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Ubiquitination in host immune response to human papillomavirus infection

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Abstract

Human papillomavirus (HPV) infection with low-risk or high-risk subtypes is very common. Infection with HPVs is often a major causative factor for the development of cutaneous benign lesions, cervical cancer, and a number of other tumors. The mechanisms of host immunity to prevent and control HPV infection still remain unclear. The importance of ubiquitination (or ubiquitylation) as an intracellular proteasomal-mediated protein degradation pathway, and as an important modulator for the regulation of many fundamental cellular processes has been valued over the last decade. Although the molecular and cellular mechanisms are not completely established, the critical role of ubiquitination in host immune response to HPV infection has become increasingly apparent. This review summarizes current knowledge on the possible role that ubiquitination plays in regulating the host immune response during HPV infection. Targeting the components of the ubiquitin system might offer potential therapeutic strategies for HPV-related diseases in the future.

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Acknowledgments

We apologize to the many authors whose publications are not cited directly because of space limitations. This work is supported by grants from National Natural Science Foundation of China (No. 81071302).

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Correspondence to Hao Cheng.

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Zhou, Q., Zhu, K. & Cheng, H. Ubiquitination in host immune response to human papillomavirus infection. Arch Dermatol Res 303, 217–230 (2011). https://doi.org/10.1007/s00403-011-1141-0

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  • DOI: https://doi.org/10.1007/s00403-011-1141-0

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