Mouse IgG2a (1b allotype specific), FITC

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known as: Mouse IgG2a (1b allotype specific), FITC
Catalog number: genta-YNShMIgG2a1bF
Product Quantity: 1 ml.
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Supplier: Accu

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Gene target: igg2a 1b allotype specific

Related genes to: Mouse IgG2a (1b allotype specific), FITC

Symbol : 1b NIH gene
LocusTag : AL352_gp2
description : 1b
type of gene : protein-coding
Modification date : 2016-05-06

Related Pathways to: Mouse IgG2a (1b allotype specific), FITC

Related product to: Mouse IgG2a (1b allotype specific), FITC

Related Articles about: Mouse IgG2a (1b allotype specific), FITC

Asperentin B, a New Inhibitor of the Protein Tyrosine Phosphatase 1B.

In the frame of studies on secondary metabolites produced by fungi from deep-sea environments we have investigated inhibitors of enzymes playing key roles in signaling cascades of biochemical pathways relevant for the treatment of diseases. Here we report on a new inhibitor of the human protein tyrosine phosphatase 1B (PTP1B), a target in the signaling pathway of insulin. A new asperentin analog is produced by an Aspergillussydowii strain isolated from the sediment of the deep Mediterranean Sea. Asperentin B (1) contains an additional phenolic hydroxy function at C-6 and exhibits an IC50 value against PTP1B of 2 μM in vitro, which is six times stronger than the positive control, suramin. Interestingly, asperentin (2) did not show any inhibition of this enzymatic activity. Asperentin B (1) is discussed as possible therapeutic agents for type 2 diabetes and sleeping sickness. - Source :PubMed

Effects of Src Kinase Inhibition on Expression of Protein Tyrosine Phosphatase 1B after Brain Hypoxia in a Piglet Animal Model.

Protein tyrosine phosphatases (PTPs) in conjunction with protein tyrosine kinases (PTKs) regulate cellular processes by posttranslational modifications of signal transduction proteins. PTP nonreceptor type 1B (PTP-1B) is an enzyme of the PTP family. We have previously shown that hypoxia induces an increase in activation of a class of nonreceptor PTK, the Src kinases. In the present study, we investigated the changes that occur in the expression of PTP-1B in the cytosolic component of the brain of newborn piglets acutely after hypoxia as well as long term for up to 2 weeks. - Source :PubMed

Binding of coronin 1B to TβRI negatively regulates the TGFβ1 signaling pathway.

Coronin 1B is an actin-binding protein that regulates several actin-dependent cellular processes including migration and endocytosis. However, the role of coronin 1B in the tumor growth factor (TGF)β signaling pathway is largely unknown. Here, we investigated whether coronin 1B affects the TGFβ signaling cascade and found that coronin 1B negatively regulates the TGFβ signaling pathway. Immunoprecipitation and glutathione-S-transferase-pulldown assays revealed that coronin 1B directly associated with TGFβ receptor I (TβRI). Overexpression of coronin 1B inhibited the TGFβ1-induced interaction between TβRI and Smad2/3 in plasmid-transfected HEK293T cells. Coronin 1B was basally bound to TβRI in vascular smooth muscle cells (VSMCs), but TGFβ1 stimulation did not affect their association, suggesting constitutive binding between coronin 1B and TβRI. Overexpression of coronin 1B suppressed TGFβ1-induced activation of a Smad-binding element-luciferase reporter construct and a plasminogen activator inhibitor (PAI)-1 promoter-luciferase reporter construct in HEK293T cells. By contrast, depletion of coronin 1B by siRNA transfection increased TGFβ1-induced Smad2/3 phosphorylation and PAI-1 expression in VSMCs. These results suggest that coronin 1B regulates the TGFβ1 signaling cascade by constitutively interacting with TβRI and inhibiting the binding of Smad2/3 to TβRI in response to TGFβ1 stimulation. - Source :PubMed

Hepatocyte nuclear factor 1b is a novel negative regulator of white adipocyte differentiation.

Hepatocyte nuclear factor 1b (HNF1b) is a transcription factor belonging to the HNF family. We aimed to investigate the role of HNF1b in white adipocyte differentiation. The expression of HNF1b was reduced in white adipose tissue (WAT) of both diet-induced and genetic obese mice and decreased during the process of 3T3-L1 adipocyte differentiation. Downregulation of HNF1b enhanced 3T3-L1 adipocyte differentiation and upregulation of HNF1b inhibited this process. Upregulation of HNF1b inhibited peroxisome proliferator-activated receptor γ (PPARγ) and its target gene expression, while downregulation of HNF1b increased those genes expression. Overexpression of PPARγ suppressed HNF1b upregulation-induced inhibition of adipocyte differentiation. HNF1b can directly bind with the promoter of PPARγ in 3T3-L1 cells, which was decreased after adipogenic differentiation. HNF1b promoted apoptotic and autophagic cell death in early differentiated adipocytes through regulation of cell cycle progress and cell death-related factors, and thus inhibited the process of mitotic clonal expansion (MCE). HNF1b acted as an antioxidant regulator through regulating various antioxidant enzymes via binding with antioxidant response element. Oxidant treatment suppressed HNF1b upregulation-induced inhibition of adipocyte differentiation. Overall, our results suggest that HNF1b is a novel negative regulator of adipocyte differentiation through regulation of PPARγ signaling, MCE and redox state.Cell Death and Differentiation advance online publication, 16 June 2017; doi:10.1038/cdd.2017.85. - Source :PubMed

Origin, prevalence and response to therapy of hepatitis C virus genotype 2k/1b chimeras.

Little is known about the epidemiology and frequency of recombinant HCV genotype 2/1 strains which may represent a challenge for direct antiviral therapy (DAA). - Source :PubMed

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