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RNA干扰(RNAi)研究之相关工具
℡ 4000-520-616
℡ 4000-520-616
SBI/PureFection™ Transfection Reagent/5 mL/LV750A-5-5 mL
产品编号:LV750A-5-5mL
市  场 价:¥24700.00
场      地:美国(厂家直采)
产品分类: 分子类>基因编辑>RNA干扰>
联系QQ:1570468124
电话号码:4000-520-616
邮      箱: info@ebiomall.com
美  元  价:$1235.00
品      牌: SBI
公      司:System Biosciences(SBI)
公司分类:
SBI/PureFection™ Transfection Reagent/5 mL/LV750A-5-5 mL
商品介绍

Overview

Increase your transfection efficiencies

With SBI’s PureFection™ Transfection Reagent, you can deliver more nucleic acid—plasmids, siRNAs, etc.—than the leading lipid-based transfection reagent for effective, efficient, and reproducible transfections.

The easy-to-use protocol consists of a rapid, one-step, 15-minute incubation with the plasmid, small RNA, or other nucleic acid you’d like to transfect. Once the incubation is done, simply add directly to target cells—no media changes are required as PureFection works in the presence of antibiotics and serum.

The fast PureFection protocol makes it well-suited for high-throughput transfection projects.

  • Highly effective transfection technology—works with most cell types
  • Cost-effective alternative to lipid-based products
  • Nanoparticle-based gene delivery with low toxicity
  • Rapid 15-minute protocol makes PureFection ideal for high-throughput transfections
  • Works with both Plasmid DNA and siRNAs

How It Works

A fast and effective method for increasing transfection efficiencies

Supporting Data

PureFection delivers higher transfection efficiencies than the leading lipid-based reagent

Resources

Protocol: PureFection Transfection Reagent
Product Sheet: PureFection Lentivirus Transfection Reagent
Brochure: Gene Delivery and Expression Products and Services

Citations

  • Quan, K, et al. (2017) Icariside II induces cell cycle arrest and apoptosis in human glioblastoma cells through suppressing Akt activation and potentiating FOXO3a activity. Am J Transl Res.2017 May 31; 9(5):2508-2519. PM ID:28560001
  • Huang, CY, et al. (2017) HSF1 phosphorylation by ERK/GSK3 suppresses RNF126 to sustain IGF-IIR expression for hypertension-induced cardiomyocyte hypertrophy. J. Cell. Physiol..2017 Apr 6;. PM ID:28383811
  • Liao, PH, et al. (2017) Phosphorylation of cofilin-1 by ERK confers HDAC inhibitor resistance in hepatocellular carcinoma cells via decreased ROS-mediated mitochondria injury. Oncogene.2017 Apr 6; 36(14):1978-1990. PM ID:27748761
  • Chen, YP, et al. (2017) Short-term Hypoxia Reverses Ox-LDL-induced CD36 and GLUT4 Switching Metabolic Pathways in H9c2 Cardiomyoblast Cells. J. Cell. Biochem..2017 Apr 4;. PM ID:28374891
  • Cheng, SY, et al. (2017) Lactate dehydrogenase downregulation mediates the inhibitory effect of diallyl trisulfide on proliferation, metastasis, and invasion in triple-negative breast cancer. Environ. Toxicol..2017 Apr 1; 32(4):1390-1398. PM ID:27566995
  • Chang, YM, et al. (2017) Alpinia oxyphylla Miq. fruit extract activates IGFR-PI3K/Akt signaling to induce Schwann cell proliferation and sciatic nerve regeneration. BMC Complement Altern Med.2017 Mar 31; 17(1):184. PM ID:28359314
  • Huang, CY, et al. (2017) Mitochondrial ROS-induced ERK1/2 activation and HSF2-mediated AT1 R upregulation are required for doxorubicin-induced cardiotoxicity.. J. Cell. Physiol..2017 Mar 14;. PM ID:28295305
  • Chen, Q, et al. (2016) FGF-2 Transcriptionally Down-Regulates the Expression of BNIP3L via PI3K/Akt/FoxO3a Signaling and Inhibits Necrosis and Mitochondrial Dysfunction Induced by High Concentrations of Hydrogen Peroxide in H9c2 Cells. Cell. Physiol. Biochem..2016 Dec 22; 40(6):1678-1691. PM ID:28006775
  • Wu, H, et al. (2016) MiR-155 is Involved in Renal Ischemia-Reperfusion Injury via Direct Targeting of FoxO3a and Regulating Renal Tubular Cell Pyroptosis. Cell. Physiol. Biochem..2016 Dec 22; 40(6):1692-1705. PM ID:28006785
  • Chang, WT, Cheng, JT & Chen, ZC. (2016) Telmisartan improves cardiac fibrosis in diabetes through peroxisome proliferator activated receptor δ (PPARδ): from bedside to bench.. Cardiovasc Diabetol.2016 Dec 1; 15(1):113. PM ID:27519769
  • Fu, CY, et al. (2016) ZAKβ antagonizes and ameliorates the cardiac hypertrophic and apoptotic effects induced by ZAKα. Cell Biochem. Funct..2016 Dec 1; 34(8):606-612. PM ID:27859413
  • Hsu, HH, et al. (2016) Taiwanin E inhibits cell migration in human LoVo colon cancer cells by suppressing MMP-2/9 expression via p38 MAPK pathway. Environ. Toxicol..2016 Nov 3;. PM ID:27807932
  • Huang, CY, et al. (2016) Doxorubicin attenuates CHIP-guarded HSF1 nuclear translocation and protein stability to trigger IGF-IIR-dependent cardiomyocyte death. Cell Death Dis.2016 Nov 3; 7(11):e2455. PM ID:27809308
  • Dotimas, JR, et al. (2016) Diabetes regulates fructose absorption through thioredoxin-interacting protein. Elife.2016 Oct 11; 5. PM ID:27725089
  • Chatterjee, B, et al. (2016) p38α MAPK disables KMT1A-mediated repression of myogenic differentiation program. Skelet Muscle.2016 Aug 23; 6:28. PM ID:27551368
  • Feng, CC, et al. (2016) Hypoxia suppresses myocardial survival pathway through HIF-1α-IGFBP-3-dependent signaling and enhances cardiomyocyte autophagic and apoptotic effects mainly via FoxO3a-induced BNIP3 expression. Growth Factors.2016 Aug 1; 34(3-4):73-86. PM ID:27366871
  • Yeh, Y, et al. (2016) Hypoxia Augments Increased HIF-1 [alpha] and Reduced Survival Protein p-Akt in Gelsolin (GSN)-Dependent Cardiomyoblast Cell Apoptosis. Cell Biochem Biophys.2016 May 18; 74:221–228. Link:Cell Biochem Biophys
  • Chen, YP, et al. (2016) Palmitic acid interferes with energy metabolism balance by adversely switching the SIRT1-CD36-fatty acid pathway to the PKC zeta-GLUT4-glucose pathway in cardiomyoblasts. J. Nutr. Biochem..2016 May 1; 31:137-49. PM ID:27133433
  • Gjymishka, A, et al. (2016) miR-133b Regulation of Connective Tissue Growth Factor: A Novel Mechanism in Liver Pathology. Am. J. Pathol..2016 May 1; 186(5):1092-102. PM ID:26945106
  • Elias, A, et al. (2016) Cancer-specific binary expression system activated in mice by bacteriophage HK022 Integrase. Sci Rep.2016 Apr 27; 6:24971. PM ID:27117628
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品牌介绍

