目录号 | 产品详情 | 靶点 | |
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T36433 | Virus Protease Antiviral | ||
A2ti-2 是一种亲和力较低且具有选择性的膜联蛋白 A2/S100A10 异四聚体 (A2t) 抑制剂(IC50 : 230 μM)。A2ti-2 具有抗病毒活性,可选择性破坏 A2 和 S100A10 之间的蛋白质相互作用,可防止人乳头瘤病毒 16 型 (HPV16) 感染。 | |||
T15172 | Others | ||
DSHS00884 is a potent inhibitor of human papillomavirus E6 (IC50: 10 μM). | |||
T71941 | |||
Lig3 is an inhibitor against high-risk strains of human papillomavirus (HPV) E6 oncoprotein. | |||
T28534 | |||
RH02007 is an inhibitor of the human papillomavirus (HPV) E6 oncoprotein. | |||
T76960 | |||
Verpasep caltespen (HspE7) 是一种重组融合蛋白,来源于Mycobacterium bovis Calmette-Guérin 热休克蛋白 65 (Hsp65),其 C 末端与HPV16 的 E7 蛋白共价连接。Verpasep caltespen 可用于人乳头瘤病毒 (HPV)引起的癌前病变和癌性病变研究。 | |||
T36858 | |||
C12 Galactosylceramide is a bioactive sphingolipid. It inhibits IL-4 production by 53.84% in EL4 T cells when used at a concentration of 10 μM. C12 Galactosylceramide reduces the growth of human papillomavirus type 16-associated tumors in mice and reduces tumor recurrence following surgical removal or chemotherapy. It also reduces natural killer T cell activity, delays the onset of proteinuria, and improves survival in a mouse model of systemic lupus. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPK-01466 | HLA-A*02:01&B2M&HPV 16 E6 (KLPQLCTEL) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Human papillomavirus (HPV) 16 infection is a necessary condition for the pathogenesis and development of cervical cancer. The E6 protein is expressed by the HPV16 E6 gene and promotes malignant phenotype transformation, which is an important mechanism for the occurrence and development of cervical cancer.
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TMPK-01467 | HLA-A*02:01&B2M&HPV 16 E6 (KLPQLCTEL) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Human papillomavirus (HPV) 16 infection is a necessary condition for the pathogenesis and development of cervical cancer. The E6 protein is expressed by the HPV16 E6 gene and promotes malignant phenotype transformation, which is an important mechanism for the occurrence and development of cervical cancer.
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TMPH-01584 | KRT7 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Blocks interferon-dependent interphase and stimulates DNA synthesis in cells. Involved in the translational regulation of the human papillomavirus type 16 E7 mRNA (HPV16 E7).
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TMPY-00190 | ULBP-6 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
ULBP6/RAET1L, is a polymorphic locus that expresses a functional transcript. ULBP6 had a more restricted expression profile in cell lines and primary human tissues than other NKG2D ligands, but expression was detected in several human papillomavirus-positive cervical carcinoma cell lines and was inducible on infection with human CMV. Expression of ULBP6 on target cells induced a significant increase in NK-cell killing.
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TMPK-00479 | AGER Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
The receptor for advanced glycation end products (AGER) is an oncogenic transmembranous receptor up-regulated in various human cancers. AGER promotes proliferation, migration, and inhibits apoptosis of squamous cervical cancer and might function as a tumor promoter in cervical cancer. Our study provides novel evidence for a potential role of AGER in bridging human papillomavirus (HPV)-induced inflammation and cervical cancer.
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TMPY-00575 | ULBP-6 Protein, Human, Recombinant (His) | Human | HEK293 | ||
ULBP6/RAET1L, is a polymorphic locus that expresses a functional transcript. ULBP6 had a more restricted expression profile in cell lines and primary human tissues than other NKG2D ligands, but expression was detected in several human papillomavirus-positive cervical carcinoma cell lines and was inducible on infection with human CMV. Expression of ULBP6 on target cells induced a significant increase in NK-cell killing.
