Catherine Arden

Summary

Affiliation: University of Newcastle
Country: UK

Publications

  1. pmc Susceptibility of glucokinase-MODY mutants to inactivation by oxidative stress in pancreatic β-cells
    Kirsty S Cullen
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, U K
    Diabetes 60:3175-85. 2011
  2. pmc Glucose induces protein targeting to glycogen in hepatocytes by fructose 2,6-bisphosphate-mediated recruitment of MondoA to the promoter
    John L Petrie
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom
    Mol Cell Biol 33:725-38. 2013
  3. doi request reprint Fructose 2,6-bisphosphate is essential for glucose-regulated gene transcription of glucose-6-phosphatase and other ChREBP target genes in hepatocytes
    Catherine Arden
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
    Biochem J 443:111-23. 2012
  4. doi request reprint Inhibition of glucokinase translocation by AMP-activated protein kinase is associated with phosphorylation of both GKRP and 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase
    Mohammed H Mukhtar
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK
    Am J Physiol Regul Integr Comp Physiol 294:R766-74. 2008
  5. ncbi request reprint A role for PFK-2/FBPase-2, as distinct from fructose 2,6-bisphosphate, in regulation of insulin secretion in pancreatic beta-cells
    Catherine Arden
    Institute of Cellular Medicine, The Medical School, Leech Bld Level 4, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
    Biochem J 411:41-51. 2008
  6. pmc Glucagon induces translocation of glucokinase from the cytoplasm to the nucleus of hepatocytes by transfer between 6-phosphofructo 2-kinase/fructose 2,6-bisphosphatase-2 and the glucokinase regulatory protein
    Kirsty S Cullen
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
    Biochim Biophys Acta 1843:1123-34. 2014
  7. pmc A novel mechanism for regulating hepatic glycogen synthesis involving serotonin and cyclin-dependent kinase-5
    Susan J Tudhope
    Institute of Cellular Medicine, The Medical School, Newcastle University, Newcastle upon Tyne, UK
    Diabetes 61:49-60. 2012
  8. pmc Elevated glucose represses liver glucokinase and induces its regulatory protein to safeguard hepatic phosphate homeostasis
    Catherine Arden
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, U K
    Diabetes 60:3110-20. 2011
  9. ncbi request reprint Contributions of glucokinase and phosphofructokinase-2/fructose bisphosphatase-2 to the elevated glycolysis in hepatocytes from Zucker fa/fa rats
    Victoria A Payne
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
    Am J Physiol Regul Integr Comp Physiol 293:R618-25. 2007
  10. ncbi request reprint Cell biology assessment of glucokinase mutations V62M and G72R in pancreatic beta-cells: evidence for cellular instability of catalytic activity
    Catherine Arden
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
    Diabetes 56:1773-82. 2007

Collaborators

  • James A M Shaw
  • Jelena Mann
  • Anna L Gloyn
  • Loranne Agius
  • Kirsty S Cullen
  • John L Petrie
  • Susan J Tudhope
  • Victoria A Payne
  • Ziad H Al-oanzi
  • Julius Kieswich
  • Muhammad M Yaqoob
  • Mohammed H Mukhtar
  • Alex J Lange
  • Finbarr P M O'Harte
  • Howard C Towle
  • Laura J Hampson
  • Fiona Malcomson
  • Lloyd Potts
  • Chung Chi Wang
  • Franz M Matschinsky
  • Salmaan Khan
  • Andrew Harbottle

Detail Information

Publications10

  1. pmc Susceptibility of glucokinase-MODY mutants to inactivation by oxidative stress in pancreatic β-cells
    Kirsty S Cullen
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, U K
    Diabetes 60:3175-85. 2011
    ..We tested the hypothesis that GK mutants that cause maturity-onset diabetes of the young (GK-MODY) show compromised activity and posttranslational regulation in β-cells...
  2. pmc Glucose induces protein targeting to glycogen in hepatocytes by fructose 2,6-bisphosphate-mediated recruitment of MondoA to the promoter
    John L Petrie
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom
    Mol Cell Biol 33:725-38. 2013
    ..Phosphometabolite activation of MondoA and ChREBP and their recruitment to target genes is consistent with a mechanism for gene regulation to maintain intracellular phosphate homeostasis...
  3. doi request reprint Fructose 2,6-bisphosphate is essential for glucose-regulated gene transcription of glucose-6-phosphatase and other ChREBP target genes in hepatocytes
    Catherine Arden
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
    Biochem J 443:111-23. 2012
    ....
  4. doi request reprint Inhibition of glucokinase translocation by AMP-activated protein kinase is associated with phosphorylation of both GKRP and 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase
    Mohammed H Mukhtar
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK
    Am J Physiol Regul Integr Comp Physiol 294:R766-74. 2008
    ....
  5. ncbi request reprint A role for PFK-2/FBPase-2, as distinct from fructose 2,6-bisphosphate, in regulation of insulin secretion in pancreatic beta-cells
    Catherine Arden
    Institute of Cellular Medicine, The Medical School, Leech Bld Level 4, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
    Biochem J 411:41-51. 2008
    ..It is concluded that PFK-2/FBPase-2 protein rather than its product fructose 2,6-P(2) is the over-riding determinant of glucose-induced insulin secretion through regulation of glucokinase activity or subcellular targeting...
  6. pmc Glucagon induces translocation of glucokinase from the cytoplasm to the nucleus of hepatocytes by transfer between 6-phosphofructo 2-kinase/fructose 2,6-bisphosphatase-2 and the glucokinase regulatory protein
    Kirsty S Cullen
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
    Biochim Biophys Acta 1843:1123-34. 2014
    ..Given that glucagon excess contributes to the pathogenesis of diabetes, glucagon may play a role in the defect in glucokinase translocation and activity evident in animal models and human diabetes. ..
  7. pmc A novel mechanism for regulating hepatic glycogen synthesis involving serotonin and cyclin-dependent kinase-5
    Susan J Tudhope
    Institute of Cellular Medicine, The Medical School, Newcastle University, Newcastle upon Tyne, UK
    Diabetes 61:49-60. 2012
    ..The opposing effects of serotonin, mediated by distinct 5-HT receptors, could explain why drugs targeting serotonin function can cause either diabetes or hypoglycemia in humans...
  8. pmc Elevated glucose represses liver glucokinase and induces its regulatory protein to safeguard hepatic phosphate homeostasis
    Catherine Arden
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, U K
    Diabetes 60:3110-20. 2011
    ..The induction of hepatic glucose 6-phosphatase (G6pc) by glucose presents a paradox of glucose-induced glucose intolerance. We tested whether glucose regulation of liver gene expression is geared toward intracellular homeostasis...
  9. ncbi request reprint Contributions of glucokinase and phosphofructokinase-2/fructose bisphosphatase-2 to the elevated glycolysis in hepatocytes from Zucker fa/fa rats
    Victoria A Payne
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
    Am J Physiol Regul Integr Comp Physiol 293:R618-25. 2007
    ..Cumulatively, this study provides support for coordinate roles for glucokinase and PFK2 in the elevated hepatic glycolysis in fa/fa rats...
  10. ncbi request reprint Cell biology assessment of glucokinase mutations V62M and G72R in pancreatic beta-cells: evidence for cellular instability of catalytic activity
    Catherine Arden
    Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
    Diabetes 56:1773-82. 2007
    ..These results suggest that cellular loss of GK catalytic activity rather than impaired translation or enhanced protein degradation may account for the hyperglycemia in subjects with V62M and G72R mutations...