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Leukocyte Ig-like receptors (LIRs) are a family of immunoreceptors expressed predominantly on monocytes and B cells and at lower levels on dendritic cells and natural killer (NK) cells. Additionally we are shipping Leukocyte Immunoglobulin-Like Receptor, Subfamily A (Without TM Domain), Member 3 Antibodies (30) and Leukocyte Immunoglobulin-Like Receptor, Subfamily A (Without TM Domain), Member 3 Proteins (13) and many more products for this protein.
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Letter: LILRA3 gene deletion is not involved in the giant cell arteritis and systemic sclerosis predisposition in Spanish patients.
LILRA3 significantly reversed Nogo (show RTN4 ELISA Kits)-66-mediated inhibition of neurite outgrowth and promoted synapse formation in primary cortical neurons through regulation of the ERK (show EPHB2 ELISA Kits)/MEK (show MAP2K1 ELISA Kits) pathway.
Experiments point towards a beneficial role for LILRA3 in virus infections, especially in ssRNA viruses, like HIV, that engage TLR8 (show TLR8 ELISA Kits); however, the potentially beneficial role of LILRA3 is abrogated during a HIV infection.
LILRA3 gene deletion was not associated with Multiple Sclerosis susceptibility and did not affect the age of disease onset, clinical subtype or disease severity.
Evidence showed lack of significant association between LILRA3 deletion and multiple sclerosis pathogenesis. [meta-analysis]
LILRA3 is a new susceptibility factor for systemic lupus erythematosus (SLE) and primary Sjogren's syndrome (pSS (show CDSN ELISA Kits)). It predisposes to certain phenotypes such as leucopenia, thrombocytopenia, autoantibody positivity and increased disease activity.
The current study was conducted to investigate the association of rs103294 of LILRA3 with benign prostatic hyperplasia risk.
ILT6 deletion polymorphism does not appear to be a lupus susceptibility gene in South Indian Tamils, but may behave as a genetic modifier of autoantibody phenotype by influencing the production of anti-Ro60 (show TROVE2 ELISA Kits) and anti-Ro52 (show TRIM21 ELISA Kits) autoantibodies
LILRA3 is an immunostimulatory molecule, whose deficiency is associated with higher frequency of B-non-Hodgkin's lymphoma.
functional LILRA3 is a novel genetic risk factor for rheumatoid arthritis (RA), especially in males. It appears to highly predispose to ACPA (show PRTN3 ELISA Kits)-positive RA and confers an increased risk of disease severity in patients with early RA.
Leukocyte Ig-like receptors (LIRs) are a family of immunoreceptors expressed predominantly on monocytes and B cells and at lower levels on dendritic cells and natural killer (NK) cells. All LIRs in subfamily B have an inhibitory function (see, e.g., LILRB1, MIM 604811). LIRs in subfamily A, with short cytoplasmic domains lacking an immunoreceptor tyrosine-based inhibitory motif (ITIM) and with transmembrane regions containing a charged arginine residue, may initiate stimulatory cascades (see LILRA1, MIM 604810). One member of subfamily A (LILRA3) lacks a transmembrane region and is presumed to be a soluble receptor (Borges et al., 1997
CD85 antigen-like family member E
, immunoglobulin-like transcript 6
, leucocyte immunoglobulin-like receptor
, leukocyte immunoglobulin-like receptor 4
, leukocyte immunoglobulin-like receptor A3
, leukocyte immunoglobulin-like receptor subfamily A member 3
, monocyte inhibitory receptor HM43/HM31