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#33550378   2021/02/08 To Up

Activation of bovine oocytes by protein synthesis inhibitors: New findings on the role of MPF/MAPKs†.

The present study evaluated the mechanism by which protein synthesis inhibitors activate bovine oocytes. The aim was to analyze the dynamics of MPF and MAPKs. MII oocytes were activated with ionomycin (Io), ionomycin+anisomycin (ANY) and ionomycin+cycloheximide (CHX) and by in vitro fertilization (IVF). The expression of cyclin B1, p-CDK1, p-ERK1/2, p-JNK and p-P38 were evaluated by immunodetection and the kinase activity of ERK1/2 was measured by enzyme assay. Evaluations at 1, 4 and 15 hours, post-activation (hpa) showed that the expression of cyclin B1 was not modified by the treatments. ANY inactivated MPF by p-CDK1Thr14-Tyr15 at 4 hpa (p < 0.05), CHX increased pre-MPF (p-CDK1Thr161 and p-CDK1Thr14-Tyr15) at 1 hpa and IVF increased p-CDK1Thr14-Tyr15 at 17 hpf (p < 0.05). ANY and CHX reduced the levels of p-ERK1/2 at 4 hpa (p < 0.05) and its activity at 4 and 1 hpa, respectively (p < 0.05). Meanwhile, IVF increased p-ERK1/2 at 6 hpf (p < 0.05); however, its kinase activity decreased at 6 hpf (p < 0.05). p-JNK in ANY, CHX and IVF oocytes decreased at 4 hpa (p < 0.05). p-P38 was only observed at 1 hpa, with no differences between treatments. In conclusion, activation of bovine oocytes by ANY, CHX and IVF inactivates MPF by CDK1-dependent specific phosphorylation without cyclin B1 degradation. ANY or CHX promoted this inactivation, which seemed to be more delayed in the physiological activation (IVF). Both inhibitors modulated MPF activity via an ERK1/2-independent-pathway, whereas IVF activated the bovine oocytes via an ERK1/2-dependent pathway. Finally, ANY does not activate the JNK and P38 kinase pathways.
Cecilia Valencia, Felipe Alonso Pérez, Carola Matus, Ricardo Felmer, María Elena Arias

1347 related Products with: Activation of bovine oocytes by protein synthesis inhibitors: New findings on the role of MPF/MAPKs†.

200 1mg20mg1mg1mg50.00 ug100 5 G200 1mg100g100

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#33526654   // To Up

The GRAS-type SCL28 transcription factor controls the mitotic cell cycle and division plane orientation.

Gene expression is reconfigured rapidly during the cell cycle to execute the cellular functions specific to each phase. Studies conducted with synchronized plant cell suspension cultures have identified hundreds of genes with periodic expression patterns across the phases of the cell cycle, but these results may differ from expression occurring in the context of intact organs. Here, we describe the use of fluorescence-activated cell sorting to analyze the gene expression profile of G2/M cells in the growing root. To this end, we isolated cells expressing the early mitosis cell cycle marker from root tips. Transcriptome analysis of these cells allowed identification of hundreds of genes whose expression is reduced or enriched in G2/M cells, including many not previously reported from cell suspension cultures. From this dataset, we identified SCL28, a transcription factor belonging to the GRAS family, whose messenger RNA accumulates to the highest levels in G2/M and is regulated by MYB3R transcription factors. Functional analysis indicates that promotes progression through G2/M and modulates the selection of cell division planes.
Camila Goldy, José-Antonio Pedroza-Garcia, Natalie Breakfield, Toon Cools, Rodrigo Vena, Philip N Benfey, Lieven De Veylder, Javier Palatnik, Ramiro E Rodriguez

2315 related Products with: The GRAS-type SCL28 transcription factor controls the mitotic cell cycle and division plane orientation.

1111200ug1961 ml

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#33485844   2021/01/21 To Up

PCGF3 promotes the proliferation and migration of non-small cell lung cancer cells via the PI3K/AKT signaling pathway.

