搜索结果: 'gmp t cell activator'

EasySep™ HLA嵌合全血CD4正选试剂盒

对来源于新鲜全血、白膜层或 LRS 锥样本的人 CD4⁺ 细胞进行免疫磁珠正选分离

EasySep™ HLA嵌合全血CD8正选试剂盒

对来源于新鲜全血、白膜层或 LRS 锥样本的人 CD8⁺ 细胞进行免疫磁珠正选分离

EasySep™小鼠CD4正选试剂盒II 免疫磁珠正选小鼠CD4+细胞的分选试剂盒

RosetteSep™人CD4去除抗体混合物 免疫密度去除试剂混合物

重组小鼠IL-33 白介素33

TWS119 WNT通路激活剂；抑制GSK3β

L. Zhu et al. ( 2018) Scientific reports 8 1 6028

Involvement of AMP-activated Protein Kinase (AMPK) in Regulation of Cell Membrane Potential in a Gastric Cancer Cell Line.

Membrane potential (Vmem) is a key bioelectric property of non-excitable cells that plays important roles in regulating cell proliferation. However,the regulation of Vmem itself remains largely unexplored. We found that,under nutrient starvation,during which cell division is inhibited,MKN45 gastric cancer cells were in a hyperpolarized state associated with a high intracellular chloride concentration. AMP-activated protein kinase (AMPK) activity increased,and expression of cystic fibrosis transmembrane conductance regulator (CFTR) decreased,in nutrient-starved cells. Furthermore,the increase in intracellular chloride concentration level and Vmem hyperpolarization in nutrient-starved cells was suppressed by inhibition of AMPK activity. Intracellular chloride concentrations and hyperpolarization increased after over-activation of AMPK using the specific activator AICAR or suppression of CFTR activity using specific inhibitor GlyH-101. Under these conditions,proliferation of MKN45 cells was inhibited. These results reveal that AMPK controls the dynamic change in Vmem by regulating CFTR and influencing the intracellular chloride concentration,which in turn influences cell-cycle progression. These findings offer new insights into the mechanisms underlying cell-cycle arrest regulated by AMPK and CFTR. View Publication

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100-0530

100-0531

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GlyH-101

科学海报

Cell Isolation of Human Memory B Cells

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Conference：

AAI 2011

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Y. Zhang et al. (aug 2019) Nature communications 10 1 3667

PTPsigma inhibitors promote hematopoietic stem cell regeneration.

Receptor type protein tyrosine phosphatase-sigma (PTPsigma) is primarily expressed by adult neurons and regulates neural regeneration. We recently discovered that PTPsigma is also expressed by hematopoietic stem cells (HSCs). Here,we describe small molecule inhibitors of PTPsigma that promote HSC regeneration in vivo. Systemic administration of the PTPsigma inhibitor,DJ001,or its analog,to irradiated mice promotes HSC regeneration,accelerates hematologic recovery,and improves survival. Similarly,DJ001 administration accelerates hematologic recovery in mice treated with 5-fluorouracil chemotherapy. DJ001 displays high specificity for PTPsigma and antagonizes PTPsigma via unique non-competitive,allosteric binding. Mechanistically,DJ001 suppresses radiation-induced HSC apoptosis via activation of the RhoGTPase,RAC1,and induction of BCL-XL. Furthermore,treatment of irradiated human HSCs with DJ001 promotes the regeneration of human HSCs capable of multilineage in vivo repopulation. These studies demonstrate the therapeutic potential of selective,small-molecule PTPsigma inhibitors for human hematopoietic regeneration. View Publication

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产品号#：

03434

03444

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MethoCult™ GF M3434

挂图

Human Hematopoietic Stem and Progenitor Cell Phenotyping Overview of subset surface markers, frequencies and assays for analysis

Pyle AD et al. (MAR 2006) Nature biotechnology 24 3 344--50

Neurotrophins mediate human embryonic stem cell survival.

Growth of human embryonic stem (hES) cells as a pluripotent population requires a balance between survival,proliferation and self-renewal signals. Here we demonstrate that hES cells express receptors of the tropomyosin-related kinase (TRK) family,which mediate antiapoptotic signals. We show that three TRK ligands,brain-derived neurotrophic factor,neurotrophin 3 and neurotrophin 4,are survival factors for hES cells. Addition of neurotrophins to hES cell cultures effects a 36-fold improvement in their clonal survival. hES cell cultures maintained in medium containing neurotrophins remain diploid and retain full developmental potency. In the presence of neurotrophins,TRK receptors in hES cells are phosphorylated; TRK receptor inhibition leads to hES cell apoptosis. The survival activity of neurotrophins in hES cells is mediated by the phosphatidylinositol-3-kinase pathway but not the mitogen-activated protein kinase pathway. Neurotrophins improve hES cell survival and may facilitate their manipulation and the development of high-throughput screens to identify factors responsible for hES cell differentiation. View Publication

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产品号#：

02508

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