System Biosciences,简称SBI,美国加州湾区新成立的生技公司,致力于独特、创新生物技术之开发,以研发利于基因及蛋白质功能鉴定、研究之崭新方法和工具为宗旨。 现阶段研发重心为RNA干扰(RNAi)研究之相关工具。 System Biosciences (SBI) 致力于开发独特、革新的技术,为客户研究蛋白组学和基因组学功能提供研究工具。SBI 是专业的慢病毒产品公司,提供基于慢病毒的所有相关产品、质粒、试剂盒及相关配套试剂和慢病毒延伸产品如IPS细胞多功能性诱导试剂盒和RNAi筛选文库。

SBI focuses on developing unique, innovative technologies that provide researchers with the tools to investigate and understand genomic and proteomic function. Our mission is to provide tools for the genome-wide analysis of the mechanisms that regulate cellular processes and biological responses.

Headquartered in Palo Alto about 30 miles south of San Francisco, SBI is geographically surrounded by highly successful research biotech companies (e.g., Affymetrix, Life Technologies, and Genentech) and some of the premier life science institutes in the world, including Stanford and the University of California, San Francisco.

As a small private biotechnology company, SBI capitalizes on a rich network of consultants and colleagues and continually collaborates to accelerate its development of innovative and novel applications. Currently, SBI has partnerships with over thirty scientists from several institutes.System Biosciences (SBI) consists of a highly motivated team committed to realizing the potential of its mission to develop and bring to market unique and innovative technology to investigate and understand genomic and proteomic function.

Possessing a diverse range of experience and knowledge, SBI's management and staff bring the skills, talent, and interest needed to support the company's continuing rapid growth.

A strong and proven background in creative research and product development with proficiency in genetic analysis, microarray technology, and cell biology

Extensive business development and management experience

A keen understanding of the needs of life scientists

Expertise in developing, marketing, and supporting consistent, high-quality research products

A clear focus on the need to build and maintain lasting customer relationships through support, service, and close customer interaction

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