Each of the four intracellular cysteines of CD36 is essential for insulin- or AMP-activated protein kinase-induced CD36 translocation

Oort, M.; Drost, Rinske; Janβen, Linda; Doorn, J.M. Van; Kerver, Jana; Horst, Dick J. Van der; Luiken, Joost J. F. P.; Rodenburg, Kees C. W.

doi:10.3109/13813455.2013.876049

Cited by 21 publications

(10 citation statements)

References 47 publications

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“…The evident plasma membrane localization of CD36 found in patients with NASH prompted the investigation of the possible mechanism(s) regulating the distribution of this protein. Previous studies demonstrated that insulin increases CD36 palmitoylation and rapidly stimulates the surface expression of CD36 in muscle cells[34,35]. In addition, Thorne et al consistently found that palmitoylation is necessary for the efficient incorporation of CD36 into plasma membrane rafts in melanoma cells[23].…”

mentioning

confidence: 97%

CD36 palmitoylation disrupts free fatty acid metabolism and promotes tissue inflammation in non-alcoholic steatohepatitis

Zhao

Zhang

Luo

et al. 2018

Journal of Hepatology

191

164

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Fatty acid translocase CD36 (CD36) is a multifunctional membrane protein which contributes to the development of liver steatosis. In the present study, we demonstrated that the localization of CD36 on the plasma membrane of hepatocytes is increased in patients with non-alcoholic steatohepatitis. Blocking the palmitoylation of CD36 reduces CD36 distribution in hepatocyte plasma membranes and protects mice from non-alcoholic steatohepatitis. The inhibition of CD36 palmitoylation not only improved fatty acid metabolic disorders but also reduced the inflammatory response in vitro and in vivo. The present study suggests that CD36 palmitoylation is important for non-alcoholic steatohepatitis development and inhibition of CD36 palmitoylation could be used to cure non-alcoholic steatohepatitis.

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mentioning

confidence: 97%

CD36 palmitoylation disrupts free fatty acid metabolism and promotes tissue inflammation in non-alcoholic steatohepatitis

Zhao

Zhang

Luo

et al. 2018

Journal of Hepatology

191

164

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“…It has been demonstrated that plasma membrane localization and the LCFA transport function of CD36 rely on cysteine S-acylation with LCFAs, such as palmitate ( 37 ). In adipocytes, palmitoyl acyltransferases DHHC4 and DHHC5 have been shown to acylate CD36 ( 38 ).…”

Section: Resultsmentioning

confidence: 99%

Fatty acid mobilization from adipose tissue is mediated by CD36 posttranslational modifications and intracellular trafficking

Daquinag¹,

Gao²,

Fussell³

et al. 2021

JCI Insight

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The mechanism controlling long-chain fatty acid (LCFA) mobilization from adipose tissue (AT) is not well understood. Here, we investigated how the LCFA transporter CD36 regulates this process. By using tissue-specific knockout mouse models, we show that CD36 in both adipocytes and endothelial cells mediates both LCFA deposition into and release from AT. We demonstrate the role of adipocytic and endothelial CD36 in promoting tumor growth and chemoresistance conferred by AT-derived LCFA. We show that dynamic cysteine S-acylation of CD36 in adipocytes, endothelial cells, and cancer cells mediates intercellular LCFA transport.We demonstrate that lipolysis induction in adipocytes triggers CD36 de-acylation and deglycosylation, as well as its dissociation from interacting proteins, prohibitin-1 (PHB), and annexin 2 (ANX2). Our data indicate that lipolysis triggers caveolar endocytosis and translocation of CD36 from the cell membrane to lipid droplets. This study suggests a mechanism for both outside-in and inside-out cellular LCFA transport regulated by CD36 Sacylation and its interactions with PHB and ANX2.

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“…Acyl protein thioesterase 1 (APT1), one of the depalmitoylating enzymes, can depalmitoylate CD36 by recruiting tyrosine kinase SYK to induce the uptake of FAs and assist in weight gain in high-fat-diet (HFD)-fed mice [49]. Furthermore, despite insulin stress and AMPK activation, mutation in one of these four sites can impede CD36 translocation from the endosomes to the plasma membrane, indicating that palmitoylation is indispensable for the cycling of CD36 [50]. However, palmitoylation of CD36 in cardiac diseases has not been studied.…”

Section: Post-translational Regulation Of Cd36mentioning

confidence: 99%

CD36 Signaling in Diabetic Cardiomyopathy

Zhang

Fan

et al. 2021

Aging and disease

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Cluster of differentiation 36 (CD36), also referred to as scavenger receptor B2, has been shown to serve multiple functions in lipid metabolism, inflammatory signaling, oxidative stress, and energy reprogramming. As a scavenger receptor, CD36 interacts with various ligands, such as oxidized low-density lipoprotein (oxLDL), thrombospondin 1 (TSP-1), and fatty acid (FA), thereby activating specific downstream signaling pathways. Cardiac CD36 is mostly expressed on the surface of cardiomyocytes and endothelial cells. The pathophysiological process of diabetic cardiomyopathy (DCM) encompasses diverse metabolic abnormalities, such as enhanced transfer of cardiac myocyte sarcolemmal FA, increased levels of advanced glycation end-products, elevation in oxidative stress, impaired insulin signaling cascade, disturbance in calcium handling, and microvascular rarefaction which are closely related to CD36 signaling. This review presents a summary of the CD36 signaling pathway that acts mainly as a long-chain FA transporter in cardiac myocytes and functions as a receptor to bind to numerous ligands in endothelial cells. Finally, we summarize the recent basic research and clinical findings regarding CD36 signaling in DCM, suggesting a promising strategy to treat this condition.

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Each of the four intracellular cysteines of CD36 is essential for insulin- or AMP-activated protein kinase-induced CD36 translocation

Cited by 21 publications

References 47 publications

CD36 palmitoylation disrupts free fatty acid metabolism and promotes tissue inflammation in non-alcoholic steatohepatitis

CD36 palmitoylation disrupts free fatty acid metabolism and promotes tissue inflammation in non-alcoholic steatohepatitis

Fatty acid mobilization from adipose tissue is mediated by CD36 posttranslational modifications and intracellular trafficking

CD36 Signaling in Diabetic Cardiomyopathy

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