搜索结果: 'gmp t cell activator'

抗人CD4，clone RPA-T4 抗人、黑猩猩CD4的小鼠Monoclonal IgG1抗体
CMV （pp65）肽库 用于免疫细胞激活的巨细胞病毒（pp65）肽库
EasySep™人CD3正选试剂盒II 人CD3+细胞的免疫磁珠正选试剂盒
EasySep™小鼠CD90.1正选试剂盒
对来源于小鼠脾细胞、淋巴结或外周血的 CD90.1⁺（Thy1.1⁺）细胞进行免疫磁珠正选分离
新品
人IgG ELISpot抗体配对试剂盒 用于检测和计数分泌人免疫球蛋白G的细胞
新品
人TNF-α ELISpot试剂盒 用于检测和计数分泌人肿瘤坏死因子-α的细胞
新品
人IL-4 ELISpot试剂盒 用于检测和计数分泌人白介素-4的细胞
新品
人颗粒酶B ELISpot试剂盒 用于检测和计数分泌人颗粒酶B的细胞
Cool B et al. ( 2006) Cell metabolism 3 6 403--416

Identification and characterization of a small molecule AMPK activator that treats key components of type 2 diabetes and the metabolic syndrome.

AMP-activated protein kinase (AMPK) is a key sensor and regulator of intracellular and whole-body energy metabolism. We have identified a thienopyridone family of AMPK activators. A-769662 directly stimulated partially purified rat liver AMPK (EC50 = 0.8 microM) and inhibited fatty acid synthesis in primary rat hepatocytes (IC50 = 3.2 microM). Short-term treatment of normal Sprague Dawley rats with A-769662 decreased liver malonyl CoA levels and the respiratory exchange ratio,VCO2/VO2,indicating an increased rate of whole-body fatty acid oxidation. Treatment of ob/ob mice with 30 mg/kg b.i.d. A-769662 decreased hepatic expression of PEPCK,G6Pase,and FAS,lowered plasma glucose by 40%,reduced body weight gain and significantly decreased both plasma and liver triglyceride levels. These results demonstrate that small molecule-mediated activation of AMPK in vivo is feasible and represents a promising approach for the treatment of type 2 diabetes and the metabolic syndrome. View Publication

产品类型：

产品号#：

72922

72924

73252

73254

产品名：

A769662

A769662, 50 mg

二甲双胍 (Hydrochloride)

二甲双胍 (Hydrochloride)
Zhou Y et al. (MAR 2014) Cell death and differentiation 21 3 462--474

The miR-106b˜25 cluster promotes bypass of doxorubicin-induced senescence and increase in motility and invasion by targeting the E-cadherin transcriptional activator EP300.

Resistance to chemotherapeutic treatment,which is indirectly responsible for many cancer deaths,is normally associated with an aggressive phenotype including increased cell motility and acquisition of invasive properties. Here we describe how breast cancer cells overcome doxorubicin-induced senescence and become drug resistant by overexpression of the microRNA (miR)-106b˜25 cluster. Although all three miRs in the cluster contribute to the generation of doxorubicin resistance,miR-25 is the major contributor to this phenotype. All three miRs in this cluster target EP300,a transcriptional activator of E-cadherin,resulting in cells acquiring a phenotype characteristic of cells undergoing epithelial-to-mesenchymal transition (EMT),including an increase in both cell motility and invasion,as well as the ability to proliferate after treatment with doxorubicin. These findings provide a novel drug resistance/EMT regulatory pathway controlled by the miR-106b˜25 cluster by targeting a transcriptional activator of E-cadherin. View Publication

产品类型：

产品号#：

01700

01705

01702

产品名：

ALDEFLUOR™ 试剂盒

ALDEFLUOR™ DEAB试剂, 1.5 mM, 1 mL

ALDEFLUOR™检测缓冲液
RosetteSep™人CD3去除抗体混合物 免疫密度去除试剂混合物
SpinSep™密度梯度离心液
密度梯度离心液