The adiponectin receptor AdipoR2 and its Caenorhabditis elegans homolog PAQR-2 prevent membrane rigidification by exogenous saturated fatty acids

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The adiponectin receptor AdipoR2 and its Caenorhabditis elegans homolog PAQR-2 prevent membrane rigidification by exogenous saturated fatty acids

Dietary fatty acids can be incorporated directly into phospholipids. This poses a specific challenge to cellular membranes since their composition, hence properties, could greatly vary with different diets. That vast variations in diets are tolerated therefore implies the existence of regulatory mechanisms that monitor and regulate membrane compositions. Here we show that the adiponectin recept...

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The Adiponectin Receptor Homologs in C. elegans Promote Energy Utilization and Homeostasis

Adiponectin is an adipokine with insulin-sensitising actions in vertebrates. Its receptors, AdipoR1 and AdipoR2, are PAQR-type proteins with 7-transmembrane domains and topologies reversed that of GPCR's, i.e. their C-termini are extracellular. We identified three adiponectin receptor homologs in the nematode C. elegans, named paqr-1, paqr-2 and paqr-3. These are differently expressed in the in...

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PAQR-2 Regulates Fatty Acid Desaturation during Cold Adaptation in C. elegans

C. elegans PAQR-2 is homologous to the insulin-sensitizing adiponectin receptors in mammals, and essential for adaptation to growth at 15°C, a low but usually acceptable temperature for this organism. By screening for novel paqr-2 suppressors, we identified mutations in genes involved in phosphatidylcholine synthesis (cept-1, pcyt-1 and sams-1) and fatty acid metabolism (ech-7, hacd-1, mdt-15, ...

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Polyunsaturated fatty acids and neurotransmission in Caenorhabditis elegans.

Changes in PUFA (polyunsaturated fatty acid) metabolism can cause mental retardation and cognitive impairment. However, it is still unclear why altered levels of PUFAs result in neuronal dysfunction. Recent studies on the nematode Caenorhabditis elegans suggest that PUFA depletion may cause cognitive impairment by compromising communication among neurons. Pharmacological and electrophysiologica...

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ژورنال

عنوان ژورنال: PLOS Genetics

سال: 2017

ISSN: 1553-7404

DOI: 10.1371/journal.pgen.1007004