CD36 deficiency and absent myocardial iodine-123-(R,S)-15-(p-iodophenyl)-3-methylpentadecanoic acid uptake in a girl with cardiomyopathy

Teraguchi, Masayuki; Ohkohchi, Hiroyuki; Ikemoto, Yumiko; Higashino, Hirohiko; Kobayashi, Yohnosuke

doi:10.1007/s00431-002-1118-2

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…succinogenes NosZ is unique in exhibiting a C-terminal extension of about 200 residues that carries a single heme cbinding motif (CNGCH). This is in line with the previous characterization of the purified W. succinogenes enzyme as a cytochrome c N 2 O reductase [10]. The cytochrome c domain might function as an electron donor to the Cu A center.…”

Section: Cytochrome C N 2 O Reductasesupporting

confidence: 91%

“…The gene arrangement within this cluster is unique as compared to other known nos gene clusters [9]. The previously purified cytochrome c N 2 O reductase of W. succinogenes is encoded by the nosZ gene [10]. The W. succinogenes nos locus includes conventional nosD, -F, -Y and -L genes although their arrangement is atypically interrupted by several open reading frames.…”

Section: Organization Of the Nos Gene Cluster Of W Succinogenesmentioning

confidence: 99%

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The unprecedented nos gene cluster of Wolinella succinogenes encodes a novel respiratory electron transfer pathway to cytochrome c nitrous oxide reductase

et al. 2004

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reductases exhibiting conservation of all residues ligating the two multinuclear copper centers but carries an unprecedented Cterminal monoheme cytochrome c domain. Notably, the N 2 O reductase pre-protein is synthesized with a Sec-dependent signal peptide, rather than the usually observed twin-arginine signal sequence, implying that the copper and heme cofactors are both incorporated in the periplasm. The nos gene cluster further consists of four adjacent open reading frames which are predicted to encode two monoheme c-type cytochromes as well as homologs of NapG and NapH. The latter proteins are thought to function in quinol oxidation coupled to cytochrome c reduction in electron transport to periplasmic nitrate reductase. While the accessory genes nosD, -F, -Y and -L are present in W. succinogenes, homologs of nosR and nosX are absent from the genome. We hypothesize that the nos gene cluster of W. succinogenes encodes a complete electron transport chain catalyzing N 2 O reduction by menaquinol, a pathway which might also be relevant to other bacteria.

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Section: Cytochrome C N 2 O Reductasesupporting

confidence: 91%

Section: Organization Of the Nos Gene Cluster Of W Succinogenesmentioning

confidence: 99%

The unprecedented nos gene cluster of Wolinella succinogenes encodes a novel respiratory electron transfer pathway to cytochrome c nitrous oxide reductase

et al. 2004

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“…The abnormal plasma lipids in humans with CD36 deficiency or with polymorphisms in the CD36 gene reflect at least in part abnormal peripheral clearance of plasma FA, since impaired tissue FA uptake has been documented in humans with CD36 deficiency (161, 213, 220). A contribution of defective lipid processing by the small intestine to lipid abnormalities is strongly suggested by findings of postprandial lipemia and of high levels of apoB48 in CD36-deficient subjects (111).…”

Section: Fatty Acid and Sterol Traffickingmentioning

confidence: 99%

Role of the Gut in Lipid Homeostasis

Abumrad

Davidson

2012

Physiological Reviews

292

245

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Intestinal lipid transport plays a central role in fat homeostasis. Here we review the pathways regulating intestinal absorption and delivery of dietary and biliary lipid substrates, principally long-chain fatty acid, cholesterol, and other sterols. We discuss the regulation and functions of CD36 in fatty acid absorption, NPC1L1 in cholesterol absorption, as well as other lipid transporters including FATP4 and SRB1. We discuss the pathways of intestinal sterol efflux via ABCG5/G8 and ABCA1 as well as the role of the small intestine in high-density lipoprotein (HDL) biogenesis and reverse cholesterol transport. We review the pathways and genetic regulation of chylomicron assembly, the role of dominant restriction points such as microsomal triglyceride transfer protein and apolipoprotein B, and the role of CD36, l-FABP, and other proteins in formation of the prechylomicron complex. We will summarize current concepts of regulated lipoprotein secretion (including HDL and chylomicron pathways) and include lessons learned from families with genetic mutations in dominant pathways (i.e., abetalipoproteinemia, chylomicron retention disease, and familial hypobetalipoproteinemia). Finally, we will provide an integrative view of intestinal lipid homeostasis through recent findings on the role of lipid flux and fatty acid signaling via diverse receptor pathways in regulating absorption and production of satiety factors.

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“…Moreover, deregulation of proteins of carbohydrate metabolism, the actin cytoskeleton, and extracellular matrix remodeling were observed in DCM patients [65]. The association between Escherichia coli infection and DCM was established in a patient who was diagnosed as DCM after the onset of hemolytic uremic syndrome caused by pathogenic Escherichia coli infection [66]. In addition, leukocyte transendothelial migration was found to be pivotal to the inflammatory response [67], which could lead to direct injury or severe host disease, such as DCM [68].…”

Section: Resultsmentioning

confidence: 98%

Prioritizing Disease Candidate Proteins in Cardiomyopathy-Specific Protein-Protein Interaction Networks Based on “Guilt by Association” Analysis

Wan

Chen

et al. 2013

PLoS ONE

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The cardiomyopathies are a group of heart muscle diseases which can be inherited (familial). Identifying potential disease-related proteins is important to understand mechanisms of cardiomyopathies. Experimental identification of cardiomyophthies is costly and labour-intensive. In contrast, bioinformatics approach has a competitive advantage over experimental method. Based on “guilt by association” analysis, we prioritized candidate proteins involving in human cardiomyopathies. We first built weighted human cardiomyopathy-specific protein-protein interaction networks for three subtypes of cardiomyopathies using the known disease proteins from Online Mendelian Inheritance in Man as seeds. We then developed a method in prioritizing disease candidate proteins to rank candidate proteins in the network based on “guilt by association” analysis. It was found that most candidate proteins with high scores shared disease-related pathways with disease seed proteins. These top ranked candidate proteins were related with the corresponding disease subtypes, and were potential disease-related proteins. Cross-validation and comparison with other methods indicated that our approach could be used for the identification of potentially novel disease proteins, which may provide insights into cardiomyopathy-related mechanisms in a more comprehensive and integrated way.

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CD36 deficiency and absent myocardial iodine-123-(R,S)-15-(p-iodophenyl)-3-methylpentadecanoic acid uptake in a girl with cardiomyopathy

Cited by 11 publications

References 20 publications

The unprecedented nos gene cluster of Wolinella succinogenes encodes a novel respiratory electron transfer pathway to cytochrome c nitrous oxide reductase

The unprecedented nos gene cluster of Wolinella succinogenes encodes a novel respiratory electron transfer pathway to cytochrome c nitrous oxide reductase

Role of the Gut in Lipid Homeostasis

Prioritizing Disease Candidate Proteins in Cardiomyopathy-Specific Protein-Protein Interaction Networks Based on “Guilt by Association” Analysis

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