Does Rft1 flip an N-glycan lipid precursor?

Nature ◽  
2008 ◽  
Vol 454 (7204) ◽  
pp. E3-E4 ◽  
Author(s):  
Christian G. Frank ◽  
Sumana Sanyal ◽  
Jeffrey S. Rush ◽  
Charles J. Waechter ◽  
Anant K. Menon
Keyword(s):  
2014 ◽  
Vol 290 (7) ◽  
pp. 4225-4237 ◽  
Author(s):  
Santosh Phuyal ◽  
Tore Skotland ◽  
Nina Pettersen Hessvik ◽  
Helena Simolin ◽  
Anders Øverbye ◽  
...  
Keyword(s):  

2005 ◽  
Vol 47 (3) ◽  
pp. 633-642 ◽  
Author(s):  
Hongying Zheng ◽  
Richard I. Duclos ◽  
Conor C. Smith ◽  
Harrison W. Farber ◽  
Raphael A. Zoeller

2017 ◽  
Vol 23 (14) ◽  
pp. 3781-3793 ◽  
Author(s):  
Roopali Saxena ◽  
Chunhua Yang ◽  
Mukkavilli Rao ◽  
Ravi Chakra Turaga ◽  
Chakravarthy Garlapati ◽  
...  

2015 ◽  
Vol 309 (8) ◽  
pp. R805-R813 ◽  
Author(s):  
Nicholas V. DiPatrizio ◽  
Miki Igarashi ◽  
Vidya Narayanaswami ◽  
Conor Murray ◽  
Joseph Gancayco ◽  
...  

The endocannabinoids are lipid-derived signaling molecules that control feeding and energy balance by activating CB1-type cannabinoid receptors in the brain and peripheral tissues. Previous studies have shown that oral exposure to dietary fat stimulates endocannabinoid signaling in the rat small intestine, which provides positive feedback that drives further food intake and preference for fat-rich foods. We now describe an unexpectedly broader role for cholinergic signaling of the vagus nerve in the production of the endocannabinoid, 2-arachidonoyl- sn-glycerol (2-AG), in the small intestine. We show that food deprivation increases levels of 2-AG and its lipid precursor, 1,2-diacylglycerol, in rat jejunum mucosa in a time-dependent manner. This response is abrogated by surgical resection of the vagus nerve or pharmacological blockade of small intestinal subtype-3 muscarinic acetylcholine (m3 mAch) receptors, but not inhibition of subtype-1 muscarinic acetylcholine (m1 mAch). We further show that blockade of peripheral CB1 receptors or intestinal m3 mAch receptors inhibits refeeding in fasted rats. The results suggest that food deprivation stimulates 2-AG-dependent CB1 receptor activation through a mechanism that requires efferent vagal activation of m3 mAch receptors in the jejunum, which, in turn, may promote feeding after a fast.


2003 ◽  
Vol 20 (1) ◽  
pp. 35-46 ◽  
Author(s):  
B. Jouzel ◽  
A.-L. Pennarun ◽  
C. Prost ◽  
D. Renard ◽  
D. Poncelet ◽  
...  

2020 ◽  
Vol 20 (5) ◽  
Author(s):  
Mike F Renne ◽  
Xue Bao ◽  
Anton I P M de Kroon

Abstract The presence of the water soluble glycerophospholipid precursors choline and inositol in culture media highly affects lipid biosynthesis and regulation thereof. We report that widely used media ingredients contain trace amounts of choline and inositol that are not mentioned on the product label, influencing experimental outcome.


2004 ◽  
Vol 279 (19) ◽  
pp. 19614-19627 ◽  
Author(s):  
Isabella Imhof ◽  
Isabelle Flury ◽  
Christine Vionnet ◽  
Carole Roubaty ◽  
Diane Egger ◽  
...  

In humans andSaccharomyces cerevisiaethe free glycosylphosphatidylinositol (GPI) lipid precursor contains several ethanolamine phosphate side chains, but these side chains had been found on the protein-bound GPI anchors only in humans, not yeast. Here we confirm that the ethanolamine phosphate side chain added by Mcd4p to the first mannose is a prerequisite for the addition of the third mannose to the GPI precursor lipid and demonstrate that, contrary to an earlier report, an ethanolamine phosphate can equally be found on the majority of yeast GPI protein anchors. Curiously, the stability of this substituent during preparation of anchors is much greater ingpi7Δsec18double mutants than in either single mutant or wild type cells, indicating that the lack of a substituent on the second mannose (caused by the deletion ofGPI7) influences the stability of the one on the first mannose. The phosphodiester-linked substituent on the second mannose, probably a further ethanolamine phosphate, is added to GPI lipids by endoplasmic reticulum-derived microsomesin vitrobut cannot be detected on GPI proteins of wild type cells and undergoes spontaneous hydrolysis in saline. Genetic manipulations to increase phosphatidylethanolamine levels ingpi7Δ cells by overexpression ofPSD1restore cell growth at 37 °C without restoring the addition of a substituent to Man2. The three putative ethanolamine-phosphate transferases Gpi13p, Gpi7p, and Mcd4p cannot replace each other even when overexpressed. Various models trying to explain how Gpi7p, a plasma membrane protein, directs the addition of ethanolamine phosphate to mannose 2 of the GPI core have been formulated and put to the test.


2003 ◽  
Vol 20 (1) ◽  
pp. 35-46 ◽  
Author(s):  
B. Jouzel ◽  
A.-L. Pennarun ◽  
C. Prost ◽  
D. Renard ◽  
D. Poncelet ◽  
...  

1993 ◽  
Vol 294 (3) ◽  
pp. 635-638 ◽  
Author(s):  
A Tabernero ◽  
J P Bolaños ◽  
J M Medina

The rate of synthesis of phospholipid and sterol species from L-lactate in neurons and astrocytes in primary culture was studied. Both types of cells actively utilized lactate as lipid precursor, although the rate of lipogenesis was about 2-fold greater in astrocytes than in neurons. The incorporation of lactate into phospholipids was significantly higher than that into sterols in both types of cells, but the ratio of phospholipid/sterol synthesis was much higher in astrocytes than in neurons. Phosphatidylcholine (PC) was the main phospholipid synthesized in both types of cells, followed by phosphatidylethanolamine (PE), phosphatidylserine and phosphatidylinositol. No detectable synthesis of sphingomyelins was observed. The ratio of PC/PE synthesis was about 2-fold higher in astrocytes than in neurons. The main sterol synthesized in neurons was lanosterol, followed by desmosterol. However, the main sterol synthesized in astrocytes was desmosterol, followed by lanosterol and cholesterol. The different ratios of phospholipid/sterol and PC/PE synthesis found in neurons and astrocytes may result in different membrane fluidity being higher in astrocytes than in neurons. This may be associated with differences in the functionality of both types of cells.


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