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  4. Recombinant Human papillomavirus type 16 Protein E6 (E6)

Recombinant Human papillomavirus type 16 Protein E6 (E6)

In Stock
  • 货号：
    CSB-YP365854HML
  • 规格：
    ￥1500
  • 图片：
    • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
  • 其他：

产品详情

  • 纯度：
    Greater than 90% as determined by SDS-PAGE.
  • 基因名：
  • Uniprot No.：
  • 别名：
    E6; Protein E6
  • 种属：
    Human papillomavirus type 16
  • 蛋白长度：
    Full Length
  • 来源：
    Yeast
  • 分子量：
    21.2 kDa
  • 表达区域：
    1-158aa
  • 氨基酸序列
    MHQKRTAMFQDPQERPRKLPQLCTELQTTIHDIILECVYCKQQLLRREVYDFAFRDLCIVYRDGNPYAVCDKCLKFYSKISEYRHYCYSLYGTTLEQQYNKPLCDLLIRCINCQKPLCPEEKQRHLDKKQRFHNIRGRWTGRCMSCCRSSRTRRETQL
    Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
  • 蛋白标签：
    N-terminal 6xHis-tagged
  • 产品提供形式：
    Liquid or Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 缓冲液：
    Tris-based buffer,50% glycerol
  • 储存条件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期：
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 货期：
    3-7 business days
  • 注意事项：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet & COA：
    Please contact us to get it.

