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Relevant bibliographies by topics / H-Fatty Acid Binding Protein

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Academic literature on the topic 'H-Fatty Acid Binding Protein'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "H-Fatty Acid Binding Protein"

1

FUJII, Hiroshi. "Fatty Acid-binding Proteins: Their Structure, Function and Gene Expression." Journal of Japan Atherosclerosis Society 24, no. 7-8 (1996): 353–61. http://dx.doi.org/10.5551/jat1973.24.7-8_353.

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ZIMMERMAN, Aukje W., Martin RADEMACHER, Heinz RüTERJANS, Christian LüCKE, and Jacques H. VEERKAMP. "Functional and conformational characterization of new mutants of heart fatty acid-binding protein." Biochemical Journal 344, no. 2 (November 24, 1999): 495–501. http://dx.doi.org/10.1042/bj3440495.

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In this study we investigated the possible involvement of several amino acids (not located in the ligand-binding centre) in fatty acid binding and conformational stability of heart fatty acid-binding protein (H-FABP). We prepared recombinant human H-FABP proteins with mutations in the hydrophobic patch (Phe4, Trp8 and Phe64), portal region (Phe16), hinge region (Leu66, Gly67), second portal region (Glu72) and at the protein surface (Lys21) respectively. Oleic acid-binding affinity and conformational stability of human H-FABP are significantly decreased or completely lost by mutation of Trp8 or Phe16. NMR spectra confirmed that these residues are important for the stability of the protein fold. Substitution of Phe4 or Phe64 resulted in less stability, but oleic acid-binding affinity was not affected. Mutation of Lys21 had no effect on either structural integrity or fatty acid-binding affinity. Replacement of Leu66 or Gly67 did not affect fatty acid binding, but protein stability was reduced. Finally, mutation of Glu72 to Ser caused no change of affinity, but NMR spectra and urea-denaturation curves showed the extremely poor stability of this mutant. In conclusion, no relationship was observed between fatty acid-binding affinity and conformational stability.

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Wilkinson, T. C., and D. C. Wilton. "Studies on fatty acid-binding proteins. The binding properties of rat liver fatty acid-binding protein." Biochemical Journal 247, no. 2 (October 15, 1987): 485–88. http://dx.doi.org/10.1042/bj2470485.

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1. The fluorescent fatty acid probe 11-(dansylamino)undecanoic acid binds to rat liver fatty acid-binding protein with a 1:1 stoichiometry. 2. The binding of the fluorescent probe is competitive with long-chain fatty acids. 3. Binding displacement studies were performed with a wide range of fatty acids and other ligands and identified C16 and C18 fatty acids as the preferred fatty acids for rat liver fatty acid-binding protein. No preference was observed for unsaturated fatty acids within this group. 4. Fatty acyl-CoA binds less well than the corresponding fatty acid.

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Carey, J. O., P. D. Neufer, R. P. Farrar, J. H. Veerkamp, and G. L. Dohm. "Transcriptional regulation of muscle fatty acid-binding protein." Biochemical Journal 298, no. 3 (March 15, 1994): 613–17. http://dx.doi.org/10.1042/bj2980613.

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Heart fatty acid-binding protein (H-FABP) is present in a wide variety of tissues but is found in the highest concentration in cardiac and red skeletal muscle. It has been proposed that the expression of H-FABP correlates directly with the fatty acid-oxidative capacity of the tissue. In the present study, the expression of H-FABP was measured in red and white skeletal muscle under two conditions in which fatty acid utilization is known to be increased: streptozotocin-induced diabetes and fasting. Protein concentration, mRNA concentration and transcription rate were measured under both conditions. The level of both protein and mRNA increased approximately 2-fold under each condition. The transcription rate was higher in red skeletal muscle than in white muscle, was increased 2-fold during fasting, but was unchanged by streptozotocin-induced diabetes. In addition to supporting the hypothesis that H-FABP is induced during conditions of increased fatty acid utilization, these findings demonstrate that the regulation of H-FABP expression may or may not be at the level of transcription depending on the stimulus.

