Mouse Autoimmune Regulator (AIRE) ELISA Kit

Este producto es parte de AIRE - Autoimmune Regulator
Mouse Autoimmune Regulator (AIRE) ELISA Kit
715€ (96 tests)

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Name
Mouse Autoimmune Regulator (AIRE) ELISA Kit
Category
ELISA Kits
Provider
Abbexa
Reference
abx153694
Tested Applications
ELISA

Description

Mouse Autoimmune Regulator (AIRE) ELISA Kit is an ELISA Kit for the in vitro quantitative measurement of Mouse Autoimmune Regulator (AIRE) concentrations in tissue homogenates and other biological fluids. This assay has high sensitivity and excellent specificity for detection of Autoimmune Regulator (AIRE)

Documentos del producto

Instrucciones
Data sheet
Descargar

Especificaciones del producto

Category
ELISA Kits
Immunogen Target
Autoimmune Regulator (AIRE)
Reactivity
Mouse
Detection Method
Colorimetric
Assay Data
Quantitative
Assay Type
Sandwich
Test Range
0.156 ng/ml - 10 ng/ml
Sensitivity
< 0.06 ng/ml
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Size 1
96 tests
Size 2
5 × 96 tests
Size 3
10 × 96 tests
Form
Standard Form: Lyophilized
Tested Applications
ELISA
Sample Type
Tissue homogenates and other biological fluids.
Availability
Shipped within 5-7 working days.
Storage
Shipped at 4°C. Upon receipt, store the kit according to the storage instruction in the kit's manual.
Dry Ice
No
Alias
AIRE1,APECED,APS1,APSI,PGA1
Background
Elisa Kits for: AIRE
Status
RUO
Note
THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR THERAPEUTIC PROCEDURES. The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments. Please note that our kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein.
The stability of the kit is determined by the rate of activity loss. The loss rate is less than 5% within the expiration date under appropriate storage conditions. To minimize performance fluctuations, operation procedures and lab conditions should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same user throughout.

Background

The Autoimmune Regulator (AIRE) is a protein encoded by the AIRE gene, and it plays a critical role in immune tolerance and the prevention of autoimmune diseases. AIRE is primarily expressed in a specialized type of cell called medullary thymic epithelial cells (mTECs) found in the thymus gland. AIRE functions as a transcriptional regulator, controlling the expression of a wide range of tissue-specific antigens (TSAs) within mTECs. These TSAs represent proteins that are normally expressed in various tissues. By inducing the expression of TSAs in the thymus, AIRE ensures that developing T cells encounter a diverse array of self-antigens during their maturation process.The exposure of developing T cells to self-antigens in the thymus is crucial for their selection and education. T cells that recognize self-antigens too strongly or too weakly are eliminated or rendered tolerant, respectively, through a process known as central tolerance. AIRE-mediated expression of TSAs in mTECs is a key mechanism by which central tolerance is maintained, helping to prevent the development of autoimmune responses against self-tissues. Mutations in the AIRE gene lead to a rare autoimmune disorder known as autoimmune polyendocrine syndrome type 1 (APS-1), also called autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). APS-1 is characterized by the development of multiple autoimmune diseases affecting various endocrine organs, such as the adrenal glands, parathyroid glands, and pancreas, as well as other tissues. These autoimmune manifestations result from defects in central tolerance due to impaired AIRE function, leading to the escape of autoreactive T cells from thymic deletion.

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