2C+an+inhibitor+of+heat-shock+protein+90+%28Hsp90%29%2C+in+UVR-induced+skin+carcinogenesis.+Skin+exposure+to+UVR+induces+the+activation+of+multiple+signal+transduction+pathways+culminating+in+activation+of+transcription+factors+%28AP1%2C+NF-%CE%BAB%2C+Stat3%2C+and+so+on%29+and+constitutive+expression+of+genes+%28e.g.%2C+cytokines%2C+COX-2%2C+cyclin+D1%2C+Survivin%2C+and+so+on%29+essential+for+squamous+cell+carcinomas+%28SCCs%29+development.+The+molecular+targets+in+UVR-induced+skin+carcinogenesis+require+Hsp90+for+their+maturity%2C+stability%2C+and+activity.+17AAG+inhibits+UVR-induced+SCC+via+inhibition+of+Hsp90+ATPase+activity+essential+for+the+stability+of+UVR-activated+signal+transduction+pathways..jpg "Journal of Investigative Dermatology , DOI: ( /jid ) Copyright © 2015 The Society for Investigative Dermatology, Inc Terms and Conditions.")
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Journal of Investigative Dermatology 2015 135, 945-947DOI: (10
Journal of Investigative Dermatology , DOI: ( /jid ) Copyright © 2015 The Society for Investigative Dermatology, Inc Terms and Conditions
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