Erik Renström

författare

• 2013
  • Effect of Common Genetic Variants Associated with Type 2 Diabetes and Glycemic Traits on α- and β-cell Function and Insulin Action in Man.
• 2012
  • A systems genetics approach identifies genes and pathways for type 2 diabetes in human islets.
  • Impact of transcription factor 7-like 2 (TCF7L2) on pancreatic islet function and morphology in mice and men.
  • Increased DNA Methylation and Decreased Expression of PDX-1 in Pancreatic Islets from Patients with Type 2 Diabetes.
  • Islet amyloid polypeptide triggers limited complement activation and binds complement inhibitor C4b-binding protein, which enhances fibril formation.
  • Reduced Insulin Exocytosis in Human Pancreatic β-cells With Gene Variants Linked to Type 2 Diabetes.
  • Role of TCF7L2 risk variant and dietary fibre intake on incident type 2 diabetes.
  • Secreted frizzled-related protein 4 reduces insulin secretion and is overexpressed in type 2 diabetes.
  • Survival of pancreatic beta cells is partly controlled by a TCF7L2-p53-p53INP1-dependent pathway.
  • The adult human brain harbors multipotent perivascular mesenchymal stem cells.
  • The human L-type calcium channel Ca(v)1.3 regulates insulin release and polymorphisms in CACNA1D associate with type 2 diabetes.
  • Truncated and Full-Length Thioredoxin-1 Have Opposing Activating and Inhibitory Properties for Human Complement with Relevance to Endothelial Surfaces.
  • γ-Aminobutyric acid (GABA) signalling in human pancreatic islets is altered in type 2 diabetes.
• 2010
  • ClC-3-A Granular Anion Transporter Involved in Insulin Secretion? Response
  • Complement inhibitor C4b-binding protein (C4BP) binding to islet amyloid polypeptide prevents complement activation and further fibril formation in the endocrine pancreas
  • Complement receptor C5aR is expressed in pancreatic islets and affects glucose-induced insulin and glucagon secretion
  • Enhancement of glucagon secretion in mouse and human pancreatic alpha cells by protein kinase C (PKC) involves intracellular trafficking of PKCalpha and PKCdelta.
  • GLP-1 inhibits and adrenaline stimulates glucagon release by differential modulation of N- and L-type Ca2+ channel-dependent exocytosis.
  • Molecular Function of TCF7L2: Consequences of TCF7L2 Splicing for Molecular Function and Risk for Type 2 Diabetes.
  • Overexpression of Alpha2A-Adrenergic Receptors Contributes to Type 2 Diabetes.
  • Polymorphisms in CACNA1D affect insulin release and channel expression and associate with type 2 diabetes
  • TCF7L2-conferred apoptosis in pancreatic beta cells involves the p53 pathway
  • The interactions of thioredoxin and the complement system
  • The role of wnt antagonists in impaired beta cell exocytosis
• 2009
  • Autologous hematopoietic stem cell transplantation in type 1-diabetes.
  • Bone marrow transplantation stimulates pancreatic β-cell replication after tissue damage.
  • Complement factors are expressed in pancreatic islets and affect glucose induced insulin secretion
  • Evaluation of chloride channel-3 as a potential target for TCF7L2-dependent impairment of insulin secretion
  • Glutaredoxin-1 mediates NADPH-dependent stimulation of calcium-dependent insulin secretion.
  • Hyperactivity in adrenergic signalling via alpha2A receptors contributes to human type 2 diabetes
  • Rapid changes in surface expression of L-type Cav1.2 channels in stimulated INS-1 cells
  • Suppression of sulfonylurea- and glucose-induced insulin secretion in vitro and in vivo in mice lacking the chloride transport protein ClC-3.
  • The impact of differential splicing of TCF7L2 on target gene expression in human islet of Langerhans
  • Unique splicing pattern of the TCF7L2 gene in human pancreatic islets.
• 2008
  • CAPS1 and CAPS2 Regulate Stability and Recruitment of Insulin Granules in Mouse Pancreatic beta Cells.
  • NADPH as a putative regulator of voltage-gated Ca2+ channels in pancreatic beta cells
  • Why treatment fails in type 2 diabetes.
• 2007
  • Polymorphisms in the gene encoding the voltage-dependent Ca(2+) channel Ca (V)2.3 (CACNA1E) are associated with type 2 diabetes and impaired insulin secretion
  • R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion
• 2006
  • Anaplerosis via pyruvate carboxylase is required for the fuel-induced rise in the ATP:ADP ratio in rat pancreatic islets.
  • Failure of Transplanted Bone Marrow Cells to Adopt a Pancreatic {beta}-Cell Fate.
  • Separately inherited defects in insulin exocytosis and beta-cell glucose metabolism contribute to type 2 diabetes.
  • Tomosyn-1 is involved in a post-docking event required for pancreatic beta-cell exocytosis
• 2005
  • CaV2.3 calcium channels control second-phase insulin release.
  • Myosin 5a controls insulin granule recruitment during late-phase secretion.
