PMID- 10403784
OWN - NLM
STAT- MEDLINE
DCOM- 19990805
LR  - 20101118
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 260
IP  - 2
DP  - 1999 Jul 5
TI  - 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).
PG  - 416-25
AB  - 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.
CI  - Copyright 1999 Academic Press.
FAU - Schaffler, A
AU  - Schaffler A
AD  - Institute for Clinical Chemistry and Laboratory Medicine, University of
      Regensburg, Germany.
FAU - Orso, E
AU  - Orso E
FAU - Palitzsch, K D
AU  - Palitzsch KD
FAU - Buchler, C
AU  - Buchler C
FAU - Drobnik, W
AU  - Drobnik W
FAU - Furst, A
AU  - Furst A
FAU - Scholmerich, J
AU  - Scholmerich J
FAU - Schmitz, G
AU  - Schmitz G
LA  - eng
SI  - GENBANK/AJ131459
SI  - GENBANK/AJ131460
SI  - GENBANK/AJ131461
SI  - GENBANK/AJ131462
SI  - GENBANK/AJ131463
PT  - Journal Article
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Adiponectin)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - 3T3 Cells
MH  - Adiponectin
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Chromosome Mapping
MH  - *Chromosomes, Human, Pair 1
MH  - Exons
MH  - Genetic Linkage
MH  - *Genetic Predisposition to Disease
MH  - Humans
MH  - Hyperlipidemia, Familial Combined/*genetics
MH  - In Situ Hybridization, Fluorescence
MH  - *Intercellular Signaling Peptides and Proteins
MH  - Introns
MH  - Lymphocyte Activation
MH  - Mice
MH  - Molecular Sequence Data
MH  - Promoter Regions, Genetic
MH  - Proteins/*genetics
MH  - RNA, Messenger/genetics
MH  - Sequence Homology, Nucleic Acid
MH  - T-Lymphocytes/*metabolism
MH  - Tumor Necrosis Factor-alpha/*genetics
EDAT- 1999/07/15 00:00
MHDA- 1999/07/15 00:01
CRDT- 1999/07/15 00:00
PHST- 1999/07/15 00:00 [pubmed]
PHST- 1999/07/15 00:01 [medline]
PHST- 1999/07/15 00:00 [entrez]
AID - 10.1006/bbrc.1999.0865 [doi]
AID - S0006-291X(99)90865-3 [pii]
PST - ppublish
SO  - Biochem Biophys Res Commun. 1999 Jul 5;260(2):416-25. doi:
      10.1006/bbrc.1999.0865.