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LÜCKE, Christian, Martin RADEMACHER, Aukje W. ZIMMERMAN, Herman T. B. VAN MOERKERK, Jacques H. VEERKAMP, and Heinz RÜTERJANS. "Spin-system heterogeneities indicate a selected-fit mechanism in fatty acid binding to heart-type fatty acid-binding protein (H-FABP)." Biochemical Journal 354, no. 2 (February 22, 2001): 259–66. http://dx.doi.org/10.1042/bj3540259.

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Recent advances in the characterization of fatty acid-binding proteins (FABPs) by NMR have enabled various research groups to investigate the function of these proteins in aqueous solution. The binding of fatty acid molecules to FABPs, which proceeds through a portal region on the protein surface, is of particular interest. In the present study we have determined the three-dimensional solution structure of human heart-type FABP by multi-dimensional heteronuclear NMR spectroscopy. Subsequently, in combination with data collected on a F57S mutant we have been able to show that different fatty acids induce distinct conformational states of the protein backbone in this portal region, depending on the chain length of the fatty acid ligand. This indicates that during the binding process the protein accommodates the ligand molecule by a ‘selected-fit’ mechanism. In fact, this behaviour appears to be especially pronounced in the heart-type FABP, possibly due to a more rigid backbone structure compared with other FABPs, as suggested by recent NMR relaxation studies. Thus differences in the dynamic behaviours of these proteins may be the key to understanding the variations in ligand affinity and specificity within the FABP family.

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PRINSEN, Clemens F. M., and Jacques H. VEERKAMP. "Fatty acid binding and conformational stability of mutants of human muscle fatty acid-binding protein." Biochemical Journal 314, no. 1 (February 15, 1996): 253–60. http://dx.doi.org/10.1042/bj3140253.

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Human muscle fatty acid-binding protein (M-FABP) is a 15 kDa cytosolic protein which may be involved in fatty acid transfer and modulation of non-esterified fatty acid concentration in heart, skeletal muscle, kidney and many other tissues. Crystallographic studies have suggested the importance of the amino acids Thr-40, Arg-106, Arg-126 and Tyr-128 for the hydrogen bonding network of the fatty acid carboxylate group. Two phenylalanines at 16 and 57 are positioned to interact with the acyl chain of the fatty acid. We prepared 13 mutant proteins by site-directed mutagenesis and tested them for fatty acid binding and stability. Substitution of amino acids Phe-16, Arg-106 or Arg-126 created proteins which showed a large decrease in or complete loss of oleic acid binding. Substitution of Phe-57 by Ser or Val and of Tyr-128 by Phe had no great effect. The stability of the mutant proteins was tested by denaturation studies on the basis of fatty acid binding or tryptophan fluorescence and compared with that of the wild-type M-FABP. There was no direct relationship between fatty acid-binding activity and stability. Less stable mutants (F57S and Y128F) did not show a marked change in fatty acid-binding activity. Substitution of Arg-126 by Gln or Arg-106 by Thr eliminated binding activity, but the former mutant protein showed wild-type stability, in contrast to the latter. The results are in agreement with crystallographic data.

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Shearer, Jane, Patrick T. Fueger, Jeffrey N. Rottman, Deanna P. Bracy, Bert Binas, and David H. Wasserman. "Heart-type fatty acid-binding protein reciprocally regulates glucose and fatty acid utilization during exercise." American Journal of Physiology-Endocrinology and Metabolism 288, no. 2 (February 2005): E292—E297. http://dx.doi.org/10.1152/ajpendo.00287.2004.

