CD95 Human ELISA Kit (DEIA1429)

Regulatory status: For research use only, not for use in diagnostic procedures.

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cell culture extracts, tissues extracts
Species Reactivity
Intended Use
For the quantitative measurement of Human CD95 concentrations in cell and tissue lysates.
Contents of Kit
1. CD95 Microplate
2. Wash Buffer Concentrate (20X)
3. Standards
4. Sample Diluent Buffer
5. Assay Diluent
6. Detection Antibody CD95
7. HRP-Streptavidin concentrate
8. TMB One-Step Substrate Reagent
9. Stop Solution
10. Cell lysate buffer
All kit components of this kit are stable at 2-8°C. For more detailed information, please download the following document on our website.
Detection Range
2.74 pg/mL-2000 pg/mL
5 pg/mL
Standard Curve


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Neutrophil apoptosis in asymptomatic Human Immunodeficiency Virus infection


Authors: Maria Cooke, Paula; Caula, Cinthya; Angel Orsilles, Miguel

In recent years it has been determined that neutrophils are highly versatile and sophisticated cells whose functions go far beyond the elimination of microorganisms. In Human Immunodeficiency Virus (HIV) infection, the role of neutrophils is not fully characterized but it is now clear that the relationship between neutrophils and HIV is much more complex than previously thought. The aims of this study were to evaluate the effect of HIV infection on neutrophil cell death and the expression of surface molecules on neutrophils in patients with asymptomatic infection and without antiretroviral treatment (ART). In HIV seropositive patients without antiretroviral therapy there was an increase in the early apoptosis of neutrophils in relation to the control groups. This increased apoptosis does not depend on the activation of the extrinsic or intrinsic pathway. In these patients there was an increase in the expression of TLR2 which, together with the increase of early apoptosis, could be indicative of an activated phenotype of neutrophils. In conclusion, this study provides information on aspects related to the apoptosis of neutrophils in early stages of HIV infection and therefore contributes to a better understanding of the effect of this virus on components of the innate immune response.

Meta-analysis of mouse transcriptomic studies supports a context-dependent astrocyte reaction in acute CNS injury versus neurodegeneration


Authors: Das, Sudeshna; Li, Zhaozhi; Noori, Ayush; Hyman, Bradley T.; Serrano-Pozo, Alberto

Background Neuronal damage in acute CNS injuries and chronic neurodegenerative diseases is invariably accompanied by an astrocyte reaction in both mice and humans. However, whether and how the nature of the CNS insult-acute versus chronic-influences the astrocyte response, and whether astrocyte transcriptomic changes in these mouse models faithfully recapitulate the astrocyte reaction in human diseases remains to be elucidated. We hypothesized that astrocytes set off different transcriptomic programs in response to acute versus chronic insults, besides a shared "pan-injury" signature common to both types of conditions, and investigated the presence of these mouse astrocyte signatures in transcriptomic studies from human neurodegenerative diseases. Methods We performed a meta-analysis of 15 published astrocyte transcriptomic datasets from mouse models of acute injury (n= 6) and chronic neurodegeneration (n= 9) and identified pan-injury, acute, and chronic signatures, with both upregulated (UP) and downregulated (DOWN) genes. Next, we investigated these signatures in 7 transcriptomic datasets from various human neurodegenerative diseases. Results In mouse models, the number of UP/DOWN genes per signature was 64/21 for pan-injury and 109/79 for acute injury, whereas only 13/27 for chronic neurodegeneration. The pan-injury-UP signature was represented by the classic cytoskeletal hallmarks of astrocyte reaction (GfapandVim), plus extracellular matrix (i.e.,Cd44,Lgals1, Lgals3, Timp1), and immune response (i.e.,C3, Serping1, Fas, Stat1, Stat2, Stat3). The acute injury-UP signature was enriched in protein synthesis and degradation (both ubiquitin-proteasome and autophagy systems), intracellular trafficking, and anti-oxidant defense genes, whereas the acute injury-DOWN signature included genes that regulate chromatin structure and transcriptional activity, many of which are transcriptional repressors. The chronic neurodegeneration-UP signature was further enriched in astrocyte-secreted extracellular matrix proteins (Lama4,Cyr61,Thbs4), while the DOWN signature included relevant genes such asAgl(glycogenolysis),S1pr1(immune modulation), andSod2(anti-oxidant). Only the pan-injury-UP mouse signature was clearly present in some human neurodegenerative transcriptomic datasets. Conclusions Acute and chronic CNS injuries lead to distinct astrocyte gene expression programs beyond their common astrocyte reaction signature. However, caution should be taken when extrapolating astrocyte transcriptomic findings from mouse models to human diseases.

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