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TMPY-05411 | Human Papilloma Virus type 58 (HPV 58) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05399 | Human Papilloma Virus type 6 (HPV 6) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPH-02301 | VPS35 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Acts as component of the retromer cargo-selective complex (CSC). The CSC is believed to be the core functional component of retromer or respective retromer complex variants acting to prevent missorting of selected transmembrane cargo proteins into the lysosomal degradation pathway. The recruitment of the CSC to the endosomal membrane involves RAB7A and SNX3. The CSC seems to associate with the cytoplasmic domain of cargo proteins predominantly via VPS35; however, these interactions seem to be of low affinity and retromer SNX proteins may also contribute to cargo selectivity thus questioning the classical function of the CSC. The SNX-BAR retromer mediates retrograde transport of cargo proteins from endosomes to the trans-Golgi network (TGN) and is involved in endosome-to-plasma membrane transport for cargo protein recycling. The SNX3-retromer mediates the retrograde endosome-to-TGN transport of WLS distinct from the SNX-BAR retromer pathway. The SNX27-retromer is believed to be involved in endosome-to-plasma membrane trafficking and recycling of a broad spectrum of cargo proteins. The CSC seems to act as recruitment hub for other proteins, such as the WASH complex and TBC1D5. Required for retrograde transport of lysosomal enzyme receptor IGF2R and SLC11A2. Required to regulate transcytosis of the polymeric immunoglobulin receptor (pIgR-pIgA). Required for endosomal localization of WASHC2C. Mediates the association of the CSC with the WASH complex via WASHC2. Required for the endosomal localization of TBC1D5.; (Microbial infection) The heterotrimeric retromer cargo-selective complex (CSC) mediates the exit of human papillomavirus from the early endosome and the delivery to the Golgi apparatus.
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TMPY-05400 | Human Papilloma Virus type 11 (HPV 11) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05405 | Human Papilloma Virus type 35 (HPV 35) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05401 | Human Papilloma Virus type 16 (HPV 16) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05403 | Human Papilloma Virus type 31 (HPV 31) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05407 | Human Papilloma Virus type 45 (HPV 45) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05409 | Human Papilloma Virus type 52 (HPV 52) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05402 | Human Papilloma Virus type 18 (HPV 18) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05410 | Human Papilloma Virus type 56 (HPV 56) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05406 | Human Papilloma Virus type 39 (HPV 39) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05412 | Human Papilloma Virus type 59 (HPV 59) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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TMPY-05404 | Human Papilloma Virus type 33 (HPV 33) L1 Protein-VLP | HPV | Baculovirus-Insect Cells | ||
Papillomaviruses are highly species-specific and can cause squamous epithelial and fibroepithelial tumors in their hosts. Human papillomaviruses (HPVs) are associated with benign and malignant hyperproliferation of cells, with a wide variety of clinical manifestations ranging from condyloma acuminatum to cervical carcinoma. HPV infection is the most common sexually transmitted disease. More than 4 HPV types so far identified are known to infect the genital tract. Genital HPVs are divided into `low risk' HPVs such as HPV 6 and 11 and ‘high risk’ HPV types such as 16, 18, 31, 33, 35, 39, 45 and 52, 58 which are responsible for more than 95% of HPV-induced cervical cancer. Vaccination against these high-risk types seems to be the most feasible prevention for cervical cancer. Indeed, clinical trials have shown prophylactic HPV vaccines to be effective against HPV infection, cervical intraepithelial neoplasia (CIN), and genital warts, but protection is type-specific and the currently developed vaccines target only a few types. These vaccines are based on papillomavirus-like particles (VLPs) composed of the major capsid protein, L1. The L1 protein self assembles into VLPs when expressed at high levels in eukaryotic or insect cells. VLPs are composed of 36 copies of L1 protein organized into 72 pentamers, so-called capsomeres, to form particles that are immunologically indistinguishable from native virions. Experimentally induced VLP antisera are mostly type-specific for neutralization. Minor cross-neutralization has been observed only between closely related HPV types, e.g. HPV6 and 11, HPV18 and 45, or HPV16 and 31. Structure analysis has revealed the presence of several hypervariable loops on the outer surface of the capsid. With a few exceptions, all HPV-neutralizing monoclonal antibodies analyzed so far are type-specific and recognize conformational epitopes within surface-exposed hypervariable loops of the major capsid protein L1.
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