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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) 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,

(2) 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,

(3) 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,

(4) The clinical pattern of nephrotic syndrome in children has no effect on the concentration of soluble urokinase receptor (suPAR) in serum and urine.[TOP]

Pubmed ID :29775445
Publication Date : //
Concentration of soluble urokinase receptor (suPAR) was regarded as viable marker to differentiate the focal segmental glomerulosclerosis (FSGS) from other glomerulopathies and also as predictive parameter for progression of renal disease.

Authors : Ochocińska Agnieszka, Jarmużek Wioletta, Janas Roman,

(5) 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,

(6) 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,

(7) Seminal suPAR Levels as Marker of Abacterial Male Accessory Gland Inflammation in Hypogonadism.[TOP]

Pubmed ID :29667546
Publication Date : //
Recent evidences suggest that hypogonadism is an important risk factor for lower urinary tract symptoms and benign prostatic hyperplasia. Several papers have discussed the role of chronic inflammation in the development of BPH, which may be modulated by the hypogonadal state. Soluble Urokinase-type Plasminogen Activator Receptor (suPAR), known protein marker of systemic inflammation, can be assayed in the seminal plasma and represents a reliable and sensitive marker of inflammation for the Male Accessory Gland Inflammation (MAGI).

Authors : Milardi Domenico, Grande Giuseppe, Autilio Chiara, Mancini Francesca, De Marinis Laura, Marana Riccardo, Zuppi Cecilia, Urbani Andrea, Pontecorvi Alfredo, Baroni Silvia,

(8) The association between receptor activator of nuclear factor kappa-β ligand and clinical attachment level among waterpipe smoker.[TOP]

Pubmed ID :29491583
Publication Date : //
Higher levels of receptor activator of nuclear factor kappa-β ligand, i.e., RANKL, were reported among periodontitis patients compared with their healthy peers. This study aimed to measure the salivary level of RANKL among waterpipe smokers and to find the possible correlation between salivary level of RANKL and clinical periodontal parameters.

Authors : Al-Mufti Saif Muhammed Taher, Saliem Saif Sehaam, Abdulbaqi Hayder Raad,

(9) Mangiferin inhibits apoptosis and oxidative stress via BMP2/Smad-1 signaling in dexamethasone-induced MC3T3-E1 cells.[TOP]

Pubmed ID :29484386
Publication Date : //
Mangiferin is a xanthone glucoside, which possesses antioxidant, antiviral, antitumor and anti-inflammatory functions, and is associated with gene regulation. However, it remains unknown whether mangiferin protects osteoblasts, such as the MC3T3-E1 cell line, against glucocorticoid-induced damage. In the present study, MC3T3-E1 cells were treated with dexamethasone (Dex), which is a well-known synthetic glucocorticoid, in order to establish a glucocorticoid-induced cell injury model. After Dex and/or mangiferin treatment, cell viability, apoptosis and reactive oxygen species (ROS) production was measured by Cell Counting kit-8 (CCK-8) and flow cytometry, respectively, and the concentration of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and macrophage colony-stimulating factor (M-CSF) was measured by ELISA. The expression of bone morphogenetic protein 2 (BMP2), phosphorylated‑SMAD family member 1 (p-Smad-1), t-Smad-1, osterix (OSX), osteocalcin (OCN), osteoprotegerin (OPG), receptor activator of nuclear factor-κB (RANK), RANK ligand (RANKL), B‑cell lymphoma 2 (Bcl-2) and Bcl‑2‑associated X protein (Bax) was measured by real-time PCR and/or western blot analysis. The results indicated that pretreatment of MC3T3-E1 cells with mangiferin for 3 h prior to exposure to Dex for 48 h significantly attenuated Dex-induced injury and inflammation, as demonstrated by increased cell viability, and decreases in apoptosis, ROS generation, and the secretion of TNF-α, IL-6 and M-CSF. In addition, pretreatment with mangiferin markedly reduced Dex-induced BMP2 and p‑Smad-1 downregulation, and corrected the expression of differentiation‑ and apoptosis‑associated markers, including alkaline phosphatase, OSX, OCN, OPG, RANK, RANKL, Bcl-2 and Bax, which were altered by Dex treatment. Similar to the protective effects of mangiferin, overexpression of BMP2 suppressed not only Dex-induced cytotoxicity, but also ROS generation, and the secretion of TNF-α, IL-6 and M-CSF. In conclusion, the results of the present study are the first, to the best of our knowledge, to demonstrate that mangiferin protects MC3T3-E1 cells against Dex-induced apoptosis and oxidative stress by activating the BMP2/Smad-1 signaling pathway.

Authors : Ding Ling-Zhi, Teng Xiao, Zhang Zhao-Bo, Zheng Chang-Jun, Chen Shi-Hong,

(10) Ang-(1-7) protects HUVECs from high glucose-induced injury and inflammation via inhibition of the JAK2/STAT3 pathway.[TOP]

Pubmed ID :29484371
Publication Date : //
Angiotensin (Ang)‑1‑7, which is catalyzed by angiotensin‑converting enzyme 2 (ACE2) from angiotensin‑II (Ang‑II), exerts multiple biological and pharmacological effects, including cardioprotective effects and endothelial protection. The Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway has been demonstrated to be involved in diabetes‑associated cardiovascular complications. The present study hypothesized that Ang‑(1‑7) protects against high glucose (HG)‑induced endothelial cell injury and inflammation by inhibiting the JAK2/STAT3 pathway in human umbilical vein endothelial cells (HUVECs). HUVECs were treated with 40 mmol/l glucose (HG) for 24 h to establish a model of HG‑induced endothelial cell injury and inflammation. Protein expression levels of p‑JAK2, t‑JAK2, p‑STAT3, t‑STAT3, NOX‑4, eNOS and cleaved caspase‑3 were tested by western blotting. CCK‑8 assay was performed to assess cell viability of HUVECs. Apoptotic cell death was analyzed by Hoechst 33258 staining. Mitochondrial membrane potential (MMP) was obtained using JC‑1. Superoxide dismutase (SOD) activity was tested by SOD assay kit. Interleukin (IL)‑1β, IL‑10, IL‑12 and TNF‑α levels in culture media were tested by ELISA. The findings demonstrated that exposure of HUVECs to HG for 24 h induced injury and inflammation. This injury and inflammation were significantly ameliorated by pre‑treatment of cells with either Ang‑(1‑7) or AG490, an inhibitor of the JAK2/STAT3 pathway, prior to exposure of the cells to HG. Exposure of the cells to HG also increased the phosphorylation of JAK2/STAT3 (p‑JAK2 and p‑STAT3). Increased activation of the JAK2/STAT3 pathway was attenuated by pre‑treatment with Ang‑(1‑7). To the best of our knowledge, the findings from the present study provided the first evidence that Ang‑(1‑7) protects against HG‑induced injury and inflammation by inhibiting activation of the JAK2/STAT3 pathway in HUVECs.

Authors : Chen Jianfang, Zhang Wei, Xu Qing, Zhang Jihua, Chen Wei, Xu Zhengrong, Li Chaosheng, Wang Zhenhua, Zhang Yao, Zhen Yulan, Feng Jianqiang, Chen Jun, Chen Jingfu,