MOUSE ANTI HUMAN CD4 APC

Price:
430 EUR
516 USD
356 GBP
known as: MOUSE ANTI HUMAN CD4 APC
Catalog number: genta-ABS0170
Product Quantity: 100 TESTS
Category:
Supplier: AbD

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Gene target: cd4 apc

Related genes to: MOUSE ANTI HUMAN CD4 APC

Symbol : Apc NIH gene
chromosome : Un
description : adenomatous polyposis coli
type of gene : protein-coding
Other designations : Adenomatous polyposis coli protein
Modification date : 2016-02-20
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 HUMAN CD4 APC

Gene about :Cd4
Pathway :Rn Cytokines and Inflammatory Response (BioCarta)
Cd4
Gene about :APC
Pathway :Sc Cell Cycle and Cell Division
APC

Related product to: MOUSE ANTI HUMAN CD4 APC

Related Articles about: MOUSE ANTI HUMAN CD4 APC

Corrigendum: CD32a is a marker of a CD4 T-cell HIV reservoir harbouring replication-competent proviruses.

This corrects the article DOI: 10.1038/nature21710. - Source :PubMed

Structural echocardiographic abnormalities seen in HIV/AIDS patients are independent of cd4 count.

The human immunodeficiency virus (HIV) infection remains one of the most daunting public health challenges today. Cardiac involvement in HIV/acquired immune deficiency syndrome (AIDS) is frequent and has been recognized on autopsy since the emergence of the pandemic. The objective of the study was to assess the pattern of structural echocardiographic (echo) findings in HIV/AIDS patients and compare this to the echo findings in apparently healthy HIV-negative controls. - Source :PubMed

Differential Requirements for Tcf1 Long Isoforms in CD8(+) and CD4(+) T Cell Responses to Acute Viral Infection.

In response to acute viral infection, activated naive T cells give rise to effector T cells that clear the pathogen and memory T cells that persist long-term and provide heightened protection. T cell factor 1 (Tcf1) is essential for several of these differentiation processes. Tcf1 is expressed in multiple isoforms, with all isoforms sharing the same HDAC and DNA-binding domains and the long isoforms containing a unique N-terminal β-catenin-interacting domain. In this study, we specifically ablated Tcf1 long isoforms in mice, while retaining expression of Tcf1 short isoforms. During CD8(+) T cell responses, Tcf1 long isoforms were dispensable for generating cytotoxic CD8(+) effector T cells and maintaining memory CD8(+) T cell pool size, but they contributed to optimal maturation of central memory CD8(+) T cells and their optimal secondary expansion in a recall response. In contrast, Tcf1 long isoforms were required for differentiation of T follicular helper (TFH) cells, but not TH1 effectors, elicited by viral infection. Although Tcf1 short isoforms adequately supported Bcl6 and ICOS expression in TFH cells, Tcf1 long isoforms remained important for suppressing the expression of Blimp1 and TH1-associated genes and for positively regulating Id3 to restrain germinal center TFH cell differentiation. Furthermore, formation of memory TH1 and memory TFH cells strongly depended on Tcf1 long isoforms. These data reveal that Tcf1 long and short isoforms have distinct, yet complementary, functions and may represent an evolutionarily conserved means to ensure proper programming of CD8(+) and CD4(+) T cell responses to viral infection. - Source :PubMed

Potent inhibition of HIV-1 replication in resting CD4 T cells by resveratrol and pterostilbene.

HIV-1 infection of resting CD4 T cells plays a crucial and numerically dominant role during virus transmission at mucosal sites and during subsequent acute replication and T cell depletion. Resveratrol and pterostilbene are plant stilbenoids associated with several health promoting benefits. Resveratrol has been shown to inhibit replication of several viruses, including herpes simplex 1 and 2, papillomaviruses, SARS virus and influenza virus. Alone, resveratrol does not inhibit HIV-1 infection of activated T cells, but it does synergize with nucleoside reverse transcriptase inhibitors in these cells to inhibit reverse transcription. Here, we demonstrate that resveratrol and pterostilbene completely block HIV-1 infection at low micromolar dose in resting CD4 T cells, primarily at the reverse transcription step. The anti-HIV effect was fully reversed by exogenous deoxynucleosides and Vpx, a simian immunodeficiency virus protein that increases dNTP levels. These findings are consistent with the reported ability of resveratrol to inhibit ribonucleotide reductase and to lower dNTP levels in cells. This study supports the potential use of resveratrol, pterostilbene or related compounds as adjuvants in anti-HIV pre-exposure prophylaxis (PrEP) formulations. - Source :PubMed

Cytokines affecting CD4(+)T regulatory cells in transplant tolerance. III. Interleukin-5 (IL-5) promotes survival of alloantigen-specific CD4(+) T regulatory cells.

CD4(+)T cells mediate antigen-specific allograft tolerance, but die in culture without activated lymphocyte derived cytokines. Supplementation of the media with cytokine rich supernatant, from ConA activated spleen cells, preserves the capacity of tolerant cells to transfer tolerance and suppress rejection. rIL-2 or rIL-4 alone are insufficient to maintain these cells, however. We observed that activation of naïve CD4(+)CD25(+)FOXP3(+)Treg with alloantigen and the Th2 cytokine rIL-4 induces them to express interleukin-5 specific receptor alpha (IL-5Rα) suggesting that IL-5, a Th2 cytokine that is produced later in the immune response may promote tolerance mediating Treg. This study examined if recombinant IL-5(rIL-5) promoted survival of tolerant CD4(+), especially CD4(+)CD25(+)T cells. CD4(+)T cells, from DA rats tolerant to fully allogeneic PVG heart allografts surviving over 100days without on-going immunosuppression, were cultured with PVG alloantigen and rIL-5. The ability of these cells to adoptively transfer tolerance to specific-donor allograft and suppress normal CD4(+)T cell mediated rejection in adoptive DA hosts was examined. Tolerant CD4(+)CD25(+)T cells' response to rIL-5 and expression of IL-5Rα was also assessed. rIL-5 was sufficient to promote transplant tolerance mediating CD4(+)T cells' survival in culture with specific-donor alloantigen. Tolerant CD4(+)T cells cultured with rIL-5 retained the capacity to transfer alloantigen-specific tolerance and inhibited naïve CD4(+)T cells' capacity to effect specific-donor graft rejection. rIL-5 promoted tolerant CD4(+)CD25(+)T cells' proliferation in vitro when stimulated with specific-donor but not third-party stimulator cells. Tolerant CD4(+)CD25(+)T cells expressed IL-5Rα. This study demonstrated that IL-5 promoted the survival of alloantigen-specific CD4(+)CD25(+)T cells that mediate transplant tolerance. - Source :PubMed

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