CD36 is a sensor of diacylglycerides

By K. Hoebe, P. Georgel, S. Rutschmann, Xin Du, Suzanne Mudd, K. Crozat, Sosathya Sovath, L. Shamel, T. Hartung, U. Zähringer and 1 more. Nature, 2005

945 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/3ba9d5eff087c7850b9fe553f2155bcefb9afd9d

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Citations in the corpus

DAMPening Inflammation by Modulating TLR Signalling (2010, background): “CD36 is a sensor of diacylated lipopeptides recognised by TLR2/TLR6 [67].”
The interleukin‐1 receptor/Toll‐like receptor superfamily: 10 years of progress (2008, background): “Mal appears to be required to stabilize MyD88 recruitment and also provides an extra level of control on TLR2 and TLR4 signaling.”
CD14 controls the LPS-induced endocytosis of Toll-like Receptor 4 (2011, background): “To determine the specificity of the role of CD14 for TLR4-mediated IFN expression, we examined the expression of cytokines and IFN-regulated genes in WT and CD14-deficient cells stimulated with TLR2 ligands.”
Dectin-1: a signalling non-TLR pattern-recognition receptor (2006, background): “Although this is mediated mainly by the TLRs, the non-TLR PRRs ( Table 1 ) can contribute to this response by the presentation of PAMPs to the TLRs ? such as described for CD36 (Ref”
CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer (2009, background): “We therefore tested whether fibrillar β-amyloid peptide (1-42) (Aβ1-42) could activate TLR4-TLR6 signaling via CD36.”
The immunology of sepsis (2008, background): “aureus demonstrate that cellular responses to the bacterium reside to a large extent in response to the diacylated lipoprotein of the cell surface, recognized by TLR2 and TLR6 [29–31].”
The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors (2010, background): “These include CD36, which acts together with the TLR2-TLR6 heterodimer to mediate the sensing of some but not all TLR2 agonist”
The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9 (2006, background): “Immunodeficiency states in which TLR signaling is altered or abolished have been systematically created and identified using the random germline mutagen N -ethyl- N -nitrosoure”