產(chǎn)品編號(hào) | bs-0990R |
英文名稱 | HPV16 E6 Rabbit pAb |
中文名稱 | 人類乳頭狀瘤病毒16抗體 |
別 名 | E6; Human Papilloma Virus; Human papillomavirus type 16 E6; Human papillomavirus type 16; Protein E6; E6 protein; HPV16 E6; HPV16-E6; VE6_HPV16. |
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Specific References (6) | bs-0990R has been referenced in 6 publications.
[IF=7.46] Yanjie Chen. et al. A portable multi-signal readout sensing platform based on plasmonic MXene induced signal amplification for point of care biomarker detection. Sensor Actuat B-Chem. 2022 Feb;352:131059
[IF=4.848] Tang Jia-Yi. et al. HPV 16 E6/E7 Promote the Glucose Uptake of GLUT1 in Lung Cancer Through Downregulation of TXNIP Due to Inhibition of PTEN Phosphorylation. Front Oncol. 2020 Nov;10:2470 WB ; Humann.
[IF=3.65] Shao, Jian-Shuang, et al. "HPV16 E6/E7 upregulates HIF-2α and VEGF by inhibiting LKB1 in lung cancer cells." Tumor Biology 39.7 (2017): 1010428317717137. WB ; Human.
[IF=3.182] NJ Gu et al. HPV 16 E6/E7 up-regulate the expression of both HIF-1α and GLUT1 by inhibition of RRAD and activation of NF-κB in lung cancer cells. Journal of Cancer 2019; 10(27): 6903-6909. WB ; Human.
[IF=2.8] Yang, J. H., et al. "Long-term persistent infection of HPV 16 E6 up-regulate SP1 and hTERT by inhibiting LKB1 in lung cancer cells." PloS one 12.8 (2017): e0182775. WB ; Human.
[IF=2.61] Yue Hu. et al. Human papillomavirus 16 (HPV 16) E6 but not E7 inhibits the antitumor activity of LKB1 in lung cancer cells by downregulating the expression of KIF7. Thorac Cancer. 2020 Nov;11(11):3175-3180 WB ; Human.
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研究領(lǐng)域 | 腫瘤 細(xì)菌及病毒 |
抗體來(lái)源 | Rabbit |
克隆類型 | Polyclonal |
交叉反應(yīng) | Human (predicted: HPV16) |
產(chǎn)品應(yīng)用 | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=1ug/Test
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
理論分子量 | 11 kDa |
檢測(cè)分子量 | |
性 狀 | Liquid |
濃 度 | 1mg/ml |
免 疫 原 | KLH conjugated synthetic peptide derived from human HPV16 E6: 85-158/158 |
亞 型 | IgG |
純化方法 | affinity purified by Protein A |
緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
PubMed | PubMed |
產(chǎn)品介紹 |
Human papilloma viruses (HPVs) can be classified as either high risk or low risk according to their association with cancer. HPV16 and HPV18 are the most common of the high risk group while HPV6 and HPV11 are among the low risk types. Approximately 90% of cervical cancers contain HPV DNA of the high risk types. Mutational analysis have shown that the E6 and E7 genes of the high risk HPVs are necessary and sufficient for HPV transforming function. The specific interactions of the E6 and E7 proteins with p53 and pRB, respectively, correlate with HPV high and low risk classifications. The high risk HPV E7 proteins bind to pRB with a higher affinity than do the low risk HPV proteins, and only the high risk HPV E6 proteins form detectable complexes with p53 in vitro. Function: 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 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/E6P targets several other substrates to degradation via the proteasome including host NFX1-91, 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 Bak, 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. Subunit: Forms a complex E6-AP ubiquitin-protein ligase which interacts with human TP53. Binds to human FBLN1 and MPDZ (By similarity). Interacts with human NFX1 and MAGI3. Interacts with human IRF3; this interaction inhibits the establishment of antiviral state. Interacts with human TYK2; this interaction inhibits JAK-STAT activation by interferon alpha. Subcellular Location: Host nucleus matrix. Similarity: Belongs to the papillomaviridae E6 protein family. Database links: Entrez Gene: 1489078 HPV16 E6 |
產(chǎn)品圖片 |
Tissue/cell: human cervical carcinoma; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min;
Incubation: Anti-HPV16-E6 Polyclonal Antibody, Unconjugated(bs-0990R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Blank control(black line):Hela.
Primary Antibody (green line): Rabbit Anti-HPV16 E6 antibody (bs-0990R)
Dilution:1ug/Test;
Secondary Antibody(white blue line): Goat anti-rabbit IgG-AF488
Dilution: 0.5ug/Test.
Isotype control(orange line): Normal Rabbit IgG
Protocol
The cells were fixed with 4% PFA (10min at room temperature)and then permeabilized with 90% ice-cold methanol for 20 min at -20℃, The cells were then incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.
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