LTB4R

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LTB4R

A gene on chromosome 14q11.2-q12 that encodes a low-affinity G protein-coupled receptor for leukotrienes, including leukotriene B4. LTB4R mediates chemotaxis of granulocytes and macrophages by activating a phosphatidylinositol-calcium second messenger system. It is highly expressed in the heart, skeletal muscle and lymphoid tissue.
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LTB4 is an extremely pro-inflammatory lipid mediator that can exert its activity by binding to receptors BLT1 or BLT2 [23].
Serhan, "Resolvin E1 selectively interacts with leukotriene B4 receptor BLT1 and ChemR23 to regulate inflammation," Journal of Immunology, vol.
For instance, as is the case for c[PLA.sub.2][alpha]-deficient mice, mice lacking [LTC.sub.4] synthase ([LTC.sub.4]S), [LTD.sub.4] receptor (CysLT1), [LTB.sub.4] receptor (BLT1), or [PGD.sub.2] receptor (DP1) are protected from asthma, (25-27) revealing the critical role of the c[PLA.sub.2][alpha]-[LTB.sub.4]/[LTC.sub.4]/[PGD.sub.2] axis in this allergic disease.
The LTs exert their actions through interaction with specific 7-transmembrane G-protein-coupled cell surface receptors, BLT1 and BLT2, representing the high and low-affinity receptor for LTB4, respectively, and CysLT1 receptor (CysLT1R) and CysLT2 receptor (CysLT2R) activated by the CysLTs [6, 7] plus a recently discovered LTE4-specific receptor known as CysLTER that was identified in [CysLT.sub.1]R/[CysLT.sub.2]R double-deficient mice [8].
Rola-Pleszczynski, "Involvement of BLT1 endocytosis and Yes kinase activation in leukotriene B4-induced neutrophil degranulation," The Journal of Immunology, vol.
have shown that mice lacking the gene encoding the LTB4 receptor, BLT1, manifested decreased inflammation in adipose tissue and liver and were protected from systemic glucose and insulin intolerance compared to WT littermates [18].
Inhibition of atherogenesis in BLT1 -deficient mice reveals a role for LTB4 and BLT1 in smooth muscle cell recruitment.
Thus, the Elves of Tol Eressea in the Book of Lost Tales were small indeed, a notion that Tolkien would strongly regret later (BLT1 32).
We also chose one gene (BLT1) involved in the regulation of immune response and regulated by promoter hypermethylation (26).
Moreover, a recent study has demonstrated that LTB4 receptor 1 (BLT1) and CXCR2 promoted the recruitment of neutrophils at psoriatic lesional sites and that these cells would secrete IL-1[beta], perpetuating psoriatic inflammation [72] (Table 1).
The involved cell surface receptors include macrophage mannose receptor, toll-like receptor 2 (TLR-2), C-type lectin receptor Dectin-1, and leukotriene B4 receptor (BLT1) [55].