The Polycomb Group Ring Finger 3 (PCGF3) protein has been reported to be significantly upregulated in pancreatic islet tumors and related to signal transduction; however, its detailed mechanisms and biological roles in other tumors, including non-small cell lung cancer (NSCLC), remain unclear. This study investigated the function of PCGF3 in NSCLC and further elucidated its mechanism of action. The immunohistochemical analysis of 86 selected lung cancer tissues revealed that PCGF3 was highly expressed in NSCLC tissues and positively correlated with lymph node metastasis and p-TNM staging. Additionally, PCGF3 promoted cell proliferation in lung cancer by regulating CyclinB1, CyclinD1, and CDK4 expression, and also promoting their migration by regulating RhoA, RhoC, and CDC42. Furthermore, PCGF3 affected both the proliferation and migration of lung cancer cells by regulating the PI3K/AKT pathway, as verified by inhibiting this pathway using LY294002. The findings of this study suggested that PCGF3 is associated with poor prognosis in patients with NSCLC and could therefore be an important biomarker for treating and preventing NSCLC.
Yujiao Hu, Yu Cheng, Xizi Jiang, Yao Zhang, Huanxi Wang, Hongjiu Ren, Yitong Xu, Jun Jiang, Qiongzi Wang, Hongbo Su, Bo Zhang, Xueshan Qiu

2177 related Products with: PCGF3 promotes the proliferation and migration of non-small cell lung cancer cells via the PI3K/AKT signaling pathway.

1.5x10(6) cells1.5 x 10^6 cells2 Pieces/Box100 ug/vial

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#33364832   2020/12/14 To Up

LCN2 Mediated by IL-17 Affects the Proliferation, Migration, Invasion and Cell Cycle of Gastric Cancer Cells by Targeting SLPI.

Gastric cancer occurred in China and even the whole East Asia with high incidence. The objective of this study was to investigate the role of in gastric cancer cells mediated by binding to .
Jing Xu, ShengXiang Lv, Wei Meng, Fang Zuo

2458 related Products with: LCN2 Mediated by IL-17 Affects the Proliferation, Migration, Invasion and Cell Cycle of Gastric Cancer Cells by Targeting SLPI.

5 x 50 ug50 ug96T0.5 mg96 tests1.00 flask10ml0.5 mg

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#33303057   // To Up

Chaetoglobosin G inhibits proliferation, autophagy and cell cycle of lung cancer cells through EGFR/MEK/ERK signaling pathway.

Chaetoglobosin G (CG) is a fungal secondary metabolite and shows anti-tumor effects. However, the mechanisms behind the anti-tumor effect is still unclear. In this study, we evaluated the anti-proliferation effect of CG on human NSCLC A549 cells and explored the underlying mechanisms. The anti-proliferation effect of CG on A549 cells was evaluated by MTT. The targets of CG were screened through transcriptome sequencing. A flow cytometer was used to detect cell cycle and apoptosis. Western blotting was used to analyze apoptosis, cell cycle and autophagy related protein expression. Our results showed that CG had a dose-dependent inhibitory effect on proliferation of A549 cells. Transcriptome sequencing analysis found that CG obviously induced cell cycle arrest. Flow cytometry analysis and western blot showed that CG induced G2/M arrest with p21 protein upregulation and cyclinB1 protein downregulation. Western blot analysis also indicated that p-EGFR, EGFR, p-MEk and p-ERK protein expressions decreased and autophagy protein LC3II expression increased, indicating that CG can promote autophagy through EGFR/MEK/ERK/LC3 pathway. Moreover, CG can induce apoptosis with bcl-2 protein decrease. In conclusion, this study indicated that CG obviously inhibited A549 cell proliferation, and its mechanism may induce autophagy of A549 cells through EGFR/MEK/ERK/LC3 pathway to upregulate the expression of P21, thus lead to G2/M phase arrest to exert an anti-tumor role.
Jinhua Chen, Qingfeng Guo, Jinxiang Zhang, Zhanhua Yin, Wenping Song, Baoxia He, Yongna Zhang, Wenzhou Zhang, Lin Chen

1490 related Products with: Chaetoglobosin G inhibits proliferation, autophagy and cell cycle of lung cancer cells through EGFR/MEK/ERK signaling pathway.

