MOUSE ANTI RAT CD4 (DOMAIN 1) Biotin

Price:
416 EUR
499 USD
345 GBP
known as: MOUSE ANTI RAT CD4 (DOMAIN 1) Biotin
Catalog number: genta-ABS0618
Product Quantity: 0.1 mg
Category:
Supplier: AbD

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Gene target: cd4 domain 1

Related genes to: MOUSE ANTI RAT CD4 (DOMAIN 1) Biotin

Symbol : biotin NIH gene
LocusTag : Bathy11g00270
chromosome : 11
description : biotin synthase
type of gene : protein-coding
Modification date : 2015-06-26
Symbol : cd4 NIH gene
description : T-cell surface glycoprotein CD4
type of gene : protein-coding
Modification date : 2015-09-26

Related Pathways to: MOUSE ANTI RAT CD4 (DOMAIN 1) Biotin

Gene about :domain
Pathway :Dm Notch Signaling Pathway
domain
Gene about :Cd4
Pathway :Rn Cytokines and Inflammatory Response (BioCarta)
Cd4
Gene about :biotin
Pathway :Sc Protein Modifications
biotin

Related product to: MOUSE ANTI RAT CD4 (DOMAIN 1) Biotin

Related Articles about: MOUSE ANTI RAT CD4 (DOMAIN 1) Biotin

Radiology Case of the Month: Idiopathic CD4 Lymphocytopenia.

A 39 year-old male with a history of diabetes, retinitis pigmentosa, and genital warts presented with intractable occipital headaches accompanied with nausea and vomiting. The patient had markedly depressed CD4 counts. Furthermore the patient tested negative for HIV and HTLV 1/2 and had normal immunoglobulin levels. During hospital course the patient underwent a lumbar puncture and multiple imaging exams, including both CT and MR. Except for occasional nausea and vomiting controlled by therapeutic lumbar punctures, phenergan, and dilaudid the patient's hospital course was uncomplicated. - Source :PubMed

Transcriptomic profiles of aging in naïve and memory CD4(+) cells from mice.

CD4+ T cells can be broadly divided into naïve and memory subsets, each of which are differentially impaired by the aging process. It is unclear if and how these differences are reflected at the transcriptomic level. We performed microarray profiling on RNA derived from naïve (CD44(low)) and memory (CD44(high)) CD4+ T cells derived from young (2-3 month) and old (28 month) mice, in order to better understand the mechanisms of age-related functional alterations in both subsets. We also performed follow-up bioinformatic analyses in order to determine the functional consequences of gene expression changes in both of these subsets, and identify regulatory factors potentially responsible for these changes. - Source :PubMed

pERK-dependent defective TCR-mediated activation of CD4(+) T cells in end-stage renal disease patients.

Patients with end-stage renal disease (ESRD) have an impaired immune response with a prematurely aged T-cell system. Mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase (ERK) and p38, regulate diverse cellular programs by transferring extracellular signals into an intracellular response. T cell receptor (TCR)-induced phosphorylation of ERK (pERK) may show an age-associated decline, which can be reversed by inhibiting dual specific phosphatase (DUSP) 6, a cytoplasmic phosphatase with substrate specificity to dephosphorylate pERK. The aim of this study was to assess whether ESRD affects TCR-mediated signaling and explore possibilities for intervening in ESRD-associated defective T-cell mediated immunity. - Source :PubMed

Modulation of Endoplasmic Reticulum Stress Controls CD4(+) T Cell Activation and Anti-tumor Function.

The endoplasmic reticulum (ER) is an energy-sensing organelle with intimate ties to programming cell activation and metabolic fate. T-cell receptor (TCR) activation represents a form of acute cell stress and induces mobilization of ER Ca(2+) stores. The role of the ER in programming T-cell activation and metabolic fate remains largely undefined. Gp96 is an ER protein with functions as a molecular chaperone and Ca(2+) buffering protein. We hypothesized that the ER stress response may be important for CD4(+) T-cell activation and that gp96 may be integral to this process. To test our hypothesis we utilized genetic deletion of gp96 gene Hsp90b1 in a CD4(+) T cell-specific manner. We show that gp96-deficient CD4(+) T cells cannot undergo activation-induced glycolysis due to defective Ca(2+) mobilization upon TCR engagement. We found that activating naive CD4(+) T cells while inhibiting ER Ca(2+) exchange, through pharmacological blockade of the ER Ca(2+) channel inositol trisphosphate receptor (IP3R), led to a reduction in cytosolic Ca(2+) content and generated a pool of CD62L(high)/CD44(low) CD4(+) T cells compared to wild-type (WT) matched controls. In vivo IP3R-inhibited CD4(+) T cells exhibited elevated tumor control above WT T cells. Together these data show that ER-modulated cytosolic Ca(2+) plays a role in defining CD4(+) T-cell phenotype and function. Factors associated with the ER stress response are suitable targets for T-cell based immunotherapies. - Source :PubMed

Polyfunctional response by ImmTAC (IMCgp100) redirected CD8(+) and CD4(+) T cells.

The success of immune system based cancer therapies depends on a broad immune response engaging a range of effector cells and mechanisms. Immune mobilising monoclonal TCRs against cancer (ImmTAC(™) molecules, fusion proteins consisting of a soluble, affinity enhanced TCR and an anti-CD3 scFv Ab) were previously shown to redirect CD8(+) and CD4(+) T cells against tumours. Here we present evidence that IMCgp100 (ImmTAC recognising a peptide derived from the melanoma-specific protein, gp100, presented by HLA-A*0201) efficiently redirects and activates effector and memory cells from both CD8(+) and CD4(+) repertoires. Using isolated subpopulations of T cells, we find that both terminally differentiated and effector memory CD8(+) T cells redirected by IMCgp100 are potent killers of melanoma cells. Furthermore, CD4(+) effector memory T cells elicit potent cytotoxic activity leading to melanoma cell killing upon redirection by IMCgp100. The majority of T cell subsets belonging to both the CD8(+) and CD4(+) repertoires secrete key proinflammatory cytokines (TNFα, IFNγ, IL-6) and chemokines (MIP1α-β, IP-10, MCP1). At an individual cell level, IMCgp100 redirected T cells display a polyfunctional phenotype, which is a hallmark of a potent anti-cancer response. This study demonstrates that IMCgp100 induces broad immune responses, which extend beyond the induction of CD8(+) T cell mediated cytotoxicity. These findings are of particular importance as IMCgp100 is currently undergoing clinical trials as a single agent or in combination with checkpoint inhibitors for patients with malignant melanoma. This article is protected by copyright. All rights reserved. - Source :PubMed

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