Soluble Leptin Receptor (sLEP-R) ELISA

Este producto es parte de LEPR - leptin receptor
Soluble Leptin Receptor (sLEP-R) ELISA
560€ (96 det.)

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Name
Soluble Leptin Receptor (sLEP-R) ELISA
Category
ELISA Kits
Provider
Mediagnost
Reference
R07
Tested Applications
Elisa

Description

Quantitative measurement of soluble human leptin receptor (sLEP-R) in human serum or plasma for research purposes.

Descripción

Soluble Leptin Receptor (sLEP-R) ELISA permite la medición cuantitativa del receptor de leptina humano soluble (sLEP-R) en suero o plasma humano con fines de investigación.

Documentos del producto

Instrucciones
Descargar
Data sheet

Especificaciones del producto

Category
ELISA Kits
Reactivity
Human
Assay Data
Reference Material:  Recombinant eukaryotically expressed soluble leptin receptor.
Incubation Period:  5 h
Calibrator:  8 individual standards, 0-30 ng/mL
Controls: 2 serum controls, low and high level, respectively, lyophilized
Assay Type
Sandwich
Test Range
0.0385-150 µg/L
Sensitivity
0,0385 µg/L
Recommended Dilution
1:5
Origin
Antibody:  Specific high-affinity antibodies
Size 1
96 det.
Tested Applications
Elisa
Sample Type
Serum / Plasma
Availability
3-5 days.
Storage
Shelf life: between 1 and 2 years. Inquire about availability
Store the kit at 2-8°C after receipt until its expiry date.
Alias
OBR, CD295, LEP-R
Background
Elisa Kits for: LEPR
Status
RUO
Note
Intra/Interassay Variance [%] < 10%

Background

The adipokine leptin realizes signal transduction via four different leptin receptor (LEP-R) isoforms. The amount of functionally active LEP-R, however, is affected by constitutive shedding of the extracellular domain. The product of the cleavage process, the so-called soluble leptin receptor (sLEP-R, soluble Leptin receptor), is the main binding protein for leptin in human blood and modulates its bioavailability. Concentrations of sLEP-R are differentially regulated in metabolic disorders, such as type 1 diabetes mellitus or obesity and can therefore enhance or reduce leptin sensitivity. Lipotoxicity and apoptosis increase LEP-R cleavage via ADAM10-dependent mechanisms. In contrast, although increased sLEP-R concentrations seem directly to inhibit leptin effects, reduced amounts of sLEP-R may reflect decreased membrane expression of LEP-R. These findings, in part, explain alterations of leptin sensitivity that are associated with changes in serum sLEP-R concentrations seen in metabolic disorders.

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