Ines Fathallah - Academia.edu (original) (raw)

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Papers by Ines Fathallah

Research paper thumbnail of NF- B Protects Human Papillomavirus Type 38 E6/E7-Immortalized Human Keratinocytes against Tumor Necrosis Factor Alpha and UV-Mediated Apoptosis

Journal of Virology, 2011

We have previously reported that cutaneous human papillomavirus type 38 (HPV38) displays transfor... more We have previously reported that cutaneous human papillomavirus type 38 (HPV38) displays transforming properties in in vitro and in vivo experimental models. However, the involvement of NF-B signaling in HPV38-induced cell growth transformation remains to be determined. In this study, we showed that HPV38 E6 and E7 activate NF-B and that inhibition of the pathway with the IB␣ superrepressor sensitizes HPV38E6E7-immortalized human keratinocytes to tumor necrosis factor alpha (TNF-␣)-and UVB radiationmediated apoptosis. Accordingly, inhibition of NF-B signaling resulted in the downregulation of NF-Bregulated antiapoptotic genes, including cIAP1, cIAP2, and xIAP genes. These findings demonstrate a critical role of NF-B activity in the survival of HPV38E6E7-immortalized human keratinocytes exposed to cytokine or UV radiation. Our data provide additional evidence for cooperation between beta HPV infection and UV irradiation in skin carcinogenesis.

Research paper thumbnail of EBV Latent Membrane Protein 1 Is a Negative Regulator of TLR9

The Journal of Immunology, 2010

Research paper thumbnail of NF- B Protects Human Papillomavirus Type 38 E6/E7-Immortalized Human Keratinocytes against Tumor Necrosis Factor Alpha and UV-Mediated Apoptosis

Journal of Virology, 2011

We have previously reported that cutaneous human papillomavirus type 38 (HPV38) displays transfor... more We have previously reported that cutaneous human papillomavirus type 38 (HPV38) displays transforming properties in in vitro and in vivo experimental models. However, the involvement of NF-B signaling in HPV38-induced cell growth transformation remains to be determined. In this study, we showed that HPV38 E6 and E7 activate NF-B and that inhibition of the pathway with the IB␣ superrepressor sensitizes HPV38E6E7-immortalized human keratinocytes to tumor necrosis factor alpha (TNF-␣)-and UVB radiationmediated apoptosis. Accordingly, inhibition of NF-B signaling resulted in the downregulation of NF-Bregulated antiapoptotic genes, including cIAP1, cIAP2, and xIAP genes. These findings demonstrate a critical role of NF-B activity in the survival of HPV38E6E7-immortalized human keratinocytes exposed to cytokine or UV radiation. Our data provide additional evidence for cooperation between beta HPV infection and UV irradiation in skin carcinogenesis.

Research paper thumbnail of EBV Latent Membrane Protein 1 Is a Negative Regulator of TLR9

The Journal of Immunology, 2010

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