PMID- 10358101
OWN - NLM
STAT- MEDLINE
DCOM- 19990706
LR  - 20190508
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 24
DP  - 1999 Jun 11
TI  - Complete cDNA cloning, genomic organization, chromosomal assignment, functional
      characterization of the promoter, and expression of the murine Bamacan gene.
PG  - 17384-93
AB  - Bamacan is a chondroitin sulfate proteoglycan that abounds in basement membranes.
      To gain insights into the bamacan gene regulation and transcriptional control, we
      examined the genomic organization and identified the promoter region of the mouse
      bamacan gene. Secondary structure analysis of the protein reveals a sequential
      organization of three globular regions interconnected by two alpha-helix
      coiled-coils. The N- and the C-terminal ends carry a P-loop and a DA box motif
      that can act cooperatively to bind ATP. These features as well as the high
      sequence homology with members of the SMC (structural maintenance of chromosome) 
      protein family led us to conclude that bamacan is a member of this protein
      family. The gene comprises 31 exons and is driven by a promoter that is highly
      enriched in GC sequences and lacks TATA and CAAT boxes. The promoter is highly
      functional in transient cell transfection assays, and step-wise 5' deletions
      identify a strong enhancer element between -659 and -481 base pairs that includes
      Jun/Fos proto-oncogene-binding elements. Using backcrossing experiments we mapped
      the Bam gene to distal chromosome 19, a locus syntenic to human chromosome 10q25.
      Bamacan is differentially expressed in mouse tissues with the highest levels in
      testes and brain. Notably, bamacan mRNA levels are low in normal cells and
      markedly reduced during quiescence but are highly increased when cells resume
      growth upon serum stimulation. In contrast, in all transformed cells tested,
      bamacan is constitutively overexpressed, and its levels do not change with cell
      cycle progression. These results suggest that bamacan is involved in the control 
      of cell growth and transformation.
FAU - Ghiselli, G
AU  - Ghiselli G
AD  - Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, 
      Philadelphia, Pennsylvania 19107, USA.
FAU - Siracusa, L D
AU  - Siracusa LD
FAU - Iozzo, R V
AU  - Iozzo RV
LA  - eng
SI  - GENBANK/AF141294
GR  - P01 CA21124/CA/NCI NIH HHS/United States
GR  - R01 CA39481/CA/NCI NIH HHS/United States
GR  - R01 CA47282/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Chondroitin Sulfate Proteoglycans)
RN  - 0 (Chromosomal Proteins, Non-Histone)
RN  - 0 (Cspg6 protein, mouse)
RN  - 0 (DNA, Complementary)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (SMC3 protein, human)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Composition
MH  - Base Sequence
MH  - *Cell Cycle Proteins
MH  - Cell Line, Transformed
MH  - Cell Nucleus/chemistry
MH  - Chondroitin Sulfate Proteoglycans/*biosynthesis/*genetics
MH  - Chromosomal Proteins, Non-Histone/genetics
MH  - Chromosome Mapping
MH  - Cloning, Molecular
MH  - Conserved Sequence
MH  - DNA, Complementary/genetics
MH  - Evolution, Molecular
MH  - Exons
MH  - Extracellular Space/chemistry
MH  - Female
MH  - Gene Expression
MH  - Gene Expression Regulation
MH  - Genomic Library
MH  - Membrane Glycoproteins/*biosynthesis/*genetics
MH  - Mice
MH  - Molecular Sequence Data
MH  - *Promoter Regions, Genetic
MH  - Protein Structure, Secondary
MH  - Recombinant Proteins/biosynthesis
MH  - Species Specificity
MH  - Tissue Distribution
EDAT- 1999/06/08 00:00
MHDA- 1999/06/08 00:01
CRDT- 1999/06/08 00:00
PHST- 1999/06/08 00:00 [pubmed]
PHST- 1999/06/08 00:01 [medline]
PHST- 1999/06/08 00:00 [entrez]
AID - 10.1074/jbc.274.24.17384 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Jun 11;274(24):17384-93. doi: 10.1074/jbc.274.24.17384.