Target antigen Fluorophore Clone Company, address CD28 FITC CD28.2 CD56 FITC NCAM16.2 CD69 FITC FN50 CD94 FITC HP-3D9
CD95 FITC DX2 PD-1 FITC MIH4 PD-1 BV421 MIH4 TCR[alpha][beta] FITC T10B9.1A-31 CD8 FITC SK1 CD8 APC Cy7 SK1 BD Bioscience CD8 V500 RPA-T8 Franklin Lakes, NJ, USA CD45RO APC UCHL1 CD4 Alexa Fluor 700 RPA-T4 CD3 PE UCHT1 CD3 V450 UCHT1 CD3 BV510 UCHT1 CD19 PE HIB19 CD27 PE M-T271 CD27 BV421 M-T271 CCR7 PE-Cy7 3D12 TCR[gamma][delta] FITC IMMU510 Beckman Coulter Inc.
The aim of this study was to investigate the expressions of COX-2 and
CD95 in RCCs (CC and NCC) showing different clinico-pathological characteristics, and also to determine if a relation existed between COX-2 and
CD95 expressions.
Cellular FLICE-inhibitory protein splice variants inhibit different steps of caspase-8 activation at the
CD95 death-inducing signaling complex.
This treatment resists the
CD95 (Fas) receptor which induces keratinocyte apoptosis.
Krammer, "Autocrine T-cell suicide mediated by APO-1/(Fas/
CD95)," Nature, vol.
Taking into consideration the importance of NOS and high level of UA in the realization of the process of apoptosis, development of MS and CVD, we should consider that in the human population with AH these processes are mediated by the mechanisms of changes in Fas (
CD95) / Fas-ligand system.
Northwestern Medicine scientists have demonstrated that cancer cells -- and not normal cells -- can be killed by eliminating either the FAS receptor, also known as
CD95, or its binding component,
CD95 ligand.
For instance, ceramide production has been proposed to be involved CD40,
CD95, and Fc-gamma receptor clustering [25-27].
For the treatment of arthritis, multiple mechanisms appear to be involved including the inhibition of enzymes involved in purine metabolism, leading to an accumulation of adenosine; inhibition of T cell activation and suppression of intercellular adhesion molecule expression by T cells; increasing
CD95 sensitivity of activated T cells; inhibition of methyltransferase activity, leading to (de)activation of enzyme activity relevant to immune system function [22].
Several targets of MARCH1 have been identified: B7.2, CD98,
CD95 (Fas), TfR, and MHC class II HLA-DR, -DM and -DO [6, 44, 46-50].
Manolios, "Identification and characterisation of polymorphisms in the promoter region of the human Apo-1/Fas (
CD95) gene," Molecular Immunology, vol.