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ELISA kit Activator protein 1,AP1,JUN,Pig,Proto-oncogene c-Jun,Sus scrofa,Transcription factor AP-1,V-jun avian sarcoma virus 17 oncogene homolog

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[#E1292p] ELISA kit Activator protein 1,AP1,JUN,Pig,Proto-oncogene c-Jun,Sus scrofa,Transcription factor AP-1,V-jun avian sarcoma virus 17 oncogene homolog


E1292p | ELISA kit Activator protein 1,AP1,JUN,Pig,Proto-oncogene c-Jun,Sus scrofa,Transcription factor AP-1,V-jun avian sarcoma virus 17 oncogene homolog, 96T
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(1) CYLD suppression enhances the pro-inflammatory effects and hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes by enhancing NF-κB activation.[TOP]

Pubmed ID :30285829
Publication Date : //
Rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) actively drive joint inflammation and degradation by producing inflammatory cytokines and matrix-degrading molecules, making them key factors in the pathogenesis of RA. Cylindromatosis (CYLD) is a tumor suppressor that downregulates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation by deubiquitinating NF-κB essential modulator and tumor necrosis factor receptor-associated factors 2 and 6. In this study, we aimed to determine CYLD expression in the synovium of patients with RA, analyze its correlation with NF-κB activation and clinical disease activity, further investigate CYLD expression in RA-FLSs, and explore CYLD's roles and mechanisms in the pro-inflammatory effects, proliferation, apoptosis, and cell cycles of RA-FLSs.

Authors : Zhang Le-Meng, Zhou Jing-Jing, Luo Chun-Lei,

(2) Relationship of Autophagy and Apoptosis with Total Occlusion of Coronary Arteries.[TOP]

Pubmed ID :30273932
Publication Date : //
BACKGROUND The primary aim of this study was to evaluate the level of autophagy and apoptosis enzymes in patients with coronary artery disease (CAD). Furthermore, we investigated the role of autophagy and apoptosis in the progression of coronary collateral and coronary total occlusion (TO). MATERIAL AND METHODS We enrolled 115 patients in this prospective, observational, controlled study, who were categorized into 3 groups as follows: group 1, patients with chronic TO (n=49); group 2, patients with acute TO such as myocardial infarction (n=36); and group 3, healthy control patients (n=30). We used the enzyme-linked immunosorbent assay (ELISA) kit for autophagy-related protein 5 (ATG5) and apoptosis (M30) in the plasma for these 3 groups. RESULTS Autophagy levels significantly varied among the groups (13.7±5.3 ng/mL, 11.7±3.4 ng/mL, and 7.5±3, respectively; P<0.001). In addition, apoptosis levels significantly varied among the groups (78.6±33.4 ng/mL, 64.9±30.6 ng/mL, and 47.6±18.2, respectively; P<0.001). The subgroup analysis revealed significant positive correlations between the autophagy level and the Rentrop score in contrast to apoptosis in group 1 (r=0.463; P<0.001). CONCLUSIONS This study determined that autophagy and apoptosis levels were higher in patients with CAD than in healthy controls. In contrast to the serum apoptosis level, serum autophagy levels demonstrated a significant positive correlation with the Rentrop score. Hence, an elevated autophagy level might be a potential activator and marker of the process by which the body protects itself in CAD.

Authors : Kaplan Ozgur, Demircan Gunnur,

(3) Artemisinin-Daumone Hybrid Inhibits Cancer Cell-Mediated Osteolysis by Targeting Cancer Cells and Osteoclasts.[TOP]

Pubmed ID :30205376
Publication Date : //
Bone metastasis of cancer cells decreases patient survival and quality of life. Hybridization via the covalent coupling of two bioactive natural products is a useful strategy for developing more potent anticancer agents by enhancing their bioavailability and avoiding drug resistance.

Authors : Ma Gwang Taek, Lee Sun Kyoung, Park Kwang-Kyun, Park Junhee, Son Seung Hwa, Jung Mankil, Chung Won-Yoon,

(4) TXNIP mediated the oxidative stress response in glomerular mesangial cells partially through AMPK pathway.[TOP]

Pubmed ID :30142540
Publication Date : //
Thioredoxin-interacting protein (TXNIP) plays an important role in the development of diabetic nephropathy. In the present study, we investigated role of TXNIP on oxidative stress in glomerular mesangial cells (GMCs) cultured in high glucose or normal glucose, and explored the potential mechanism related to TXNIP as well.

Authors : Xu Wenwei, Wang Ling, Li Jimin, Cai Yingying, Xue Yaoming,

(5) Luteolin induces caspase-dependent apoptosis via inhibiting the AKT/osteopontin pathway in human hepatocellular carcinoma SK-Hep-1 cells.[TOP]

Pubmed ID :30107166
Publication Date : //
Luteolin, a naturally occurring flavonoid, possesses anti-cancer effects including induction of apoptosis. This study investigated the involvement of osteopontin (OPN) in luteolin-induced apoptosis in human hepatocellular carcinoma (HCC) SK-Hep-1 cells with high OPN expression.

Authors : Im Eunji, Yeo Changhwan, Lee Eun-Ok,

(6) Hesperidin inhibits insulin-induced phosphoinositide 3-kinase/Akt activation in human pre-B cell line NALM-6.[TOP]

Pubmed ID :29893306
Publication Date : //
It has been shown that hesperidin induces apoptosis in NALM-6 cells through inhibition of nuclear factor-kappa B (NF-κB) activation.

