Recombinant Human Papilloma Virus type 18 L1 protein (VLP) (DAGF-230)

Human Papilloma Virus type 18 L1 protein (VLP), recombinant protein from E. coli

Molecular Weight
55 kDa
Alternative Names
HPV 18 L1; L1; Major capsid protein L1
> 95%(SDS-PAGE)
Batch dependent - please inquire should you have specific requirements.
500 mM Histidine 100mM NaCl 0.02%Tween80(pH6.0)
Store at -70°C, avoid repeat freeze/thaw cycles
Antigen Description
Human papillomavirus (HPV) is a DNA virus from the papillomavirus family that is capable of infecting humans. Like all papillomaviruses, HPVs establish productive infections only in keratinocytes of the skin or mucous membranes. L1 is a major capsid protein of human papilloma virus. Infection with specific types of HPV has been associated with an increased risk of developing cervical neoplasia. Does not bind DNA.
HPV 18 L1; L1; Major capsid protein L1


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Stigma as a Barrier to Care for Human Papillomavirus: A Commentary Summarizing Literature and Presenting Recommendations for Health Care Providers


Authors: Nagpal, Taniya S.; Blake, Jennifer

In this commentary, we briefly summarize knowledge on stigma associated with human papillomavirus (HPV). In addition, we provide suggestions for health care providers to de-stigmatize HPV and improve the delivery of care.

Changes in the genetic landscape during the malignization of high grade squamous intraepithelial lesion into cervical cancer


Authors: Litviakov, Nikolai, V; Ibragimova, M. K.; Tsyganov, M. M.; Shpileva, O., V; Churuksaeva, O. N.; Kolomiets, L. A.

In 5 patients, a change in the genetic landscape from HPV16 positive high-grade squamous intraepithelial lesion (HSIL) to squamous cervical cancer was traced, which occurred in these patients within the period from 7 months to 5 years after diagnosing HSIL. Materials and Methods: The DNA from paraffin blocks of dysplasia tissue and the tumor that emerged afterwards was used for the study, which was analyzed using the OncoScan FFPE microarray Assay Kit Affymetrix (USA) for genome-wide determination of gene abundance and 65 key somatic driver mutations of oncogenes and tumor suppressor genes. Results: In the study of HSIL material, somatic mutations were observed in 4/5 cases, 18 different somatic driver mutations of the NRAS, EGFR, BRAF, KRAS, IDH2 oncogenes and TP53 suppressor genes were found and almost no CNA-Copy Number Aberration was identified. HSIL malignization is associated with the appearance of secondary driver mutations in oncogenes and tumor suppressor genes and a large number of structural and numerical CNA, the frequency of which correlates with the time of dysplasia malignization into cancer with a very high correlation coefficient r = 0.98, P = 0.004. The trees of dysplasia evolution into tumor were constructed for each patient. Conclusion: According to the results of the work, it is assumed that the initiation of the development of mucosa dysplastic changes is due to primary driver mutations. The formation of secondary driver mutations and CNA are genetic mechanisms of malignant transformation, while the scenarios of the evolution of dysplasia into a tumor are individual and very diverse. (C) 2020 Elsevier Inc. All rights reserved.

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