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The role of heart-type cytosolic fatty acid-binding protein (H-FABP) in mediating whole body and muscle-specific long-chain fatty acid (LCFA) and glucose utilization was examined using exercise as a phenotyping tool. Catheters were chronically implanted in a carotid artery and jugular vein of wild-type (WT, n = 8), heterozygous (H-FABP+/−, n = 8), and null (H-FABP−/−, n = 7) chow-fed C57BL/6J mice, and mice were allowed to recover for 7 days. After a 5-h fast, conscious, unrestrained mice were studied during 30 min of treadmill exercise (0.6 mph). A bolus of [125I]-15-( p-iodophenyl)-3- R, S-methylpentadecanoic acid and 2-deoxy-[3H]glucose was administered to obtain rates of whole body metabolic clearance (MCR) and indexes of muscle LCFA (Rf) and glucose (Rg) utilization. Fasting, nonesterified fatty acids (mM) were elevated in H-FABP−/− mice (2.2 ± 0.9 vs. 1.3 ± 0.1 and 1.3 ± 0.2 for WT and H-FABP+/−). During exercise, blood glucose (mM) increased in WT (11.7 ± 0.8) and H-FABP+/− (12.6 ± 0.9) mice, whereas H-FABP−/− mice developed overt hypoglycemia (4.8 ± 0.8). Examination of tissue-specific and whole body glucose and LCFA utilization demonstrated a dependency on H-FABP with exercise in all tissues examined. Reductions in H-FABP led to decreasing exercise-stimulated Rf and increasing Rg with the most pronounced effects in heart and soleus muscle. Similar results were seen for MCR with decreasing LCFA and increasing glucose clearance with declining levels of H-FABP. These results show that, in vivo, H-FABP has reciprocal effects on glucose and LCFA utilization and whole body fuel homeostasis when metabolic demands are elevated by exercise.

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Tso, P., A. Nauli, and C. M. Lo. "Enterocyte fatty acid uptake and intestinal fatty acid-binding protein." Biochemical Society Transactions 32, no. 1 (February 1, 2004): 75–78. http://dx.doi.org/10.1042/bst0320075.

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This article reviews our current understanding of the uptake of fatty acids by the enterocytes of the intestine. The micellar solubilization of fatty acids by bile salts and the factors regulating that process are discussed. The mechanism of how micellar solubilization of fatty acids promotes the uptake of fatty acids by enterocytes and their relative importance is reviewed. Additionally, discussion of the various fatty acid transporters located at the brush border membrane of the enterocytes is included. Finally, a summary of our current understanding of the function of fatty-acid-binding proteins inside enterocytes is provided.

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Zanotti, Giuseppe. "Muscle fatty acid-binding protein." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1441, no. 2-3 (November 1999): 94–105. http://dx.doi.org/10.1016/s1388-1981(99)00163-8.

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Bronský, Jiří, Michal Karpíšek, Eva Bronská, Marta Pechová, Barbora Jančíková, Hana Kotolová, David Stejskal, Richard Průša, and Jiří Nevoral. "Adiponectin, Adipocyte Fatty Acid Binding Protein, and Epidermal Fatty Acid Binding Protein: Proteins Newly Identified in Human Breast Milk." Clinical Chemistry 52, no. 9 (September 1, 2006): 1763–70. http://dx.doi.org/10.1373/clinchem.2005.063032.

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Abstract Background: Breastfeeding may protect children from developing metabolic syndrome and other diseases later in life. We investigated novel proteins in human breast milk that might play a role in this process. Methods: We used ELISA to measure adiponectin, adipocyte and epidermal fatty acid binding proteins (AFABP, EFABP), and leptin concentrations in human breast milk obtained from 59 mothers 48 h after initiation of lactation. Using a questionnaire and medical records, we collected information about the mothers and newborns. Results: Mean (SE) adiponectin concentrations in breast milk were 13.7 (0.8), range 3.9–30.4 μg/L; AFABP concentrations 26.7 (4.4), range 1.2–137.0 μg/L; EFABP concentrations 18.1 (1.4), range 0.8–47.0 μg/L; and leptin concentrations 0.50 (0.05), range 0–1.37 μg/L. We found a significant correlation between AFABP and EFABP concentrations (r = 0.593, P <0.0001). Maternal EFABP concentrations were significantly higher in mothers who delivered boys than in those who delivered girls [21.7 (2.3) vs 15.4 (1.7) μg/L, P = 0.028] and correlated with newborn birth weight (r = 0.266, P = 0.045). Maternal leptin correlated with body weight before pregnancy (r = 0.272, P = 0.043) and at delivery (r = 0.370, P = 0.005), body mass index before pregnancy (r = 0.397, P = 0.003) and at delivery (r = 0.498, P <0.0001), body weight gain during pregnancy (r = 0.267, P = 0.047), and newborn gestational age (r = 0.266, P = 0.048). Leptin was significantly lower in mothers who delivered preterm vs term babies [0.30 (0.09) vs 0.60 (0.05) ug/L, P = 0.026]. Conclusions: Concentrations of adiponectin, AFABP, and EFABP in human breast milk are related to nutritional variables of mothers and newborns and thus may play a role in the protective effects of breastfeeding.