  • Redox control of exocytosis - Regulatory role of NADPH, thioredoxin, and glutaredoxin
  • The R6/2 transgenic mouse model of Huntington's disease develops diabetes due to deficient {beta}-cell mass and exocytosis.
  • The ablation of the Ca(v)2.3/E-type voltage-gated Ca2+ channel causes a mild phenotype despite an altered glucose induced glucagon response in isolated islets of Langerhans
• 2004
  • Enhanced cAMP/Protein Kinase A signaling determines improved insulin secretion in a clonal insulin-producing {beta}-cell line (INS-1 832/13).
  • Isoform-specific regulation of mood behavior and pancreatic beta cell and cardiovascular function by L-type Ca2+ channels
  • Large dense-core vesicle exocytosis in pancreatic beta-cells monitored by capacitance measurements
  • Temperature-Sensitive Random Insulin Granule Diffusion is a Prerequisite for Recruiting Granules for Release.
• 2003
  • Impaired insulin secretion and glucose tolerance in beta cell-selective Ca(V)1.2 Ca(2+) channel null mice.
  • Insulin granule dynamics in pancreatic beta cells
  • SUR1 Regulates PKA-independent cAMP-induced Granule Priming in Mouse Pancreatic B-cells.
• 2002
  • A Subset of 50 Secretory Granules in Close Contact With L-Type Ca(2+) Channels Accounts for First-Phase Insulin Secretion in Mouse beta-Cells.
  • Delay between fusion pore opening and peptide release from large dense-core vesicles in neuroendocrine cells.
  • Glucose dependence of insulinotropic actions of pituitary adenylate cyclase-activating polypeptide in insulin-secreting INS-1 cells.
  • Important role of phosphodiesterase 3B for the stimulatory action of cAMP on pancreatic beta -cell exocytosis and release of insulin.
  • Inositol 3,4,5,6-tetrakisphosphate inhibits insulin granule acidification and fusogenic potential.
  • Sulfonylurea-Mediated Stimulation of Insulin Exocytosis via an ATP-Sensitive K(+) Channel--Independent Action.
• 2001
  • Differential glucose responsitivity in insulin-producing cell lines derived from the INS-1 line is associated with altered Ca2+dynamics and Ca2+-evoked exocytosis
  • Fast exocytosis with few Ca(2+) channels in insulin-secreting mouse pancreatic B cells
  • Perchlorate stimulates insulin secretion by shifting the gating of L-type Ca2+ currents in mouse pancreatic B-cells towards negative potentials
  • Phosphodiesterase 3B is activated by glucose and insulin in rat islets and involved in Ca2+-stimulated exocytosis
  • Priming of insulin granules for exocytosis by granular Cl(-) uptake and acidification
• 2000
  • The Cell Physiology of Biphasic Insulin Secretion
• 1999
  • Activation of Ca(2+)-dependent K(+) channels contributes to rhythmic firing of action potentials in mouse pancreatic beta cells
  • CaM kinase II-dependent mobilization of secretory granules underlies acetylcholine-induced stimulation of exocytosis in mouse pancreatic B-cells
  • Cell biology. Glutamate primes the pump
  • The stimulatory action of tolbutamide on Ca2+-dependent exocytosis in pancreatic beta cells is mediated by a 65-kDa mdr-like P-glycoprotein
  • The voltage sensitive Lc-type Ca2+ channel is functionally coupled to the exocytotic machinery
• 1997
  • Adrenaline stimulates glucagon secretion in pancreatic A-cells by increasing the Ca2+ current and the number of granules close to the L-type Ca2+ channels
  • Components of insulin secretion: lessons to be learnt from capacitance
  • Glucagon-like peptide I and glucose-dependent insulinotropic polypeptide stimulate Ca2+-induced secretion in rat alpha-cells by a protein kinase A-mediated mechanism
  • Multisite regulation of insulin secretion by cAMP-increasing agonists: evidence that glucagon-like peptide 1 and glucagon act via distinct receptors
  • Protein kinase A-dependent and -independent stimulation of exocytosis by cAMP in mouse pancreatic B-cells
  • Rapid ATP-dependent priming of secretory granules precedes Ca(2+)-induced exocytosis in mouse pancreatic B-cells
• 1996
  • Cooling inhibits exocytosis in single mouse pancreatic B-cells by suppression of granule mobilization
  • Dynamics of the cationic, bioelectrical and secretory responses to formycin A in pancreatic islet cells
  • Neurotransmitter-induced inhibition of exocytosis in insulin-secreting beta cells by activation of calcineurin
  • PKC-dependent stimulation of exocytosis by sulfonylureas in pancreatic beta cells
• 1995
  • Co-localization of L-type Ca2+ channels and insulin-containing secretory granules and its significance for the initiation of exocytosis in mouse pancreatic B-cells
  • Glucagon-like peptide I increases cytoplasmic calcium in insulin-secreting beta TC3-cells by enhancement of intracellular calcium mobilization
• 1994
  • Ion channels, electrical activity and insulin secretion