Recombinant Human LILRA3 protein is a Human Full Length protein, in the 19 to 439 aa range, expressed in HEK 293, with >95% purity, < 1 EU/µg endotoxin level and suitable for SDS-PAGE, HPLC.
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| Application | Reactivity | Dilution info | Notes |
|---|---|---|---|
Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application HPLC | Reactivity Reacts | Dilution info - | Notes - |
Acts as a soluble receptor for class I MHC antigens. Binds both classical and non-classical HLA class I molecules but with reduced affinities compared to LILRB1 or LILRB2. Binds with high affinity to the surface of monocytes, leading to abolish LPS-induced TNF-alpha production by monocytes.
CD85e, ILT6, LIR4, LILRA3, Leukocyte immunoglobulin-like receptor subfamily A member 3, CD85 antigen-like family member E, Immunoglobulin-like transcript 6, Leukocyte immunoglobulin-like receptor 4, Monocyte inhibitory receptor HM43/HM31, ILT-6, LIR-4
Recombinant Human LILRA3 protein is a Human Full Length protein, in the 19 to 439 aa range, expressed in HEK 293, with >95% purity, < 1 EU/µg endotoxin level and suitable for SDS-PAGE, HPLC.
pH: 7.4
Constituents: 99% Phosphate Buffer, 0.88% Sodium chloride
Purity is greater than 95% as determined by SEC-HPLC and reducing SDS-PAGE.
Acts as a soluble receptor for class I MHC antigens. Binds both classical and non-classical HLA class I molecules but with reduced affinities compared to LILRB1 or LILRB2. Binds with high affinity to the surface of monocytes, leading to abolish LPS-induced TNF-alpha production by monocytes.
N-glycosylation is required for ligand binding.
LILRA3 also known as Leukocyte Immunoglobulin-Like Receptor Subfamily A Member 3 is a soluble receptor lacking a transmembrane domain. This protein has a mass of approximately 45 kDa. It is mainly expressed in immune cells such as monocytes macrophages and some lymphocytes. Researchers detect LILRA3 in serum and other body fluids which suggests its potential role outside of cellular membranes.
LILRA3 modulates immune responses by binding to unknown ligands. It does not associate with any known receptor complex because it does not possess a transmembrane or cytoplasmic domain. LILRA3 may act as a natural antagonist to other LILR receptors by interfering with their ligand interactions. This antagonism helps regulate the functions of the innate and adaptive immune responses by competing with membrane-bound LILR forms for binding with common ligands.
LILRA3 influences the pathways involved in immune regulation including the modulation of cytokine production. It has been linked to pathways associated with the inhibition of inflammation intersecting with receptors like LILRA2 and LILRB1 which are also part of the LILR family. These interactions are essential in balancing immune responses possibly by inhibiting excessive activation that could lead to inflammation or autoimmunity.
Researchers have studied LILRA3 in the context of autoimmune conditions and inflammatory disorders. Decreased levels of LILRA3 expression or activity have associations with diseases such as rheumatoid arthritis and multiple sclerosis. The interaction between LILRA3 and other family members like LILRB2 may influence disease processes by affecting immune regulation and the balance of activating and inhibitory signals within the immune system.
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