产品评价

靶点详情

  • 功能：
    Plays a major role in the induction and maintenance of cellular transformation. Acts mainly as an oncoprotein by stimulating the destruction of many host cell key regulatory proteins. E6 associates with host UBE3A/E6-AP ubiquitin-protein ligase, and inactivates tumor suppressors TP53 and TP73 by targeting them to the 26S proteasome for degradation. In turn, DNA damage and chromosomal instabilities increase and lead to cell proliferation and cancer development. The complex E6/E6AP targets several other substrates to degradation via the proteasome including host DLG1 or NFX1, a repressor of human telomerase reverse transcriptase (hTERT). The resulting increased expression of hTERT prevents the shortening of telomere length leading to cell immortalization. Other cellular targets including BAK1, Fas-associated death domain-containing protein (FADD) and procaspase 8, are degraded by E6/E6AP causing inhibition of apoptosis. E6 also inhibits immune response by interacting with host IRF3 and TYK2. These interactions prevent IRF3 transcriptional activities and inhibit TYK2-mediated JAK-STAT activation by interferon alpha resulting in inhibition of the interferon signaling pathway.
  • 基因功能参考文献：
    1. USP15 could increase the level of HPV16 E6 by inhibiting E6 degradation. PMID: 29895155
    2. Up-regulation of miR-20a by HPV16 E6 exerted growth-promoting effects by targeting PDCD6 in cervical carcinoma cells. PMID: 29710555
    3. The HPV16-E6 oncoprotein induces EMT in transgenic mice cataracts. The molecular mechanism may involve TGF-beta and Wnt/beta-catenin pathways, suggesting that the K14E6 transgenic mouse could be a useful model for the study or treatment of EMT-induced cataracts. PMID: 29888254
    4. This study provides links between the DNA damage response, the regulation of E6 human papillomavirus type 16 PDZ binding motif function, and the inhibition of p53 activity and begins to explain how virus-infected cells remain within the cell cycle, despite activation of DNA damage response pathways during productive virus infections. PMID: 29848585
    5. E6 oncogene alters host gene expression in the cervical stroma. PMID: 29073104
    6. the K14E6 versus K14E6Delta146-151 transcriptional profile provides a source of valuable data to uncover novel E6 functions in the skin. PMID: 29130045
    7. HPV16 E6 T178G mutation increases the disease risk of cervical intraepithelial neoplasia 2 and 3 PMID: 29787003
    8. the network of transcriptional interactions in HPV16-infected basal-type cervical epithelium is regulated in a concentration-dependent manner by E6/E7, via a limited number of central master-regulators. PMID: 27457222
    9. E6 association with cellular PDZ proteins promotes the nuclear localization of YAP1. PMID: 29346075
    10. Results showed that increased expression of HPV16 E6 expression level was strongly associated with malignant transformation of the cervical epithelium and the histological progression of cervical squamous cell carcinoma. PMID: 29470526
    11. human papillomavirus 16 E6, E7 genes and Long Control Region are expressed in cervical samples from Uruguayan women PMID: 29454092
    12. HPV16 E6 oncoprotein promoted the bioactivities of non-small cell lung cancer (NSCLC) cells. TLR3-Src signaling pathway might be involved in this procession by up-regulation of cytokine production. The interaction between HPV16 E6 protein and TLR3 might contribute to the poor prognosis of NSCLC. PMID: 28480962
    13. HPV16 E6-E7 promotes cancer stem-like cells phenotype in esophageal squamous cell carcinoma cells through the activation of PI3K/Akt signaling pathway PMID: 27489353
    14. Studied role of HPV16 E6 and COX-2 in invasive ductal breast cancer using qPCR and IHC, and in vitro studies. Found HPV16 E6 promoted breast cancer proliferation; Cox-2 inhibition suppressed HPV16 E6 effects on proliferation thru NF-kappaB signaling pathway. PMID: 29250535
    15. Findings indicate O-linked N-acetylglucosamine transferase (OGT) as a cellular factor involved in human papillomaviruses type 16/18 E6 and E7 expressions and cervical cancer tumorigenesis, suggesting that targeting OGT in cervical cancer may have potential therapeutic benefit. PMID: 27331873
    16. IFN-beta treatment leads to p53-indipendent apoptosis in K16 cells whereas induces senescence in K16 cells if E6 is silenced and p53 expression is restored. The levels of selected miRNAs, deregulated in K16 and K38 cells, can be modulated by IFN-beta when E6 and E7 proteins of HPV-16, but not HPV-38, are expressed. PMID: 26748726
    17. A decrease in miR-184 level by E6 oncoprotein may predict unfavorable response to cisplatin-based chemotherapy in HPV-infected non-small cell lung carcinoma patients via increasing Bcl-2 expression. PMID: 27083050
    18. Seminal studies over the last two decades have identified the transcriptional, epigenetic, and post-transcriptional roles high-risk E6 and E7 have in TERT regulation. (Review) PMID: 27863966
    19. Ablation of E6 by siRNA induces the tumor suppressor p53 and diminishes beta-defensin-3 (hBD3) in HPV-16 positive CaSki cervical cancer cells and UM-SCC-104 head and neck cancer cells. PMID: 27034006
    20. This study identifies NFX1-123 as a critical host protein partner through which 16E6 is able to subvert the immune response and in turn permit a long-lived high-risk Human papillomavirus infection. PMID: 29117186
    21. HPV E6 is capable of overriding this regulation and can promote degradation of p53 and Dlg regardless of the phosphorylation status of E6AP. PMID: 28835500
    22. Studies indicate the accuracy of HPV16 antibodies to the oncoproteins E6. PMID: 28316084
    23. Lactate and glucose production were enhanced in E6-transduced keratinocytes, likely due to raised levels of metabolic enzymes, but independent of(HIF-1alpha activity. PMID: 28857035
