PMID- 10078554
OWN - NLM
STAT- MEDLINE
DCOM- 19990330
LR  - 20190515
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 48
IP  - 3
DP  - 1999 Mar
TI  - Structure and promoter activity of an islet-specific glucose-6-phosphatase
      catalytic subunit-related gene.
PG  - 543-51
AB  - In liver and kidney, the terminal step in the gluconeogenic pathway is catalyzed 
      by glucose-6-phosphatase (G-6-Pase). This enzyme is actually a multicomponent
      system, the catalytic subunit of which was recently cloned. Numerous reports have
      also described the presence of G-6-Pase activity in islets, although the role of 
      G-6-Pase in this tissue is unclear. Arden and associates have described the
      cloning of a novel cDNA that encodes an islet-specific G-6-Pase catalytic
      subunit-related protein (IGRP) (Arden SD, Zahn T, Steegers S, Webb S, Bergman B, 
      O'Brien RM, Hutton JC: Molecular cloning of a pancreatic islet-specific
      glucose-6-phosphatase catalytic subunit related protein (IGRP). Diabetes
      48:531-542, 1999). We screened a mouse BAC library with this cDNA to isolate the 
      IGRP gene, which spans approximately 8 kbp of genomic DNA. The exon/intron
      structure of the IGRP gene has been mapped and, as with the gene encoding the
      liver/kidney G-6-Pase catalytic subunit, it is composed of five exons. The sizes 
      of these exons are 254 (I), 110 (II), 112 (III), 116 (IV), and 1284 (V) bp,
      similar to those of the G-6-Pase catalytic subunit gene. Two interspecific
      backcross DNA mapping panels were used to unambiguously localize the IGRP gene
      (map symbol G6pc-rs) to the proximal portion of mouse chromosome 2. The IGRP gene
      transcription start site was mapped by primer extension analysis, and the
      activity of the IGRP gene promoter was analyzed in both the islet-derived HIT
      cell line and the liver-derived HepG2 cell line. The IGRP and G-6-Pase catalytic 
      subunit gene promoters show a reciprocal pattern of activity, with the IGRP
      promoter being approximately 150-fold more active than the G-6-Pase promoter in
      HIT cells.
FAU - Ebert, D H
AU  - Ebert DH
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University Medical 
      School, Nashville, Tennessee 37232-0615, USA.
FAU - Bischof, L J
AU  - Bischof LJ
FAU - Streeper, R S
AU  - Streeper RS
FAU - Chapman, S C
AU  - Chapman SC
FAU - Svitek, C A
AU  - Svitek CA
FAU - Goldman, J K
AU  - Goldman JK
FAU - Mathews, C E
AU  - Mathews CE
FAU - Leiter, E H
AU  - Leiter EH
FAU - Hutton, J C
AU  - Hutton JC
FAU - O'Brien, R M
AU  - O'Brien RM
LA  - eng
SI  - GENBANK/AF118761
SI  - GENBANK/AF118762
SI  - GENBANK/AF118763
SI  - GENBANK/AF118764
SI  - GENBANK/AF118765
SI  - GENBANK/AF118766
SI  - GENBANK/AH007666
GR  - F32 DK009865/DK/NIDDK NIH HHS/United States
GR  - CA68485/CA/NCI NIH HHS/United States
GR  - DK20593/DK/NIDDK NIH HHS/United States
GR  - RR 08911/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Genetic Markers)
RN  - 0 (Proteins)
RN  - EC 3.1.3.9 (Glucose-6-Phosphatase)
RN  - EC 3.1.3.9. (G6PC2 protein, human)
RN  - EC 3.1.3.9. (G6pc2 protein, mouse)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Carcinoma, Hepatocellular
MH  - *Chromosome Mapping
MH  - Exons
MH  - Gene Library
MH  - Genetic Markers
MH  - Glucose-6-Phosphatase/*genetics
MH  - Humans
MH  - Introns
MH  - Islets of Langerhans/*metabolism
MH  - Kidney/metabolism
MH  - Liver/metabolism
MH  - Liver Neoplasms
MH  - Mice
MH  - Molecular Sequence Data
MH  - *Promoter Regions, Genetic
MH  - Proteins/chemistry/*genetics
MH  - Sequence Alignment
MH  - Sequence Homology, Nucleic Acid
MH  - Tumor Cells, Cultured
EDAT- 1999/03/17 00:00
MHDA- 1999/03/17 00:01
CRDT- 1999/03/17 00:00
PHST- 1999/03/17 00:00 [pubmed]
PHST- 1999/03/17 00:01 [medline]
PHST- 1999/03/17 00:00 [entrez]
AID - 10.2337/diabetes.48.3.543 [doi]
PST - ppublish
SO  - Diabetes. 1999 Mar;48(3):543-51. doi: 10.2337/diabetes.48.3.543.