Isolation, Cloning, and Expression of Fatty-Acid Binding Proteins fromFasciola gigantica

1997 ◽  
Vol 85 (1) ◽  
pp. 86-91 ◽  
Author(s):  
Peter M. Smooker ◽  
Danielle E. Hickford ◽  
Sam A. Vaiano ◽  
Terry W. Spithill
Keyword(s):  
Fatty Acid ◽  
Binding Proteins ◽  
Cloning And Expression ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding

The expression pattern of a novel gene encoding brain-fatty acid binding protein correlates with neuronal and glial cell development

Development ◽  
1994 ◽  
Vol 120 (9) ◽  
pp. 2637-2649 ◽  
Author(s):  
A. Kurtz ◽  
A. Zimmer ◽  
F. Schnutgen ◽  
G. Bruning ◽  
F. Spener ◽  
...  
Keyword(s):  
Nervous System ◽  
Fatty Acid ◽  
Expression Pattern ◽  
Glial Cells ◽  
Binding Proteins ◽  
Cloning And Expression ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding ◽  
Radial Glial Cells ◽  
Radial Glial

Fatty acid binding proteins (FABPs) are a multigene family of small intracellular proteins that bind hydrophobic ligands. In this report we describe the cloning and expression pattern of a novel member of this gene family that is specifically expressed in the developing and adult nervous system and thus was designated brain (B)-FABP. B-FABP is closely related to heart (H)-FABP with 67% amino acid identity. B-FABP expression was first detected at mouse embryonic day 10 in neuroepithelial cells and its pattern correlates with early neuronal differentiation. Upon further development, B-FABP was confined to radial glial cells and immature astrocytes. B-FABP mRNA and protein were found in glial cells of the peripheral nervous system such as satellite cells of spinal and cranial ganglia and ensheathing cells of the olfactory nerve layer from as early as embryonic day 11 until adulthood. In the adult mouse brain, B-FABP was found in the glia limitans, in radial glial cells of the hippocampal dentate gyrus and Bergman glial cells. These findings suggest a function of B-FABP during neurogenesis or neuronal migration in the developing nervous system. The partially overlapping expression pattern with that of cellular retinoid binding proteins suggests that B-FABP is involved in the metabolism of a so far unknown hydrophobic ligand with potential morphogenic activity during CNS development.

scholarly journals Fatty acid transfer between multilamellar liposomes and fatty acid-binding proteins.

1984 ◽  
Vol 259 (21) ◽  
pp. 13395-13401 ◽  
Author(s):  
P Brecher ◽  
R Saouaf ◽  
J M Sugarman ◽  
D Eisenberg ◽  
K LaRosa
Keyword(s):  
Fatty Acid ◽  
Binding Proteins ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding ◽  
Multilamellar Liposomes

scholarly journals Increased Levels of Adipocyte and Epidermal Fatty Acid-Binding Proteins in Acute Lymphoblastic Leukemia Survivors

2021 ◽  
Vol 10 (8) ◽  
pp. 1567
Author(s):  
Katarzyna Konończuk ◽  
Eryk Latoch ◽  
Beata Żelazowska-Rutkowska ◽  
Maryna Krawczuk-Rybak ◽  
Katarzyna Muszyńska-Rosłan
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Acute Lymphoblastic Leukemia ◽  
Binding Proteins ◽  
Lymphoblastic Leukemia ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Significant Difference

Childhood cancer survivors are highly exposed to the development of side effects after many years of cessation of anticancer treatment, including altered lipid metabolism that may result in an increased risk of overweight and metabolic syndrome. Adipocyte (A-FABP) and epidermal (E-FABP) fatty acid-binding proteins are expressed in adipocytes and are assumed to play an important role in the development of lipid disturbances leading to the onset of metabolic syndrome. The aim of this study was to investigate the association between serum A-FABP and E-FABP levels, overweight, and components of the metabolic syndrome in acute lymphoblastic leukemia survivors. Sixty-two acute lymphoblastic leukemia (ALL) survivors (34 females) were included in the study. The mean age at the time of the study was 12.41 ± 4.98 years (range 4.71–23.43). Serum levels of A-FABP and E-FABP were analyzed using a commercially available ELISA kit. The ALL survivors presented statistically higher A-FABP levels in comparison with the healthy controls (25.57 ± 14.46 vs. 15.13 ± 7.61 ng/mL, p < 0.001). The subjects with body mass index (BMI) above the normal range (18 overweight, 10 obese) had a greater level of A-FABP compared to the ALL group with normal BMI (32.02 ± 17.10 vs. 20.33 ± 9.24 ng/mL, p = 0.006). Of all participants, 53.23% had at least one risk factor of metabolic syndrome; in this group, only the A-FABP level showed a statistically significant difference compared to the healthy control group (30.63 ± 15.91 vs. 15.13 ± 7.61 ng/mL, p < 0.001). The subjects with two or more metabolic risk factors (16.13%) presented higher levels of both A-FABP (33.62 ± 17.16 vs. 15.13 ± 7.61 ng/mL, p = 0.001) and E-FABP (13.37 ± 3.62 vs. 10.12 ± 3.21 ng/mL, p = 0.021) compared to the controls. Univariable regression models showed significant associations between BMI and systolic blood pressure with the A-FABP level (coeff. 1.02 and 13.74, respectively; p < 0.05). In contrast, the E-FABP level was only affected by BMI (coeff. 0.48; p < 0.01). The findings reported herein suggest that the increased levels of A-FABP and E-FABP may be involved in the pathogenesis of overweight and the onset of metabolic syndrome in acute lymphoblastic leukemia. However, further longitudinal, prospective studies of fatty acid-binding proteins and their potential role in the pathogenesis of obesity and metabolic syndrome in ALL survivors remain to be performed.

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