MOUSE ANTI HUMAN CD58 Azide Free

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889 EUR
1066 USD
737 GBP
known as: MOUSE ANTI HUMAN CD58 Azide Free
Catalog number: genta-ABS0443
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd58

Related genes to: MOUSE ANTI HUMAN CD58 Azide Free

Symbol : cd58 NIH gene
dbXrefs : Ensembl:ENSAMXG00000016789
chromosome : Un
description : CD58 molecule
type of gene : protein-coding
Modification date : 2016-02-21

Related Pathways to: MOUSE ANTI HUMAN CD58 Azide Free

Related product to: MOUSE ANTI HUMAN CD58 Azide Free

Related Articles about: MOUSE ANTI HUMAN CD58 Azide Free

Association of CD58 gene polymorphisms with NMO spectrum disorders in a Han Chinese population.

This study aimed to perform a comprehensive assessment of the association between CD58 polymorphisms and the risk of neuromyelitis optica spectrum disorders (NMOSD) in a Han Chinese population. Nine single-nucleotide polymorphisms (SNPs) were genotyped in 230 NMOSD patients and 487 healthy controls. Five SNPs were significantly associated with an increased risk of NMOSD (rs2300747, rs1335532, rs56302466, rs1016140, and rs12044852). The haplotype TAGCCCAA significantly increased the risk of NMOSD, while TATTACGG reduced the risk. In conclusion, this study identified a new NMOSD susceptibility variant, rs56302466, and suggested that CD58 polymorphisms are associated with the risk of NMOSD in Han Chinese. - Source :PubMed

[Research Progress on Relationship between CD58 Molecule and ALL and Lymphoma -Review].

Lymphocyte function-associated antigen-3 (LFA-3/CD58) is a cell-surface glycoprotein, it can bind to CD2 and activate the costimulation pathways of T lymphocytes and natural killer (NK) cells, maximizing the cytolysis of target cells by cytotoxic T lymphocytes (CTL) and NK cells. Some studies have demonstrated that in acute lymphoblastic leukemia(ALL) and lymphomas, lack of CD58 on the tumor cells may fail to activate the T lymphocytes and NK cells, resulting in feeble cytotoxic effect and subsequently escape from immune surveillance, making the disease become more complicated and liable to relapse. Therefore, this article aims to review the structure, biological characteristics of CD58 on the tumor cells and its relationship with ALL and lymphomas. - Source :PubMed

Leishmania donovani resistant to Ambisome or Miltefosine exacerbates CD58 expression on NK cells and promotes trans-membrane migration in association with CD2.

Visceral leishmaniasis (VL) is a disease that is associated with compromised immunity and drug un-responsiveness as well as with the emergence of drug resistance in Leishmania donovani (Ld). Ld down-modulates cellular immunity by manipulating signaling agents, including a higher expression of the adhesion molecule CD58. The expression of CD58 and CD2 on natural killer (NK) cells facilitates intercellular adhesion and signaling. The influence of drug-resistant Ld on the expression of CD58 and CD2 was addressed in this study. The mean florescence intensity (MFI) of CD58 but not of CD2 was twofold higher on CD56(+) cells during VL, but was down-regulated after treatment. In addition, MFI of CD58 on CD56(+) cells was further exacerbated in VL subjects who had relapsed after Ambisome or Miltefosine treatment. The same pattern of CD58 expression was also obtained upon stimulation of healthy peripheral blood mononuclear cells with Miltefosine- or Ambisome-resistant Ld. The ratio of CD56(+)CD58(+)IFN-γ(+)/CD56(+)CD58(+)IL-10(+) cells was reduced by 6.98-fold after stimulation with Ld. Further, an antagonist to CD58 or its counter-receptor CD2 down-regulated CD56(+) NK cell recruitment across a polycarbonate trans-membrane at Ld infection sites. This study reports that factors associated with drug resistance in Ld probably promote higher expression of CD58 on CD56(+) cells and their migration to the infection site in association with CD2. - Source :PubMed

Mutations or copy number losses of CD58 and TP53 genes in diffuse large B cell lymphoma are independent unfavorable prognostic factors.

The advent of next generation sequencing (NGS) technologies has expedited the discovery of novel genetic lesions in DLBCL. The prognostic significance of these identified gene mutations is largely unknown. In this study, we performed NGS for the 27 genes most frequently implicated in 196 patients. Interestingly, TP53 mutations were found to be significantly more common in DLBCL with MYC translocations (r = 0.446, P = 0.034). While no gene mutation was found to be more prevalent in patients with DLBCL with bone marrow involvement, MYD88 mutations were more common in primary DLBCL of the CNS or testis. To evaluate the prognostic significance of the abnormalities of these 27 genes, a total of 165 patients with newly diagnosed DLBCL, NOS were included in a multivariate survival analysis. Surprisingly, in addition to the TP53 mutation, CD58 mutation was found to predict poor clinical outcome. Furthermore, copy number loss of CD58 or TP53 was also identified to be an independent negative prognostic factor. Our results have uncovered the previously unknown critical impact of gene mutations on the prognosis of DLBCL and are fundamentally important for the future design of tailored therapy for improved clinical outcomes. - Source :PubMed

CD2-CD58 interactions are pivotal for the activation and function of adaptive natural killer cells in human cytomegalovirus infection.

The existence and expansion of adaptive NK-cell subsets have been linked to HCMV infection. Phenotypically, a majority of adaptive NK cells expresses the activating receptor NKG2C and CD57. Some of the molecular factors driving the expansion of NKG2C(+) CD57(+) NK cells in HCMV infection have been identified. The direct interaction of adaptive NK cells with HCMV-infected cells, preceding the expansion, however, remains less studied. Recently, adaptive NK cells were reported to express higher levels of the co-activating receptor CD2. We explored whether CD2 was directly involved in the response of adaptive NK cells to HCMV. In a co-culture system of human PBMCs and productively infected fibroblasts, we observed an upregulation of CD69, CD25, and HLA-DR on all NK cells. However, only in adaptive NK cells was this increase largely blocked by antibodies against CD2 and CD58. Functionally, this blockade also resulted in diminished production of IFN-γ and TNF-α by adaptive human NK cells in response to HCMV-infected cells. Our results demonstrate that binding of CD2 to upregulated CD58 on infected cells is a critical event for antibody-mediated activation and subsequent effector functions of adaptive NKG2C(+) CD57(+) NK cells during the antiviral response. - Source :PubMed

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