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Dissertations / Theses on the topic "H-Fatty Acid Binding Protein"

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Sheridan, Mary T. "Studies of fatty acid binding protein." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235759.

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Vork, Michaël Maria. "Fatty acid-binding protein in rat heart." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1993. http://arno.unimaas.nl/show.cgi?fid=6232.

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Proefschrift Maastricht.
Samenvatting in het Nederlands. Ten dele eerder verschenen en nog te verschijnen art. Auteursnaam op rug en omslag: Michaël Vork. Met lit. opg. en een samenvatting in het Nederlands.

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Evans, Carol. "Studies on rat liver fatty acid-binding protein." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385122.

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Priyananda, Pramith School of Chemical Engineering &amp Industrial Chemistry UNSW. "Protein and fatty acid interactions during ultrafiltration." Awarded by:University of New South Wales. School of Chemical Engineering and Industrial Chemistry, 2006. http://handle.unsw.edu.au/1959.4/24310.

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Proteins and fatty acids often exist in solutions containing biological matter that are treated with membranes. These proteins and fatty acids interact with each other as well as with the membranes thereby affecting the flux. Binding of fatty acids to proteins results in complexes that are much larger than fatty acid molecules. Exploitation of this size difference to remove difficult to separate fatty acids from aqueous solutions by ultrafiltration was investigated in this study. In addition, the fouling of membrane by the protein-fatty acid mixtures containing free dissolved fatty acids was studied using bovine albumin (BSA)-caprylic system. Binding of caprylic acid to native and pasteurized BSA was examined by diafiltering pre equilibrated fatty acid-BSA mixtures. The rate of mass transfer of fatty acid molecules through boundary film surrounding the protein molecules was estimated using a BSA solution as the adsorbent phase in an agitated column. A stirred cell fitted with a polyethersulfone membrane (30 kDa) was used for the diafiltrations. Accumulation of fatty acid in the BSA layers fouled on the membrane was also estimated. Binding studies indicate that a native BSA molecule (at pH 6.8) could bind 7 fatty acid molecules in specific binding cavities while approximately 44 molecules are bound onto the surface. When BSA was pasteurized the specific binding decreased from 7 to 2 indicating unfolding of the molecule. In addition, the total binding capacity decreased from 44 to 24 moles/BSA mole and the rate of mass transfer decreased from 4.5/min to 3.6/min, indicating heat induced aggregation of BSA. At alkaline pH levels fatty acid anion acts as an anionic surfactant stabilizing the molecular conformation of the protein and reducing fouling. When pH was lowered to 3, flux severely declined. Unusually large accumulation of fatty acid in the deposited protein layers (caprylic/BSA ~ 10,000 moles) occurred indicating capillary condensation of undissociated fatty acids in the protein layer. Agitated column studies showed that proteins could be used as an adsorbent to remove hard to separate dissolved fatty acids from aqueous solutions. The separated protein-fatty acid complex may be further processed to manufacture animal feed.

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Peet, Daniel J. "Protein-bound fatty acids in mammalian hair fibres /." Connect to thesis, 1994. http://eprints.unimelb.edu.au/archive/00000641.

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Hagan, Robert Mark. "Liver fatty acid binding protein : relating structure to function." Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437109.

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Hopf, Lisa-Marie. "Regulation von Adipocyte fatty acid binding protein in Abhängigkeit der Nierenfunktion." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-197266.