50 ug1.5x10(6) cells1.5 x 10^6 cells5 x 50 ug0.5 mg

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#33230792   2020/11/23 To Up

Nickel carcinogenesis mechanism: cell cycle dysregulation.

Nickel (Ni) is a widely distributed metal in the environment and an important pollutant due to its widespread industrial applications. Ni has various toxicity in humans and experimental animals, including carcinogenicity. However, the carcinogenic effects of Ni remain troublesome. Cell cycle dysregulation may be an important carcinogenic mechanism and is also a potential molecular mechanism for Ni complexes anti-cancerous effects. Therefore, we conducted a literature review to summarize the effects of Ni on cell cycle. Up to now, there were three different reports on Ni-induced cell cycle arrest: (i) Ni can induce cell cycle arrest in G0/G1 phase, phosphorylation and degradation of IkappaB kinase-alpha (IKKα)-dependent cyclin D1 and phosphoinositide-3-kinase (PI3K)/serine-threonine kinase (Akt) pathway-mediated down-regulation of expressions of cyclin-dependent kinases 4 (CDK4) play important role in it; (ii) Ni can induce cell cycle arrest in S phase, but the molecular mechanism is not known; (iii) G2/M phase is the target of Ni toxicity, and Ni compounds cause G2/M cell cycle phase arrest by reducing cyclinB1/Cdc2 interaction through the activation of the ataxia telangiectasia mutated (ATM)-p53-p21 and ATM-checkpoint kinase inhibitor 1 (Chk1)/Chk2-cell division cycle 25 (Cdc25) pathways. Revealing the mechanisms of cell cycle dysregulation associated with Ni exposure may help in the prevention and treatment of Ni-related carcinogenicity and toxicology.
Hongrui Guo, Huidan Deng, Huan Liu, Zhijie Jian, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li, Xun Wang, Ling Zhao

1421 related Products with: Nickel carcinogenesis mechanism: cell cycle dysregulation.

1 kit2 Pieces/Box 100ul1 kit2 Pieces/Box2 Pieces/Box1 kit250 ml.1mg100 extractions5x5 ml

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#33196942   2020/11/16 To Up

Knockdown of TRAP1 promotes cisplatin-induced apoptosis by promoting the ROS-dependent mitochondrial dysfunction in lung cancer cells.

The tumor necrosis factor receptor-associated protein 1 (TRAP1) is associated with the occurrence and development of various diseases, including inflammation and cancer. However, the role and mechanism of TRAP1 in the development of lung cancer need to be further explored. Therefore, the purpose of this study is to investigate the role of TRAP1 in the regulation of apoptosis by cisplatin and its special mechanism. The RT-qPCR and Western blot were used to detect the mRNA and protein expression of ANGPTL4 in A549 and H1299 cells, respectively. And the cell apoptosis and cell cycle were measured by flow cytometry (FCM). The expression of genes related to apoptosis and drug resistance as well as the cell cycle regulators, including MDM2, CyclinB1, and CDK1, were detected by Western blot. Finally, the reactive oxygen species (ROS) indicator DCFH-DA was performed to detect the generation of ROS, and the mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. The results showed that the expression of TRAP1 was significantly increased in A549/DDP and H1299/DDP than A549 and H1299 cells. Further research found that knockdown of TRAP1 induced apoptosis and caused G2/M cell cycle arrest in A549/DDP and H1299/DDP cells. What is more, siTRAP1 reduced the relative JC-1 polymer monomer fluorescence ratio and decreased the ΔΨm, up-regulated the expression of Cytochrome C. Importantly, siTRAP1 induces ROS-dependent mitochondrial dysfunction. It is suggested that that TRAP1 suppresses cisplatin-induced apoptosis by promoting ROS-dependent mitochondrial dysfunction.
Xiaowei Zhang, Yu Dong, Miao Gao, Minfeng Hao, Hui Ren, Ling Guo, Hua Guo

1943 related Products with: Knockdown of TRAP1 promotes cisplatin-induced apoptosis by promoting the ROS-dependent mitochondrial dysfunction in lung cancer cells.

2 Pieces/Box

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