ArticleThe Biochemical journal1998
Signalling through the leukotriene B4 receptor involves both alphai and alpha16, but not alphaq or alpha11 G-protein subunits.
Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 54 citations in OpenAlex.
- Type 3 secretion system induced leukotriene B4 synthesis by leukocytes is actively inhibited by Yersinia pestis to evade early immune recognition.PLoS pathogens · 2024Article
- Structural insights on ligand recognition at the human leukotriene B4 receptor 1.Nature communications · 2021Article
- RvE1 uses the LTBThe ocular surface · 2020Article
- Differential Contribution of BLT1 and BLT2 to Leukotriene B4-Induced Human NK Cell Cytotoxicity and Migration.Mediators of inflammation · 2015Article
- Expression of functional leukotriene B4 receptors on human airway smooth muscle cells.The Journal of allergy and clinical immunology · 2009Article
- Sprouty4 negatively regulates protein kinase C activation by inhibiting phosphatidylinositol 4,5-biphosphate hydrolysis.Oncogene · 2009Article
- A second leukotriene B(4) receptor, BLT2. A new therapeutic target in inflammation and immunological disorders.The Journal of experimental medicine · 2000Article
- Normal hematopoiesis and inflammatory responses despite discrete signaling defects in Galpha15 knockout mice.Molecular and cellular biology · 2000Article
- cDNA cloning and characterization of guinea-pig leukotriene B4 receptor.The Biochemical journal · 1999Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
COS-7 cells transfected with the leukotriene (LT) B4 receptor (BLTR) cDNA were unable to produce LTB4-induced inositol phosphates (IPs) in spite of the presence of endogenous Galphai, Galphaq and Galpha11 proteins. Co-transfection of BLTR with Galpha16, however, resulted in high levels of IP production, which were 17-, 10- and 6-fold higher than with co-transfected Galpha11, Galphaq and Galpha14, respectively. Co-transfection of BLTR with phospholipase C (PLC) beta2, on the other hand, resulted in efficient IP production and co-transfection of BLTR with both Galpha16 and PLCbeta2 resulted in a greater than additive response.
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Registered trials
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