Disease relevance of Fabp6

• To explore a possible cause for this gender dimorphic effect, we examined the changes in expression of genes that encode liver fatty acid binding protein (L-FABP) and ileal lipid binding protein in the small intestine resulting from I-FABP deficiency [1].
• In two of five families, kidney lesions consisting of proximal tubular hyperplasia, renal cysts, and microadenomas developed in male animals; males also expressed higher levels of gamma GT/rasT24 RNA [2].
• Thus, the Spnr(GT/GT) mutant male mouse provides a unique model for some human male infertility cases [3].
• Adenoviral vector-mediated transfer of pig alpha(1, 3) GT gene into human tumor cells such as malignant melanoma A375, stomach cancer SGC-7901, and lung cancer SPC-A-1 was reported for the first time [4].
• In a previous work, our group reported that Albino Swiss male mice inoculated with T. cruzi to develop acute lethal infection by day 15 decreased parasitemia and survived when treated with total brain gangliosides (GT; 1 mg, daily) [5].

High impact information on Fabp6

• Normal, chimeric-transgenic, and transgenic mice have been used to study the axial patterns of ileal lipid-binding protein gene (Ilbp) expression during and after completion of gut morphogenesis [6].
• Ilbp is initially activated in enterocytes in bidirectional wave that expands proximally in the ileum and distally to the colon during late gestation and the first postnatal week [6].
• Although the heterogeneity of the 5' ends of gamma GT RNAs may be explained in part by alternative splicing, it is likely that multiple promoters are involved in their generation [7].
• One of these genes appears to be deleted in individuals lacking GT activity on trans-stilbene oxide [8].
• Although all the RNA samples examined contained class-alpha GT mRNA, class-mu GT mRNA was found only in individuals whose peripheral leukocytes expressed GT activity on the substrate trans-stilbene oxide [8].

Biological context of Fabp6

• The mouse ileal lipid-binding protein gene: a model for studying axial patterning during gut morphogenesis [6].
• Therefore, the I-BABP gene expression might be controlled by CS [9].
• Different constructs of human I-BABP promoter, cloned upstream of a chloramphenicol acetyltransferase (CAT) reporter gene, have been used in transfections studies [9].
• Ileal lipid-binding protein (Illbp) gene maps to mouse chromosome 11 [10].
• The ileal lipid binding protein (ILBP), a member of the intracellular lipid binding protein family, is a 14-kDa protein that has bile and fatty acids as possible physiological ligands [11].

Anatomical context of Fabp6

• I-BABP mRNA levels were significatively increased when the human enterocyte-like CaCo-2 cells were CS-deprived and repressed when CS were added to the medium [9].
• The gene encoding the human ileal bile acid-binding protein (I-BABP) is regulated by peroxisome proliferator-activated receptors [12].
• The ileal lipid-binding protein (ILBP) is the only physiologically relevant bile acid-binding protein in the cytosol of ileocytes [13].
• The results indicate that both L-FABP and ilbp levels are modestly increased in the small intestine of chow-fed mice lacking I-FABP [1].
• To elucidate the mechanisms that generate these different mRNAs we determined the transcription start sites of gamma GT kidney mRNAs and investigated the ability of the 5'-flanking regions of mRNAs I, II, IV, V, and VI to direct transcription of chloramphenicol acetyltransferase (CAT) reporter gene constructs in a mouse kidney cell line [14].

Associations of Fabp6 with chemical compounds

• A highly conserved sterol regularory element-like sequence (SRE) and a putative GC box were found in human I-BABP gene promoter [9].
• Indeed, treatment with the PPARalpha-PPARbeta/delta agonist bezafibrate led to the up-regulation of I-BABP mRNA levels in the human intestine-derived Caco-2 cells [12].
• By chemical modification and NMR structure of ILBP, arginine residue 122 was identified as the probable contact point for the negatively charged side chain of cholyltaurine [13].
• Consequently, bile acids bind to ILBP with the steroid nucleus deep inside the protein cavity and the negatively charged side chain near the entry portal [13].
• The effect of Glc deprivation (starvation) on hexose transporter (GT) polypeptide(s) (pp) was studied in 3T3-C2 murine fibroblasts [15].

Other interactions of Fabp6

• Co-transfections experiments with the mature isoforms of human sterol responsive element-binding proteins (SREBPs) and Sp1 demonstrate that the CS-mediated regulation of I-BABP gene was dependent of these transcriptional factors [9].
• We confirmed that these effects on IBABP transcription required the FXR by employing a cell-based transactivation assay [16].
• Ontogenetic development and spatial distribution of the ileal apical sodium-dependent bile acid transporter and the ileal lipid-binding protein in apoE knockout and C57BL/6 mice [17].

Analytical, diagnostic and therapeutic context of Fabp6

• Identification of the bile acid-binding site of the ileal lipid-binding protein by photoaffinity labeling, matrix-assisted laser desorption ionization-mass spectrometry, and NMR structure [13].
• Early lesions consisted of proximal tubular hyperplasia as defined by alkaline phosphatase histochemistry, gamma GT immunohistochemistry, and electron microscopy and could be correlated with the presence of rasT24 RNA within the cystic proximal tubular epithelium by in situ hybridization [2].
• Reverse transcription-mediated polymerase chain reaction detected low amounts of gamma GT RNA types I, III, and V [18].
• The expression of murine alpha(1,3) GT was characterized by RT-PCR [19].
• METHODS: Transgenic mice bearing the porcine antisense alpha(1,3) GT cDNA (nt 1alpha-640) were generated by pronuclei microinjection method [19].

References