RAB0079

Human MCP-2 / CCL8 ELISA Kit

Name: Human MCP-2 / CCL8 ELISA Kit
Brand: SIGMA

for serum, plasma, cell culture supernatant and urine

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About This Item

NACRES:

NA.32

UNSPSC Code:

41116158

Product Name

Human MCP-2 / CCL8 ELISA Kit, for serum, plasma, cell culture supernatant and urine

species reactivity

human

packaging

kit of 96 wells (12 strips x 8 wells)

technique(s)

ELISA: suitable
capture ELISA: suitable

input

sample type urine
sample type plasma
sample type serum
sample type cell culture supernatant(s)

assay range

inter-assay cv: <12%
intra-assay cv: <10%
sensitivity: 1.5 pg/mL
standard curve range: 0.82-200 pg/mL

detection method

colorimetric

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... CCL8(6355)

Related Categories

Enzyme-Linked Immunosorbent Assay (ELISA) Kits

Immunoassay Platform Solutions

Application

For research use only. Not for use in diagnostic procedures.
Please refer to the attached General ELISA KIT Procedure (sandwich, competitive & Indirect ELISA)

General description

The Human MCP-2 ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of human MCP-2 in serum, plasma, cell culture supernatants and urine.

Immunogen

Recombinant Human MCP2

Other Notes

A sample Certificate of Analysis is available for this product.
Please type the word sample in the text box provided for lot number.

pictograms

GHS05

signalword

Warning

hcodes

H290

pcodes

P234 - P390

Hazard Classifications

Met. Corr. 1

Storage Class

8A - Combustible corrosive hazardous materials

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Genetically distinct Group B Streptococcus strains induce varying macrophage cytokine responses.

Rebecca A Flaherty et al.

PloS one, 14(9), e0222910-e0222910 (2019-09-20)

Group B Streptococcus (GBS) is an opportunistic pathogen that causes preterm birth and neonatal disease. Although GBS is known to exhibit vast diversity in virulence across strains, the mechanisms of GBS-associated pathogenesis are incompletely understood. We hypothesized that GBS strains

CaSR Antagonist (Calcilytic) NPS 2143 Hinders the Release of Neuroinflammatory IL-6, Soluble ICAM-1, RANTES, and MCP-2 from Aβ-Exposed Human Cortical Astrocytes.

Anna Chiarini et al.

Cells, 9(6) (2020-06-06)

Available evidence shows that human cortical neurons' and astrocytes' calcium-sensing receptors (CaSRs) bind Amyloid-beta (Aβ) oligomers triggering the overproduction/oversecretion of several Alzheimer's disease (AD) neurotoxinseffects calcilytics suppress. We asked whether AβCaSR signaling might also play a direct pro-neuroinflammatory role in

CCL8 enhances sensitivity of cutaneous squamous cell carcinoma to photodynamic therapy by recruiting M1 macrophages.

Jie Ji et al.

Photodiagnosis and photodynamic therapy, 26, 235-243 (2019-03-25)

Antitumor immunity induced by photodynamic therapy (PDT) is believed to depend on the degree of local and systemic inflammation. The recruitment of leukocytes, in particular by the chemokine CCL8, to the sites of tissue damage has been strongly associated with

Estrogen receptor β upregulates CCL2 via NF-κB signaling in endometriotic stromal cells and recruits macrophages to promote the pathogenesis of endometriosis.

Yanling Gou et al.

Human reproduction (Oxford, England), 34(4), 646-658 (2019-03-07)

How is the activation of estrogen receptor β (ERβ) in endometriotic stromal cells (ESCs) involved in macrophage recruitment to promote the pathogenesis of endometriosis? ERβ modulates the production of C-C motif chemokine ligand 2 (CCL2) via nuclear factor kappa-light-chain-enhancer of

Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac.

Tiyash Parira et al.

Scientific reports, 7(1), 11236-11236 (2017-09-13)

Previous reports on epigenetic mechanisms involved in alcohol abuse have focus on hepatic and neuronal regions, leaving the immune system and specifically monocyte-derived dendritic cells (MDDCs) understudied. Our lab has previously shown histone deacetylases are modulated in cells derived from