Cellular binding proteins for fatty acids and retinoids: similar or specialized functions?

1993 ◽  
pp. 191-202
Author(s):  
Nathan M. Bass
Keyword(s):  
Fatty Acids ◽  
Binding Proteins

scholarly journals Interaction of fatty acids with recombinant rat intestinal and liver fatty acid-binding proteins

1991 ◽  
Vol 286 (1) ◽  
pp. 300-309 ◽  
Author(s):  
Gyorgy Nemecz ◽  
Timothy Hubbell ◽  
John R. Jefferson ◽  
John B. Lowe ◽  
Friedhelm Schroeder
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Binding Proteins ◽  
Fatty Acid Binding Proteins ◽  
Liver Fatty Acid ◽  
Fatty Acid Binding

scholarly journals Fatty acid binding proteins have the potential to channel dietary fatty acids into enterocyte nuclei

2015 ◽  
Vol 57 (2) ◽  
pp. 219-232 ◽  
Author(s):  
Adriana Esteves ◽  
Anja Knoll-Gellida ◽  
Lucia Canclini ◽  
Maria Cecilia Silvarrey ◽  
Michèle André ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Binding Proteins ◽  
Dietary Fatty Acids ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding

Fatty acid binding sites of rodent adipocyte and heart fatty acid binding proteins: characterization using fluorescent fatty acids

Biochemistry ◽  
1990 ◽  
Vol 29 (40) ◽  
pp. 9305-9311 ◽  
Author(s):  
Margo G. Wootan ◽  
Nathan M. Bass ◽  
David A. Bernlohr ◽  
Judith Storch
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Binding Sites ◽  
Binding Proteins ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding

The intestine as source of cytotoxic mediators in shock: free fatty acids and degradation of lipid-binding proteins

2008 ◽  
Vol 294 (4) ◽  
pp. H1779-H1792 ◽  
Author(s):  
Alexander H. Penn ◽  
Geert W. Schmid-Schönbein
Keyword(s):  
Fatty Acids ◽  
Cell Death ◽  
Small Intestine ◽  
Free Fatty Acids ◽  
Binding Proteins ◽  
Arterial Occlusion ◽  
Lipid Binding ◽  
Protein Fractions ◽  
Intestinal Lumen ◽  
Fatty Acid Binding

Shock and multiple organ failure remain primary causes of late-stage morbidity and mortality in victims of trauma. During shock, the intestine is subject to extensive cell death and is the source of inflammatory factors that cause multiorgan failure. We ( 34 ) showed previously that ischemic, but not nonischemic, small intestines and pancreatic protease digested homogenates of normal small intestine can generate cytotoxic factors capable of killing naive cells within minutes. Using chloroform/methanol separation of rat small intestine homogenates into lipid fractions and aqueous and sedimented protein fractions and measuring cell death caused by those fractions, we found that the cytotoxic factors are lipid in nature. Recombining the lipid fraction with protein fractions prevented cell death, except when homogenates were protease digested. Using a fluorescent substrate, we found high levels of lipase activity in intestinal homogenates and cytotoxic levels of free fatty acids. Addition of albumin, a lipid binding protein, prevented cell death, unless the albumin was previously digested with protease. Homogenization of intestinal wall in the presence of the lipase inhibitor orlistat prevented cell death after protease digestion. In vivo, orlistat plus the protease inhibitor aprotinin, administered to the intestinal lumen, significantly improved survival time compared with saline in a splanchnic arterial occlusion model of shock. These results indicate that major cytotoxic mediators derived from an intestine under in vitro conditions are free fatty acids. Breakdown of free fatty acid binding proteins by proteases causes release of free fatty acids to act as powerful cytotoxic mediators.

scholarly journals Possible Role of Fatty Acids in Milk as the Regulator of the Expression of Cytosolic Binding Proteins for Fatty Acids and Vitamin A through PPAR.ALPHA. in Developing Rats

2007 ◽  
Vol 53 (6) ◽  
pp. 515-521 ◽  
Author(s):  
Kazuki MOCHIZUKI ◽  
Hiroko MOCHIZUKI ◽  
Hiroko KAWAI ◽  
Yuko OGURA ◽  
Masaya SHIMADA ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Vitamin A ◽  
Binding Proteins

Liver cytosolic fatty acids binding proteins in rats and Psammomys obesus: modulation in diabetes

1986 ◽  
Vol 83 (4) ◽  
pp. 837-839
Author(s):  
Ruth Brandes ◽  
Ruth Tsur ◽  
Rivka Arad ◽  
Jonathan H. Adler
Keyword(s):  
Fatty Acids ◽  
Binding Proteins ◽  
Psammomys Obesus

Mutant huntingtin interacts with the sterol regulatory element-binding proteins and impairs their nuclear import

2019 ◽  
Vol 29 (3) ◽  
pp. 418-431 ◽  
Author(s):  
Alba Di Pardo ◽  
John Monyror ◽  
Luis Carlos Morales ◽  
Vaibhavi Kadam ◽  
Susanne Lingrell ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Nuclear Import ◽  
Binding Proteins ◽  
Neurodegenerative Disorder ◽  
Regulatory Element ◽  
Cholesterol Homeostasis ◽  
Mutant Huntingtin ◽  
Underlying Causes ◽  
Sterol Regulatory Element ◽  
Nuclear Levels

Abstract Brain cholesterol homeostasis is altered in Huntington’s disease (HD), a neurodegenerative disorder caused by the expansion of a CAG nucleotide repeat in the HTT gene. Genes involved in the synthesis of cholesterol and fatty acids were shown to be downregulated shortly after the expression of mutant huntingtin (mHTT) in inducible HD cells. Nuclear levels of the transcription factors that regulate lipid biogenesis, the sterol regulatory element-binding proteins (SREBP1 and SREBP2), were found to be decreased in HD models compared to wild-type, but the underlying causes were not known. SREBPs are synthesized as inactive endoplasmic reticulum-localized precursors. Their mature forms (mSREBPs) are generated upon transport of the SREBP precursors to the Golgi and proteolytic cleavage, and are rapidly imported into the nucleus by binding to importin β. We show that, although SREBP2 processing into mSREBP2 is not affected in YAC128 HD mice, mSREBP2 is mislocalized to the cytoplasm. Chimeric mSREBP2-and mSREBP1-EGFP proteins are also mislocalized to the cytoplasm in immortalized striatal cells expressing mHTT, in YAC128 neurons and in fibroblasts from HD patients. We further show that mHTT binds to the SREBP2/importin β complex required for nuclear import and sequesters it in the cytoplasm. As a result, HD cells fail to upregulate cholesterogenic genes under sterol-depleted conditions. These findings provide mechanistic insight into the downregulation of genes involved in the synthesis of cholesterol and fatty acids in HD models, and have potential implications for other pathways modulated by SREBPs, including autophagy and excitotoxicity.

The binding affinity of fatty acid-binding proteins from human, pig and rat liver for different fluorescent fatty acids and other ligands

1989 ◽  
Vol 21 (4) ◽  
pp. 407-418 ◽  
Author(s):  
Roger A. Peeters ◽  
Monique A.P.M. in't Groen ◽  
Marielle P. de Moel ◽  
Herman T.B. Van Moerkerk ◽  
Jacques H. Veerkamp
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Binding Affinity ◽  
Rat Liver ◽  
Binding Proteins ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding
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