Authors : Shahbazi Roghayeh, Cheraghpour Makan, Homayounfar Reza, Nazari Maryam, Nasrollahzadeh Javad, Davoodi Sayed Hossein,

(7) Puerarin prevents vascular endothelial injury through suppression of NF-κB activation in LPS-challenged human umbilical vein endothelial cells.[TOP]

Pubmed ID :29775893
Publication Date : //
In the present study, we aimed to explore the effects of puerarin on vascular endothelial cell injury induced by lipopolysaccharide (LPS) and its underlying mechanisms.

Authors : Deng Hua-Fei, Wang Sha, Li Lian, Zhou Qin, Guo Wan-Bei, Wang Xiao-Li, Liu Mei-Dong, Liu Ke, Xiao Xian-Zhong,

(8) [TOP]

Pubmed ID :
Publication Date : //

Authors :

(9) Exogenous hydrogen sulfide promotes hepatocellular carcinoma cell growth by activating the STAT3-COX-2 signaling pathway.[TOP]

Pubmed ID :29725404
Publication Date : //
The effects of hydrogen sulfide (HS) on cancer are controversial. Our group previously demonstrated that exogenous HS promotes the development of cancer via amplifying the activation of the nuclear factor-κB signaling pathway in hepatocellular carcinoma (HCC) cells (PLC/PRF/5). The present study aimed to further investigate the hypothesis that exogenous HS promotes PLC/PRF/5 cell proliferation and migration, and inhibits apoptosis by activating the signal transducer and activator of transcription 3 (STAT3)-cyclooxygenase-2 (COX-2) signaling pathway. PLC/PRF/5 cells were treated with 500 µmol/l NaHS (a donor of HS) for 24 h. The expression levels of phosphorylated (p)-STAT3, STAT3, cleaved caspase-3 and COX-2 were measured by western blot assay. Cell viability was detected by Cell Counting kit-8 assay. Apoptotic cells were observed by Hoechst 33258 staining. The expression of STAT3 and COX-2 messenger RNA (mRNA) was detected by semiquantitative reverse transcription-polymerase chain reaction. The production of vascular endothelial growth factor (VEGF) was evaluated by ELISA. The results indicated that treatment of PLC/PRF/5 cells with 500 µmol/l NaHS for 24 h markedly increased the expression levels of p-STAT3 and STAT3 mRNA, leading to COX-2 and COX-2 mRNA overexpression, VEGF induction, decreased cleaved caspase-3 production, increased cell viability and migration, and decreased number of apoptotic cells. However, co-treatment of PLC/PRF/5 cells with 500 µmol/l NaHS and 30 µmol/l AG490 (an inhibitor of STAT3) or 20 µmol/l NS-398 (an inhibitor of COX-2) for 24 h significantly reverted the effects induced by NaHS. Furthermore, co-treatment of PLC/PRF/5 cells with 500 µmol/l NaHS and 30 µmol/l AG490 markedly decreased the NaHS-induced increase in the expression level of COX-2. By contrast, co-treatment of PLC/PRF/5 cells with 500 µmol/l NaHS and 20 µmol/l NS-398 inhibited the NaHS-induced increase in the expression level of p-STAT3. In conclusion, the findings of the present study provide evidence that the STAT3-COX-2 signaling pathway is involved in NaHS-induced cell proliferation, migration, angiogenesis and anti-apoptosis in PLC/PRF/5 cells, and suggest that the positive feedback between STAT3 and COX-2 may serve a crucial role in hepatocellular carcinoma carcinogenesis.

Authors : Zhen Yulan, Wu Qiaomei, Ding Yiqian, Zhang Wei, Zhai Yuansheng, Lin Xiaoxiong, Weng Yunxia, Guo Ruixian, Zhang Ying, Feng Jianqiang, Lei Yiyan, Chen Jingfu,

(10) The therapeutic effect of artesunate on rosacea through the inhibition of the JAK/STAT signaling pathway.[TOP]

Pubmed ID :29693177
Publication Date : //
Acne rosacea is a type of chronic dermatosis with the characteristics of erubescence, angiotelectasis and pustule formation. However, current treatment methods are limited due to the side effects. Artesunate demonstrated a promising therapeutic efficacy with a high safety margin. HaCaT cells were treated with antibacterial peptide LL‑37 to simulate rosacea caused by Demodex folliculorum (D. folliculorum) infection. Cell Counting kit 8 and flow cytometry assays were performed to measure cellular proliferation, apoptosis, the stage of the cell cycle and reactive oxygen species generation in order to determine the level of cell damage. Then the damaged cells were treated with different concentrations of artesunate and doxycycline to determine the therapeutic effect of artesunate. Pro‑inflammatory cytokines tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑6, IL‑8 and C‑C motif chemokine 2 (MCP‑1) were measured using an ELISA, while western blotting was used to detect the expression of Janus kinase 2 (JAK2) and signal transducer and transcription activator (STAT3). As a result, LL‑37 treated HaCaT cells decreased in cell viability, had an increased apoptotic rate and cell cycle arrest, indicating that cell damage caused by rosacea was simulated. In addition, upregulated concentrations of the pro‑inflammatory cytokines TNF‑α, IL‑6, IL‑8 and MCP‑1 were attenuated in the artesunate group in a dose‑dependent fashion, indicating the therapeutic effect of artesunate. Furthermore, higher concentrations of artesunate exhibited an improved effect compared with the doxycycline group. In addition, increased expression levels of JAK2 and STAT3 following treatment with LL‑37 suggested that rosacea caused by D. folliculorum infection may lead to inflammation through the JAK/STAT signaling pathway. In conclusion, the potential mechanism by which damage occurs in rosacea was revealed and a promising therapeutic method against rosacea was demonstrated.

Authors : Li Ting, Zeng Qingwen, Chen Xingming, Wang Guojiang, Zhang Haiqing, Yu Aihua, Wang Hairui, Hu Yang,