Schaeffler, Andreas and Orso, E. and Palitzsch, Klaus-Dieter and Buechler, Christa and Drobnik, W. and Fuerst, Alois and Schoelmerich, Juergen and Schmitz, Gerd (1999) The human apM-1, an adipocyte-specific gene linked to the family of TNF's and to genes expressed in activated T cells, is mapped to chromosome 1q21.3-q23, a susceptibility locus identified for familial combined hyperlipidaemia (FCH). BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 260 (2). pp. 416-425. ISSN 0006-291X, 1090-2104
Full text not available from this repository. (Request a copy)Abstract
The human adipocyte-specific apM-1 gene encodes a secretory protein of the adipose tissue that has been suggested to play a role in the pathogenesis of obesity. The regulation of apM-1 was studied along adipocyte differentiation. While apM-1-mRNA and apM-1 protein were absent in preadipocytes and in 48 h differentiated adipocytes, they were found upregulated from day 4 to day 9 of adipocyte differentiation as shown by RNase protection assay and Western blot analysis. These data indicate that apM-1 may be a late marker of adipocyte differentiation, In human sera apM-1 protein is also detectable by Western blots using a polyclonal antibody raised against a synthetic peptide sequence of the human apM-1. The genomic structure of the human apM-1 gene together with a total of 2.7 kb of the 5'-flanking region with putative transcription factor binding sites is presented. Interestingly, sequence comparisons link the apM-1 gene to tbe family of TNF's and to genes expressed in activated T-cells. The chromosomal localization of apM-1 was investigated by FISH and mapped to human chromosome 1q21.3-1q23, a region that was identified as a susceptibility locus for Familial Combined Hyperlipidaemia (FCH) and polygenic NIDDM. These data and the chromosomal localization on chromosome 1q21.3-q23 raises the possibility that apM-1 as an adipocyte-specific secretory protein may play a rob in the pathogenesis of FCH and associated insulin resistance. Exon- and intronspecific primer sequences are presented as a basis for mutation screening of patients affected with FCH. (C) 1999 Academic Press.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TUMOR-NECROSIS-FACTOR; MOUSE OBESE GENE; ADIPOSE-TISSUE; FACTOR-ALPHA; C1Q RECEPTOR; PROTEIN; LEPTIN; COMPLEMENT; COMPONENT; ADIPSIN; apM-1; AdipoQ; Acrp-30; adipocyte; obesity; TNF-alpha, familial combined hyperlipidaemia (FCH); C1q; complement |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Chirurgie Medicine > Lehrstuhl für Innere Medizin I Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 31 Jan 2023 10:00 |
| Last Modified: | 31 Jan 2023 10:00 |
| URI: | https://pred.uni-regensburg.de/id/eprint/49132 |
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