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RAB0273

Sigma-Aldrich

Human IL-1 β ELISA Kit

for serum, plasma, cell culture supernatant and urine

Synonyme(s) :

Il-1 beta, Interleukin-1 beta

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About This Item

Code UNSPSC :
41116158
Nomenclature NACRES :
NA.84

Espèces réactives

human

Conditionnement

kit of 96 wells (12 strips x 8 wells)

Technique(s)

ELISA: suitable
capture ELISA: suitable

Entrée

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

assay range

inter-assay cv: <12%
intra-assay cv: <10%
sensitivity: 0.3 pg/mL
standard curve range: 0.48-100 pg/mL

Méthode de détection

colorimetric

Conditions d'expédition

wet ice

Température de stockage

−20°C

Informations sur le gène

human ... IL1B(3553)

Description générale

The Human IL-1 β ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of human IL-1 β in serum, plasma, cell culture supernatants and urine.

Immunogène

Recombinant Human IL-1β

Application

For research use only. Not for use in diagnostic procedures.
Human IL-1 β ELISA kit has been used to measure the concentration of interleukin 1β (IL-1 β) in cell culture supernatants.

Actions biochimiques/physiologiques

Interleukin 1β (IL-1 β) is a proinflammatory cytokine, which is implicated in induction of various acute and chronic inflammation. Hence, IL1B can be considered as a potential therapeutic target for disease associated with fibrosis and tissue remodeling. IL-1β protein increases the production of endogenous 92kDa gelatinase (matrix metalloproteinases 9 (MMP-9)) and tissue inhibitors of MMP (TIMP -1). Elevated concentration of IL-1β in synovial fluid contributes to the pathogenesis of synovitis and degenerative changes of the cartilaginous tissue and bone of the temporomandibular joint. IL-1β brings neutrophil and macrophage to the site of infection. Mutations in IL-1β gene are linked with renal manifestations and renal sequelae in Henoch-Schönlein purpura (HSP).

Autres remarques

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

Composants de kit également disponibles séparément

Réf. du produit
Description
FDS
  • RABELADAELISA 1X Assay/Sample Diluent Buffer A (Item D1)FDS
  • RABELADBELISA 5X Assay/Sample Diluent Buffer B (Item E1)FDS
  • RABSTOP3ELISA Stop Solution (Item I)FDS
  • RABTMB3ELISA Colorimetric TMB Reagent (HRP Substrate, Item H)FDS
  • RABWASH420X Wash Buffer (Item B)FDS

Pictogrammes

Corrosion
GHS05

Mention d'avertissement

Warning

Mentions de danger

H290

Conseils de prudence

P234 - P390

Classification des risques

Met. Corr. 1

Code de la classe de stockage

8A - Combustible corrosive hazardous materials

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Proinflammatory cytokines detectable in synovial fluids from patients with temporomandibular disorders.
Takahashi T
Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, 85(2), 135-141 (1998)
Chao Zhu et al.
Cell biology and toxicology (2022-10-14)
Atherosclerosis is a chronic inflammatory disease and the main pathology behind most cardiovascular diseases and the overactivation of macrophages initiates the development of atherosclerosis. However, the specific functions of oxidized low-density lipoprotein (ox-LDL) in macrophages remain elusive. Macrophages derived from
Jie Liu et al.
The Journal of international medical research, 49(3), 300060521996564-300060521996564 (2021-03-27)
Porphyromonas gingivalis (Pg) plays a critical role in the occurrence and development of atherosclerosis. Lipopolysaccharide from Pg (Pg-LPS) could lead to pyroptosis of vascular smooth muscle cells (VSMCs) and induce instability of atherosclerotic plaque. Therefore, pyroptosis of VSMCs could promote
Differential regulation of monocyte matrix metalloproteinase and TIMP-1 production by TNF-alpha, granulocyte-macrophage CSF, and IL-1 beta through prostaglandin-dependent and -independent mechanisms.
Zhang Y
Journal of Immunology, 161(6), 3071-3076 (1998)
Strain- and host species-specific inflammasome activation, IL-1? release, and cell death in macrophages infected with uropathogenic Escherichia coli.
Schaale K
Mucosal Immunology, 9(1), 124-136 (2016)
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