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Adipositas und die damit verbundenen Folgeerkrankungen sind eine der zentralen Gesund-heitsherausforderungen unserer Zeit. Dauerhafte Adipositas führt zu einer Dysregulation fettgewebseigener Peptidhormone. Diese sogenannten Adipokine stellen ein Verbindungsglied zwischen Fettgewebsakkumulation und den vielfältigen Adipositaskomplikationen des gesamten Organismus dar. Adipocyte fatty acid binding protein (AFABP) wurde in den letzten Jahren als zirkulierendes Adipokin mit diabetogenen, proinflammatorischen und proateriosklerotischen Effekten etabliert. Zu Beginn der Dissertation lagen unzureichende Erkenntnisse über die Elimination von AFABP sowie die Regulation des Adipokins bei eingeschränkter Nierenfunktion vor. Aus diesem Grund untersucht die vorliegende Arbeit die AFABP-Regulation in Abhängigkeit von der Nierenfunktion in 532 Patienten mit chronischer Niereninsuffizienz (Studienpopulation 1) und 32 Patienten mit akuter Nierenfunktionsverminderung nach Nephrektomie (Studienpopulation 2). In beiden Kohorten stiegen die medianen AFABP-Serumkonzentrationen mit abfallender Nierenfunktion an. Zudem waren Marker der Nierenfunktion in beiden Studienpopulationen die stärksten unabhängigen Prädiktoren für zirkulierendes AFABP. Untersuchungen aus der Arbeitsgruppe zur AFABP-Regulation in einem Rattenmodell der akuten Niereninsuffizienz unterstützen die klinischen Studienergebnisse. Zusammenfassend zeigen diese Ergebnisse zum ersten Mal signifikant steigende AFABP-Serumspiegel bei chronischer und akuter Nierenfunktionsstörung, sowie bei akutem Abfall der Nierenfunktion. Diese Befunde stützen die Hypothese, dass AFABP renal eliminiert wird. Inwiefern AFABP darüber hinaus in die Pathogenese der chronischen Niereninsuffizienz eingreift, muss in weiterführenden Studien beleuchtet werden.

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Adhikari, Sean. "Glucose oxidation in heart-type fatty acid binding protein null mice." Texas A&M University, 2006. http://hdl.handle.net/1969.1/4391.

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Heart-type fatty acid binding protein (H-FABP) is a major fatty acid binding factor in skeletal muscles. Genetic lack of H-FABP severely impairs the esterification and oxidation of exogenous fatty acids in soleus muscles isolated from chow-fed mice (CHOW-solei) and high fat diet-fed mice (HFD-solei), and prevents the HFD-induced accumulation of muscle triglycerides. Here, we examined the impact of H-FABP deficiency on the relationship between fatty acid utilization and glucose oxidation. Glucose oxidation was measured in isolated soleus muscles in the presence or absence of 1 mM palmitate (simple protocol) or in the absence of fatty acid after preincubation with 1 mM palmitate (complex protocol). With the simple protocol, the mutation slightly reduced glucose oxidation in CHOW-muscles, but markedly increased it in HFDmuscles; unexpectedly, this pattern was not altered by the addition of palmitate, which reduced glucose oxidation in both CHOW- and HFD-solei irrespective of the mutation. In the complex protocol, the mutation first inhibited the synthesis and accumulation of triglycerides and then their mobilization; with this protocol, the mutation increased glucose oxidation in both CHOW- and HFD-solei. We conclude: (i) H-FABP mediates a non-acute inhibition of muscle glucose oxidation by fatty acids, likely by enabling both the accumulation and mobilidoes not mediate the acute inhibitory effect of extracellular fatty acids on muscle glucose oxidation; (iii) H-FABP affects muscle glucose oxidation in opposing ways, with inhibition prevailing at high muscle triglyceride contents.zation of a critical mass of muscle triglycerides; (ii) H-FABP

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Wilkinson, T. C. I. "A study of the fatty acid-binding protein of rat liver." Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374448.

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Li, Huiying. "Adipocyte fatty acid-binding protein : a link between inflammation and vascular dysfunction /." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B44248714.

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Books on the topic "H-Fatty Acid Binding Protein"

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Glatz, Jan F. C., and Ger J. Van Der Vusse, eds. Cellular Fatty Acid-binding Proteins. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0.

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Glatz, Jan F. C., and Ger J. van der Vusse, eds. Cellular Fatty Acid-Binding Proteins II. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3096-1.

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C, Glatz Jan F., and Vusse, G. J. van der., eds. Cellular fatty acid-binding proteins: Proceedings of the 2nd International Workshop on Fatty Acid-Binding Proteins, Maastricht, August 31 and September 1, 1992. Dordrecht: Kluwer Academic Publishers, 1993.

