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MULTI SCIENCES

Human M-CSF ELISA?Kit For Protein Quantification

Human M-CSF ELISA?Kit For Protein Quantification

SKU:EK1144

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Product Details

Human M-CSF ELISA?Kit For Protein Quantification

Brand

MultiSciences

CatNum

70-EK1144

Product Name

Human M-CSF ELISA Kit

Customs Name

Human M-CSF ELISA Kit

Application

ELISA

Reactivity

Human

Assay Type

Sandwich ELISA

Suitable Sample Type

serum, plasma, cell culture supernates

Format

96-well strip plate

Storage

4℃ (unopened) standard stored at -20℃, others stored at 4℃ (opened)

Shipping Condition

4℃

Sample Volume

20 μl

Sensitivity

0.19 pg/ml

Standard Curve Range

31.25 - 2000 pg/ml

Spike Recovery Range

81 % - 116 %

Mean Spike Recovery

1.02

CV of Intra plate

2.1 % - 4.1 %

CV of Inter plate

3.1 % - 4.0 %

Components

96-well polystyrene microplate coated with a monoclonal antibody against M-CSF

Human M-CSF Standard, lyophilized

M-CSF Detect Antibody

Standard Diluent

Streptavidin-HRP

Assay Buffer (10×)

Substrate (TMB)

Stop Solution

Washing Buffer (20×)

Plate Covers

Describtion

This assay employs the quantitative sandwich enzyme immunoassay technique for the quantitative detection of human M-CSF. The Human M-CSF ELISA is for research use only. Not for diagnostic or therapeutic procedures.

Macrophage colony-stimulating factor (M-CSF), also known as colony stimulating factor 1 (CSF1), is a secreted cytokine released by osteoblasts. It is a hematopoietic growth factor that is involved in the proliferation, differentiation, and survival of monocytes, macrophages, and bone marrow progenitor cells. Locally produced M-CSF in the vessel wall contributes to the development and progression of atherosclerosis. M-CSF has been described to play a role in renal pathology including Acute kidney injury (AKI) and Chronic Renal Failure (CRF). The chronic activation of monocytes can lead to multiple metabolic, hematologic and immunologic abnormalities in patients with CRF. In the context of AKI, M-CSF has been implicated in promoting repair following AKI, but also been described in an opposing role, driving proliferation of a pro-inflammatory macrophage phenotype.