CVPx ᵀᴹ Human HPV 18 Antigen ELISA Quantitation Kit

Name: CVPx ᵀᴹ Human HPV 18 Antigen ELISA Quantitation Kit
SKU: DEIASL119
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum and Plasma

Species Reactivity

Human

Detection Method

sELISA

Intended Use

Enzyme immunoassay for quantitative analysis of HPV-18 antigen in samples.

Contents of Kit

1. Coated plate: 1 (96 wells)
2. HPV 18 Antigen Standard: Lyophilized, 10 μg/mL, 1 vial. Store at -20°C.
3. HRP-Conjugated Antibody Solution: 100×, 120 μl, 1 vial. Store at -20°C
4. HRP-Conjugated Dilution Buffer: 12 ml, l vial.
5. Sample Diluent: Ready to use, 50 ml, 1 vial.
6. Washing Buffer: 20×, 50 ml, 1 vial.
7. TMB Substrate Solution: 6 ml, 2vial.
8. Stop Solution: 7 ml, 1 vial.
9. Sealing plate film, 2 pieces.
10. Instruction manual

Storage

The HPV 18 Antigen Standard and HRP-Conjugated Antibody Solution should be stored at -20°C. Other components remain stable under the condition of 2-8°C for six months.

Precision

Detection Range

7.8～500 ng/ml

General Description

HPV is a double-stranded DNA virus with a circular genome that encodes early genes, including E1, E2, E4, E5, E6, and E7, essential for replication, transcription, and transformation, and late genes L1 and L2, encoding viral capsid proteins. The replication cycle of HPV is tightly linked to the differentiation of the infected epithelium. Indeed, viral protein production and virus assembly occur only in the upper differentiated layers of the epithelium. In the basal layer, HPV particles initially interact with the basement membrane mostly through heparan sulfate proteoglycans (HSPGs)—capsid L1 contacts, and subsequently bind to HSPGs present on the basal keratinocyte cell surface. This attachment triggers conformational changes in the L2 capsid protein, resulting in exposure of a consensus cleavage site in the L2 N-terminus, whose proteolysis facilitates further interaction of the viral capsid with secondary receptor(s) present on the keratinocyte membrane. After such binding, HPVs are generally internalized by clathrin-dependent endocytosis, which initially relies on actin-rich cell protrusions, acting as the transport mechanism along the endocytic machinery.

General Notes

Enzyme immunoassay for quantitative analysis of HPV-18 antigen in samples.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

HPV Reagents for Vaccine Research and Immunoassay Development

QA & Reviews

Q & A

Ask a Question

Q: Is it monoclonal or polyclonal?

A: This product utilizes the principle of double antibody sandwich ELISA. An HPV18-L1 monoclonal antibody is coated on the enzyme-linked immunosorbent assay (ELISA) plate. After the test sample has reacted, unbound substances are washed away. Subsequently, another HPV18-L1 monoclonal antibody labeled with HRP is added, forming a complex of the coated antibody-antigen-HRP antibody. The extent of TMB colorimetric reaction indicates the level of active HPV18-L1 antigen in intermediate vaccine production, drug substance, and the mixed solution of the 9-valent HPV vaccine (before the addition of adjuvants).

Q: It is against L1 capsid protein of HPV-18

A: Yes

Customer Reviews

References

G Protein-Coupled Receptor Genes, PTGDR1, PTGDR2, and PTGIR, Are Candidate Epigenetic Biomarkers and Predictors for Treated Patients with HPV-Associated Oropharyngeal Cancer

MICROORGANISMS

Authors: Misawa, Kiyoshi; Imai, Atsushi; Kanazawa, Takeharu; Mima, Masato; Yamada, Satoshi; Mochizuki, Daiki; Yamada, Taiki; Shinmura, Daichi; Ishikawa, Ryuji; Kita, Jyunya; Yamaguchi, Yuki; Misawa, Yuki; Mineta, Hiroyuki

Abstract

Differences in the biology of human papillomavirus (HPV)-associated oropharyngeal cancers (OPCs) and HPV-negative OPCs may have implications in patient management. Early detection is imperative to reduce HPV-associated OPC mortality. Circulating tumor DNA (ctDNA) can potentially serve as a biomarker for monitoring clinically relevant cancer-related genetic and epigenetic modifications. We analyzed the methylation status of 24 G protein-coupled receptor (GPCR) genes in verification (85 OPC primary samples) and validation (8 OPC ctDNA samples) studies using quantitative methylation-specific polymerase chain reaction (Q-MSP). The Q-MSP-based verification study with 85 OPC primary samples revealed the GPCR genes that were significantly associated with recurrence in high methylation groups (>= 14 methylated genes) with OPC and HPV-associated OPC (p < 0.001). In the Kaplan-Meier estimate and multivariate Cox proportional hazard analyses, 13 GPCR genes were significantly related to increased recurrence in the methylation group. Furthermore, the validation study on ctDNA showed that three of these genes (Prostaglandin D2 receptor 1: PTGDR1, Prostaglandin D2 receptor 2: PTGDR2, and Prostaglandin I2 Receptor: PTGIR) had a prediction performance as emerging biomarkers. We characterized the relationship between the methylation status of GPCR genes and outcomes in HPV-associated OPC. Our results highlight the potential utility of ctDNA methylation-based detection for the clinical management of HPV-associated OPC.

Structural and functional impacts of E5 genetic variants of human papillomavirus type 31

VIRUS RESEARCH

Authors: Silva, Ruany C. de O.; da Silva Junior, Antonio Humberto P.; Gurgel, Ana P. A. D.; Barros Junior, Marconi R.; Santos, Daffany L.; de Lima, Rita de C. P.; Batista, Marcus V. A.; Pena, Lindomar J.; Chagas, Barbara S.; Freitas, Antonio C.

Abstract

Persistent infections caused by high-risk human papillomavirus (HR-HPV) are important, for the development of cervical lesions, but environmental and genetic factors are also related in the process of carcinogenesis. Among the genetic factors, the genetic variants of HR-HPV appear to be related to the risk of persistent infections. Therefore, the present study investigates variants of HPV31 E5 oncogene in cervical scraping samples from Brazilian women to assess their functional and structural effects, in order to identify possible repercussions of these variants on the infectious and carcinogenic process. Our results detected nucleotide changes previously described in the HPV31 E5 oncogene, which may play a critical role in the development of cancer due to its ability to promote cell proliferation and signal transmission. In our study, the interaction percentage of the 31E5 sequence generated by the Immune Epitope Server database and the Analysis Resource (IEDB) allowed us to include possible immunogenic epitopes with the MHC-I and MHC-II molecules, which may represent a possible relationship between protein suppression of the immune system. In the structural analysis of the HPV31 E5 oncoprotein, the N5D, 148 V, P56A, F80I and V64I polymorphisms can be found inserted within transmembrane regions. The P56A mutation has been predicted to be highly stabilizing and, therefore, can cause a change in protein function. Regarding the interaction of the E5 protein from HPV31 with the signaling of NF-kB pathway, we observed that in all variants of the E5 gene from HPV-31, the activity of the NF-kB pathway was increased compared to the prototype. Our study contributes to a more refined design of studies with the E5 gene from HPV31 and provides important data for a better understanding of how variants can be distinguished under their clinical consequences.