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Huang, Wei-chün. Structural studies of enzymes in biotin and fatty acid biosynthesis. Uppsala: Dept. of Molecular Biology, Swedish University of Agricultural Sciences, 1996.

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C, Glatz Jan F., and Vusse, G. J. van der., eds. Cellular fatty-acid binding proteins. Dordrecht: Kluwer Academic Publishers, 1990.

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Jan F.C. Glatz (Editor) and Ger J. van der Vusse (Editor), eds. Cellular Fatty-Acid Binding Proteins (Developments in Molecular and Cellular Biochemistry). Springer, 2007.

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Glatz, Jan F. C., and A. T. M. Jansen. Cellular Lipid Binding Proteins. Springer London, Limited, 2012.

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Cellular Lipid Binding Proteins. Springer, 2011.

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C, Glatz Jan F., ed. Cellular lipid binding proteins. Dordrecht: Kluwer Academic Pub., 2002.

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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B7 (biotin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0011.

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Biotin is a water-soluble B vitamin (vitamin B7) which acts as a coenzyme to carboxylases and has roles in gluconeogenesis, fatty acid synthesis, and amino acid catabolism. Reduced activity of biotin-dependent enzymes (acetyl-CoA carboxylase I and II, and propionyl-CoA carboxylase) alters lipid metabolism and may impair synthesis of polyunsaturated fatty acids and prostaglandins; in addition, biotin has effects on gene expression by binding covalently to histones. Deficiency can be caused by prolonged consumption of egg whites, which contain the biotin-binding protein avidin. Smoking accelerates the degradation of biotin, which can result in marginal biotin deficiency. The effects of deficiency include disruption of immune function and lipid metabolism, with some evidence of teratogenicity in animals. Dietary deficiency is unlikely, although high consumption of egg whites should be avoided in pregnancy.

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Book chapters on the topic "H-Fatty Acid Binding Protein"

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Lassen, Dirck, Christian Lücke, Arno Kromminga, Axel Lezius, Friedrich Spener, and Heinz Rüterjans. "Solution structure of bovine heart fatty acid-binding protein (H-FABPC)." In Cellular Fatty Acid-Binding Proteins II, 15–22. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3096-1_3.

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Lefèvre, G. "Le h-FABP (Heart Fatty Acid Binding Protein)." In Les biomarqueurs en médecine d’urgence, 121–26. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0297-8_16.

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Fournier, N. C., and M. A. Richard. "Role of fatty acid-binding protein in cardiac fatty acid oxidation." In Cellular Fatty Acid-binding Proteins, 149–59. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_19.

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Knudsen, Jens. "Acyl-CoA-binding protein (ACBP) and its relation to fatty acid-binding protein (FABP): an overview." In Cellular Fatty Acid-binding Proteins, 217–23. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_27.

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Börchers, Torsten, Peter Højrup, Søren U. Nielsen, Peter Roepstorff, Friedrich Spener, and Jens Knudsen. "Revision of the amino acid sequence of human heart fatty acid-binding protein." In Cellular Fatty Acid-binding Proteins, 127–33. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_16.

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Oudenampsen, Elke, Eva-Maria Kupsch, Thomas Wissel, Friedrich Spener, and Axel Lezius. "Expression of fatty acid-binding protein from bovine heart in Escherichia coli." In Cellular Fatty Acid-binding Proteins, 75–79. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_10.

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Vergani, Lodovica, Marina Fanin, Andrea Martinuzzi, Andrea Galassi, Andrea Appi, Rosalba Carrozzo, Maurizio Rosa, and Corrado Angelini. "Liver fatty acid-binding protein in two cases of human lipid storage." In Cellular Fatty Acid-binding Proteins, 225–30. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_28.

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Veerkamp, J. H., R. J. A. Paulussen, R. A. Peeters, R. G. H. J. Maatman, H. T. B. van Moerkerk, and T. H. M. S. M. van Kuppevelt. "Detection, tissue distribution and (sub)cellular localization of fatty acid-binding protein types." In Cellular Fatty Acid-binding Proteins, 11–18. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_2.

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Sacchettini, James C., Leonard J. Banaszak, and Jeffrey I. Gordon. "Expression of rat intestinal fatty acid binding protein in E. coli and its subsequent structural analysis: a model system for studying the molecular details of fatty acid-protein interaction." In Cellular Fatty Acid-binding Proteins, 81–93. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_11.