    24. These data highlight the importance of the carboxy-terminal motif of the E6 protein and downregulation of PAR3 in tumorigenic transformation of human cervical keratinocytes. PMID: 28440909
    25. Study presented a combined molecular dynamics/infrared spectroscopy approach to the study of ligand binding (11-residue peptide derived from the C terminus of HPV16 E6) by the PDZ1 domain of MAGI1, focusing in particular on the far-infrared region of the spectrum. PMID: 28636914
    26. HPV16 E6/E7 oncogene expression in primary human epithelial cells alters miR expression in extracellular vesicles. PMID: 28500882
    27. In three warty or basaloid SCSC HPV16-DNA and E6*I-mRNA were detected. LCM-PCR confirmed HPV16 was in p16(INK4a)-positive malignant cells. However, of three usual-type SCSC, all were HPV-negative and two expressed p53 protein but not p16(INK4a). PMID: 28376081
    28. HPV-16 E6 was confirmed to regulate microRNA miR-23b indirectly through the DNA methylation of host gene C9orf3 and thus induce c-MET and inhibit apoptosis in cervical cancer cells. PMID: 28077801
    29. Our results indicate that HPV16 E6/E7 indirectly upregulated the expression of VEGF by inhibition of liver kinase B1 expression and upregulation of hypoxia-inducible factor 2alpha expression,thus propose a human papillomavirus-liver kinase B1-hypoxia-inducible factor 2A-vascular endothelial growth factor axis for the tumorigenesis of lung cancer PMID: 28720067
    30. HPV E6/E7 increased expression of DROSHA and DICER mRNA and protein in cervical carcinoma cells. PMID: 28448850
    31. Data show that p63 transcription factors modulate cell migration via Src-focal adhesion kinase (FAK) signaling in foreskin keratinocytes (HFK) expressing human papilloma virus (HPV)16 E6/E7 genes. PMID: 26001294
    32. Overall, this study supports the model that perturbation of cellular miR expression by human papillomavirus type 16 E6/E7 importantly contributes to the rewiring of cellular regulatory circuits that contributes to oncogenic transformation. PMID: 28049151
    33. Thus, Brd4 activates human papillomavirus 16 transcription at this integration site, and strong selection for E6/E7 expression can drive the formation of a super-enhancer-like element to promote oncogenesis. PMID: 27624132
    34. Collectively, these results indicate that human papillomavirus 16 E6 induces upregulation of APOBEC3B through increased levels of TEADs, highlighting the importance of the TEAD-APOBEC3B axis in carcinogenesis. PMID: 28077648
    35. A transcriptomic landscape of human papillomavirus 16 E6-regulated gene expression and splicing events in cervical cancer patients has been presented. PMID: 27859058
    36. The ubiquitylation of beta-catenin by E6AP was dependent on its E3 ubiquitin ligase activity, but it was proteasome-independent and did not require HPV16-E6. PMID: 27902311
    37. nucleotide changes in E6 occur significantly more often in the mixed form of viral DNA and in low-grade squamous intraepithelial lesions; and the variants without additional mutations may promote integration of HPV16 genome. PMID: 27801430
    38. We also found VPA suppressed oncogene E6 in a Notch-independent manner, and induced significant apoptosis in E6-overexpressing HPV positive CaSki cells. PMID: 27176495
    39. Data show that alpha-linolenic acid (ALA) decreased the expression of VEGF and COX2 proteins, and reduced the expression of Human papillomavirus type 16/18 onco-proteins E6 and E7, resulting into restoration of expression of tumor suppressor proteins, p53 and Rb in cervical cancer cell lines. PMID: 26440049
    40. Expression changes of E6 and E7 significantly promoted the protein expression of HIF-1alpha, the expression of both protein and mRNA of GLUT1, but had no effect on the expression of HIF-1alpha mRNA in lung cancer cells. PMID: 26508030
    41. our results suggest that ERK1/2 signaling pathway is involved in HPV-16 E6 but not E7 oncoprotein-induced HIF-1a, VEGF, and IL-8 expression in NSCLC cells, leading to the enhanced angiogenesis in vitro. PMID: 26931433
    42. Our data suggest that the use of HPV 16 spliced transcripts may help to predict for poorer outcomes in patients with HPV positive oropharyngeal cancer PMID: 26575468
    43. Within the limitations of this study, the immunoexpression of HPV 16/18 E6 and E7 oncoproteins may have prognostic value regarding cervical squamous intraepithelial lesions persistence in HIV-positive women. PMID: 26909984
    44. HPV16 E6/E7 Oncoproteins Alter the In Vitro Growth of CD44+NGFR+ Human Tonsillar Epithelial Cells. PMID: 26527383
    45. Human papillomavirus type 16 E6 protein, a major etiological molecule of cervical cancer, maintains high YAP protein levels in cervical cancer cells by preventing proteasome-dependent YAP degradation to drive cervical cancer cell proliferation. PMID: 26417066
    46. E6 and E7 have roles in methylation of tumor suppressor genes and inducing phenotype transformation of human cervical carcinoma cells PMID: 26329329
    47. Here we demonstrate that E7, and to a lesser extend E6, strongly reduce NFkappaB activation in response to the inflammatory mediator imiquimod. Moreover, we establish that undifferentiated keratinocytes do not express the putative receptor for imiquimod, TLR7 PMID: 26268216
    48. The data indicate for the first time that increased cytoplasmic human papillomavirus type 16 E6 levels associated with malignant progression alter Cx43 trafficking and recycling to the membrane and the E6/human Dlg interaction may be involved. PMID: 26445057
    49. High-risk HPV-type lesions might inhibit the chemokine CCL20 on Langerhans cells through E6 and E7 to escape the immune response. PMID: 26400278
    50. E6 protein functioning as a host miRna modulator and play a role of HPV induced carcinogenesis in patient diagnosed with cervical cancer. PMID: 26384051

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  • 亚细胞定位：
    Host cytoplasm. Host nucleus.
  • 蛋白家族：
    Papillomaviridae E6 protein family
  • 数据库链接：

    KEGG: vg:1489078