|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0008633,
umls-concept:C0012655,
umls-concept:C0015576,
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0020474,
umls-concept:C0024779,
umls-concept:C0039194,
umls-concept:C0086418,
umls-concept:C0205396,
umls-concept:C0208973,
umls-concept:C0812246,
umls-concept:C1171362,
umls-concept:C1456820,
umls-concept:C1515670,
umls-concept:C1517892,
umls-concept:C1704666,
umls-concept:C1708726,
umls-concept:C1879547
|
|
pubmed:issue |
2
|
|
pubmed:dateCreated |
1999-8-5
|
|
pubmed:databankReference |
|
|
pubmed:abstractText |
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 the 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 role in the pathogenesis of FCH and associated insulin resistance. Exon- and intron-specific primer sequences are presented as a basis for mutation screening of patients affected with FCH.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jul
|
|
pubmed:issn |
0006-291X
|
|
pubmed:author |
|
|
pubmed:copyrightInfo |
Copyright 1999 Academic Press.
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
5
|
|
pubmed:volume |
260
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
416-25
|
|
pubmed:dateRevised |
2010-11-18
|
|
pubmed:meshHeading |
pubmed-meshheading:10403784-3T3 Cells,
pubmed-meshheading:10403784-Adiponectin,
pubmed-meshheading:10403784-Amino Acid Sequence,
pubmed-meshheading:10403784-Animals,
pubmed-meshheading:10403784-Base Sequence,
pubmed-meshheading:10403784-Chromosome Mapping,
pubmed-meshheading:10403784-Chromosomes, Human, Pair 1,
pubmed-meshheading:10403784-Exons,
pubmed-meshheading:10403784-Genetic Linkage,
pubmed-meshheading:10403784-Genetic Predisposition to Disease,
pubmed-meshheading:10403784-Humans,
pubmed-meshheading:10403784-Hyperlipidemia, Familial Combined,
pubmed-meshheading:10403784-In Situ Hybridization, Fluorescence,
pubmed-meshheading:10403784-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:10403784-Introns,
pubmed-meshheading:10403784-Lymphocyte Activation,
pubmed-meshheading:10403784-Mice,
pubmed-meshheading:10403784-Molecular Sequence Data,
pubmed-meshheading:10403784-Promoter Regions, Genetic,
pubmed-meshheading:10403784-Proteins,
pubmed-meshheading:10403784-RNA, Messenger,
pubmed-meshheading:10403784-Sequence Homology, Nucleic Acid,
pubmed-meshheading:10403784-T-Lymphocytes,
pubmed-meshheading:10403784-Tumor Necrosis Factor-alpha
|
|
pubmed:year |
1999
|
|
pubmed:articleTitle |
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).
|
|
pubmed:affiliation |
Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, Germany.
|
|
pubmed:publicationType |
Journal Article
|