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Scapin, Giovanna, Paola Spadon, Mario Mammi, Giuseppe Zanotti, and Hugo L. Monaco. "Crystal structure of chicken liver basic fatty acid-binding protein at 2.7 Å resolution." In Cellular Fatty Acid-binding Proteins, 95–99. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_12.

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Conference papers on the topic "H-Fatty Acid Binding Protein"

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Elmasri, Harun, Elisa Ghelfi, Haiming Cao, Evgenia Gerasimovskaya, Kurt Stenmark, Gokhan Hotamisligil, and Sule Cataltepe. "Role Of Fatty Acid Binding Protein 4 In Pulmonary Angiogenesis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4934.

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Donjuán-Loredo, Guadalupe, Ricardo Espinosa-Tanguma, and Miguel Ramírez-Elías. "Characterization of fatty acid binding protein 4 (FABP4) using Raman spectroscopy." In Clinical and Translational Biophotonics. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/translational.2020.jw3a.18.

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Zelencova, Diana, Karlis Vilks, Marina Makrecka-Kuka, Edgars Liepinsh, and Kristaps Jaudzems. "Investigation of protective effects of fatty acid binding protein 3 against long-chain fatty acid derivative-induced damage." In 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-07485.

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Mukherjee, Abir, Fabian Coscia, Johannes Fahrmann, Chun-Yi Chiang, Justin Smith, Kristin Nieman, Andras Ladanyi, et al. "Abstract A15: Fatty acid binding protein 4 is indispensable for ovarian cancer metastasis." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a15.

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Sato, Hiromi, Shintarao Narita, Masanori Ishida, Soki Kashima, Ryohei Yamamoto, Atsushi Koizumi, Taketoshi Nara, et al. "Abstract 2662: Cellular retinoic acid-binding protein 2 enhances saturated fatty acid-induced prostate cancer progression." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2662.

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Stan, Dana, Carmen-Marinela Mihailescu, Rodica Iosub, Mihaela Savin, Baciu Ion, and Raluca Gavrila. "Development of an immunoassay for impedance-based detection of heart-type fatty acid binding protein." In 2012 International Semiconductor Conference (CAS 2012). IEEE, 2012. http://dx.doi.org/10.1109/smicnd.2012.6400668.

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Yang, Xiaofei, Shaogang Xu, Wentong Li, Ding Yuan, and Jiangqi Qu. "The Expression of Brain-Type Fatty Acid Binding Protein (FABP7) in Rainbow Trout (Oncorhynchus Mykiss)." In the 2018 10th International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3232059.3232062.

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Rao, Deviyani, Anne-Laure Perraud, Della Phan, and Fabienne Gally. "Cigarette smoke impairs Fatty Acid Binding Protein 5-mediated resolution of inflammation in COPD exacerbations." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp103.

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Mak, Judith C., Qian Han, Sze C. Yeung, and Mary S. Ip. "Effects Of Intermittent Hypoxia On The Expression Levels Of Fatty Acid-Binding Protein In Rat Heart." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3869.

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Sauter, E., J. Hao, X. Yan, M. Kong, and B. Li. "Abstract P5-12-07: Expression of adipocyte fatty acid binding protein promotes obesity-associated mammary tumor growth." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p5-12-07.

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Reports on the topic "H-Fatty Acid Binding Protein"

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Ganju, Ramesh. Role of Fatty Acid Binding Protein 5 (FABP5) in Breast Cancer Progression and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada592354.

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Liu, Yiliang. Omega-3 Fatty Acids and a Novel Mammary Derived Growth Inhibitor Fatty Acid Binding Protein MRG in Suppression of Mammary Tumor. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396066.

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Liu, Yiliang E. Omega-3 Fatty Acids and a Novel Mammary Derived Growth Inhibitor Fatty Acid Binding Protein MRG in Suppression of Mammary Tumor. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408070.

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Wang, Mingsheng. Breast Cancer Prevention by a Fatty Acid Binding Protein MRG-Induced Pregnancy Like Mammary Gland Differentiation. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada427084.

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