HAMSTER ANTI MOUSE TCR ALPHA_BETA BETA CHAIN Azide Free

Price:
889 EUR
1066 USD
737 GBP
known as: HAMSTER ANTI MOUSE TCR ALPHA_BETA BETA CHAIN Azide Free
Catalog number: genta-ABS0366
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: tcr alpha beta chain

Related genes to: HAMSTER ANTI MOUSE TCR ALPHA_BETA BETA CHAIN Azide Free

Symbol : betA NIH gene
LocusTag : NGR_c06990
description : choline dehydrogenase
type of gene : protein-coding
Modification date : 2016-04-19
Symbol : Tcr NIH gene
dbXrefs : FLYBASE:FBgn0003677
chromosome : 3
map location : 3-39.6 cM
description : Third chromosome alpha methyl dopa-resistant
type of gene : unknown
Modification date : 2016-05-09

Related Pathways to: HAMSTER ANTI MOUSE TCR ALPHA_BETA BETA CHAIN Azide Free

Gene about :TCR
Pathway :Rn Id Signaling Pathway
TCR

Related product to: HAMSTER ANTI MOUSE TCR ALPHA_BETA BETA CHAIN Azide Free

Related Articles about: HAMSTER ANTI MOUSE TCR ALPHA_BETA BETA CHAIN Azide Free

EGCG inhibits the oligomerization of amyloid beta (16-22) hexamer: Theoretical studies.

An extensive replica exchange molecular dynamics (REMD) simulation was performed to investigate the progress patterns of the inhibition of (-)-epigallocatechin-3-gallate (EGCG) on the Aβ16-22 hexamer. Structural variations of the oligomers without and with EGCG were monitored and analyzed in detail. It has been found that EGCG prevents the formation of Aβ oligomer through two different ways by either accelerating the Aβ oligomerization or reducing the β-content of the hexamer. It also decreases the potential "highly toxic" conformations of Aβ oligomer, which is related to the conformations having high order β-sheet sizes. Both electrostatic and van der Waals interaction energies are found to be involved to the binding process. Computed results using quantum chemical methods show that the π-π stacking is a critical factor of the interaction between EGCG and the peptides. As a result, the binding free energy of the EGCG to the Aβ peptides is slightly larger than that of the curcumin. - Source :PubMed

Transplant-Specific Quality Improvement Program Enters Beta Phase.

- Source :PubMed

FTY720 ameliorates renal fibrosis by simultaneously affecting leukocyte recruitment and TGF-β signaling in fibroblasts.

Renal fibrosis is the common final manifestation of chronic kidney diseases and usually results in end-stage renal failure. In this study, we evaluated the effect of FTY720, an analog of sphingosine 1-phosphate (S1P), as a treatment for the unilateral ureteral obstruction (UUO)-induced renal fibrosis animal model. We treated mice with FTY720 at a dosage of 1 mg/kg/day by intragastric administration from day 1 until day 7. The control group received the same amount of saline. FTY720 significantly reduced the urine albumin/creatinine ratio (UACR) in treated UUO mice. FTY720 treatment also caused a significant decrease in interstitial expansion and collagen deposition in the kidney, accompanied by reduced mononuclear cell recruitment and inflammatory cytokine expression. In addition, the expression levels of the endothelial cell adhesion molecules P-selectin and VCAM-1 were suppressed in the ligated kidney by FTY720 administration, suggesting reduced renal endothelial cell activation. Furthermore, in renal interstitial fibroblast NRK-49F cells, FTY720 significantly affected TGF-β-induced α-SMA expression and collagen synthesis by inhibiting both the Smad2/3 and PI3K/AKT/GSK3β signaling pathways. S1P1 knockdown by siRNA significantly reversed this effect in our fibroblast cell culture model. Therefore, FTY720 attenuates renal fibrosis via two different mechanisms. First, FTY720 suppresses the synthesis of extracellular matrix in interstitial fibroblasts by interfering with TGF-β signaling. Second, FTY720 affects endothelial cell activation and chemokine expression, thereby reducing immune cell recruitment into the kidney. This article is protected by copyright. All rights reserved. - Source :PubMed

Red rot resistant transgenic sugarcane developed through expression of β-1,3-glucanase gene.

Sugarcane (Saccharum spp.) is a commercially important crop, vulnerable to fungal disease red rot caused by Colletotrichum falcatum Went. The pathogen attacks sucrose accumulating parenchyma cells of cane stalk leading to severe losses in cane yield and sugar recovery. We report development of red rot resistant transgenic sugarcane through expression of β-1,3-glucanase gene from Trichoderma spp. The transgene integration and its expression were confirmed by quantitative reverse transcription-PCR in first clonal generation raised from T0 plants revealing up to 4.4-fold higher expression, in comparison to non-transgenic sugarcane. Bioassay of transgenic plants with two virulent C. falcatum pathotypes, Cf 08 and Cf 09 causing red rot disease demonstrated that some plants were resistant to Cf 08 and moderately resistant to Cf 09. The electron micrographs of sucrose storing stalk parenchyma cells from these plants displayed characteristic sucrose-filled cells inhibiting Cf 08 hyphae and lysis of Cf 09 hyphae; in contrast, the cells of susceptible plants were sucrose depleted and prone to both the pathotypes. The transgene expression was up-regulated (up to 2.0-fold in leaves and 5.0-fold in roots) after infection, as compared to before infection in resistant plants. The transgene was successfully transmitted to second clonal generation raised from resistant transgenic plants. β-1,3-glucanase protein structural model revealed that active sites Glutamate 628 and Aspartate 569 of the catalytic domain acted as proton donor and nucleophile having role in cleaving β-1,3-glycosidic bonds and pathogen hyphal lysis. - Source :PubMed

Conditional abrogation of Transforming Growth Factor Beta Receptor 1 in PTEN-inactivated endometrium promotes endometrial cancer progression in mice.

Although a putative role for TGF beta (TGFB) signaling in the pathogenesis of human endometrial cancer has long been proposed, the precise function of TGFB signaling in the development and progression of endometrial cancer remains elusive. Depletion of PTEN in the mouse uterus causes endometrial cancer. To identify the potential role of TGFB signaling in endometrial cancer, we simultaneously deleted TGFB receptor 1 (Tgfbr1) and Pten in the mouse uterus using Cre-recombinase driven by the progesterone receptor (termed Pten(d/d) ; Tgfbr1(d/d) ). We found that Pten(d/d) ; Tgfbr1(d/d) mice developed severe endometrial lesions that progressed more rapidly compared with those resulting from conditional deletion of Pten alone, suggesting that TGFB signaling synergizes with PTEN to suppress endometrial cancer progression. Remarkably, the Pten(d/d) ; Tgfbr1(d/d) mice developed distant pulmonary metastases, leading to significantly reduced life span. The development of metastasis and accelerated tumor progression in Pten(d/d) ; Tgfbr1(d/d) mice are associated with increased production of pro-inflammatory chemokines, enhanced cancer cell motility evidenced by myometrial invasion and disruption, and altered tumor microenvironment characterized by recruitment of tumor-associated macrophages. Thus, conditional deletion of Tgfbr1 in PTEN-inactivated endometrium leads to a disease that recapitulates invasive and lethal human endometrial cancer. This mouse model may be valuable for preclinical testing of new cancer therapies, particularly those targeting metastasis, one of the hallmarks of cancer and a major cause of death in endometrial cancer patients. - Source :PubMed

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