Rehabilitation in severe head injuries.
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Biomedical subjects
Publications and source records attributed to K Kristiansen.
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Acyl-CoA-Binding Protein (ACBP)/Diazepam-Binding Inhibitor (DBI) is a 10 kD protein which has been implicated in a surprisingly large number of biochemical functions. We have unambiguously demonstrated that ACBP binds acyl-CoA esters with high affinity and in vivo functions as an acyl-CoA ester pool former. We have molecularly cloned and characterized the rat ACBP gene family which comprises one expressed and four processed pseudogenes. One of these was shown to exist in two allelic forms. A comprehensive computer-aided analysis of the promoter region of the expressed ACBP gene revealed that it exhibits all the hallmarks of typical housekeeping genes. In addition, the promoter region harbors a number of potential tissue specific cis-acting elements that may in part regulate the level of ACBP expression in specialized cells.
Acyl-CoA-binding protein has been isolated independently by five different groups based on its ability to (1) displace diazepam from the GABAA receptor, (2) affect cell growth, (3) induce medium-chain acyl-CoA-ester synthesis, (4) stimulate steroid hormone synthesis, and (5) affect glucose-induced insulin secretion. In this survey evidence is presented to show that ACBP is able to act as an intracellular acyl-CoA transporter and acyl-CoA pool former. The rat ACBP genomic gene consists of 4 exons and is actively expressed in all tissues tested with highest concentration being found in liver. ACBP consists of 86 amino acid residues and contains 4 alpha-helices which are folded into a boomerang type of structure with alpha-helices 1, 2 and 4 in the one arm and alpha-helix 3 and an open loop in the other arm of the boomerang. ACBP is able to stimulate mitochondrial acyl-CoA synthetase by removing acyl-CoA esters from the enzyme. ACBP is also able to desorb acyl-CoA esters from immobilized membranes and transport and deliver these for mitochondrial beta-oxidation. ACBP efficiently protects acetyl-CoA carboxylase and the mitochondrial ADP/ATP translocase against acyl-CoA inhibition. Finally, ACBP is shown to be able to act as an intracellular acyl-CoA pool former by overexpression in yeast. The possible role of ACBP in lipid metabolism is discussed.
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A method to preserve high resolution R-bands on human lymphocyte chromosomes after in situ hybridization to 3H-labelled probes and autoradiography is presented. The technique was used to re-examine the location of the known oncogene N-myc. Due to the high resolution power of the present technique, this gene could be located to subband 2p24.1 in the human karyotype.
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