Anti-HPV11 L1 polyclonal antibody (CABT-B8787)


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Application Notes
WB: 1:200-1000
ELISA: 1:200-2000
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
HPV; L1; major capsid L1 protein; HPV-11; HPV-11 capsid; HPV11 capsid protein


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Inducible heat shock protein 70 enhances HPV31 viral genome replication and virion production during the differentiation-dependent life cycle in human keratinocytes


Authors: Song, Hebin; Moseley, Pope L.; Lowe, Stephanie L.; Ozbun, Michelle A.

Increasing data indicate heat shock proteins (HSPs) including inducible HSP70 (HSP70i) are involved in the replicative cycles of various viruses including adenoviruses (Ads), polyomaviruses (PyVs), and some RNA viruses. Cell-free system studies implicate HSP70i in human papillomavirus type 11 (HPV11) genome replication with E1 and E2 proteins, and there is evidence that HSP70 is involved in capsid assembly and disassembly for PyVs and HPVs. HSP70 expression is increased in HPV16 E6/E7 gene transduced human primary keratinocytes, and frequently detected in early stage uterine cervical cancer at levels in conjunction with lesion severity. In this study we carry out analyses in the natural host epithelial tissues to assess the role of inducible HSP70 (HSP70i) in the HPV infectious life cycle. For these studies we used the organotypic (raft) culture system to recapitulate the full viral life cycle of the high-risk HPV31. Upon heat shock of HPV31-infected organotypic tissues, we find high and sustained expression of HSP70i coincident with enhanced HPV genome replication and virion production. Whereas there is no clear effect on L1 expression levels, we find HSP70i and L1 interact and HSP70i colocalizes with and enhances the nuclear localization of L1 in differentiated cells. Ad-mediated gene transfer was used to study the effects of HSP70i in naturally HPV-infected differentiating tissues and showed results similar to those in heat shocked rafts. These results indicate that increased HSP70i augments late activities in the viral life cycle. We conclude that HSP70i contributes directly to HPV replicative viral activities and the production of infectious virions. (c) 2009 Elsevier B.V. All rights reserved.

Non-specific antiviral activity of antisense molecules targeted to the E1 region of human papillomavirus


Authors: Lewis, EJ; Agrawal, S; Bishop, J; Chadwick, J; Cristensen, ND; Cuthill, S; Dunford, P; Field, AK; Francis, J; Gibson, V; Greenham, AK; Kelly, F; Kilkushie, R; Kreider, JW; Mills, JS; Mulqueen, M; Roberts, NA; Roberts, P; Szymkowski, DE

Antisense phosphorothioate oligonucleotides (ODN1 0x5 OMe) directed against the El start region of human papillomavirus 11 (HPV11) can inhibit papillomavirus induced growth of implanted human foreskin in a mouse xenograft model. Administration of a mismatch control oligonucleotide (ODN9 0x5 OMe), in which guanine was replaced with adenine in the same model, had no effect on papilloma induced growth. However, the apparent antiviral activity of ODN1 0x5 OMe was also shown in a lethal mouse cytomegalovirus (CMV) model, in which the oligonucleotides are not expected to have antisense activity. To understand the mechanisms of action of these oligonucleotides, a mismatch oligonucleotide (ODN61 0x5 OMe) was prepared which retained the CpG motifs of ODN1 0x5 OMe. This was tested in the mouse xenograft model and shown to have moderate inhibitory activity. As a definitive experiment, a comparison was made between the efficacy of the active oligonucleotide ODN1 0x5 Oh le against two papilloma viruses HPV11 and HPV40. Both these viruses cause benign genital warts, but differ by four bases in their El sequence that was the target for ODN1 0x5 OMe. Papillomavirus induced growth in the mouse xenograft model was inhibited by ODN1 0x5 OMe in both cases, suggesting that oligonucleotide molecules have a non-specific antiviral activity that is not directly related to their antisense sequence. (C) 2000 Published by Elsevier Science B.V. All rights reserved.

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