| http://purl.uniprot.org/citations/19696098 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19696098 | http://www.w3.org/2000/01/rdf-schema#comment | "Src homology 2 domain-containing protein B (SHB) is an adapter protein involved in the regulation of beta-cell and endothelial cell function. We have recently obtained the Shb knockout mouse, and consequently, the aim of this study was to assess the effect of Shb deletion upon beta-cell function and blood glucose homeostasis. Shb-/-mice display an elevated basal blood glucose concentration, and this increase is maintained during insulin challenge in insulin sensitivity tests. To assess glucose-induced insulin secretion, pancreata were perfused, and it was observed that Shb-/-first phase insulin secretion was blunted during glucose stimulation. Gene expression of Shb-/-islets shortly after isolation was altered, with increased pancreatic and duodenal homeobox gene-1 (Pdx1) gene expression and reduced expression of Vegf-A. Islet culture normalized Pdx1 gene expression. The microvascular density of the Shb-/-islets was reduced, and islet capillary endothelial cell morphology was changed suggesting an altered microvascular function as a contributing cause to the impaired secretory activity. Capacitance measurements of depolarization-induced exocytosis indicate a direct effect on the exocytotic machinery, in particular a dramatic reduction in readily releasable granules, as responsible for the insulin-secretory defect operating in Shb-/- islets. Shb-/-mice exhibited no alteration of islet volume or beta-cell area. In conclusion, loss of Shb impairs insulin secretion, alters islet microvascular morphology, and increases the basal blood glucose concentration. The impaired insulin secretory response is a plausible underlying cause of the metabolic impairment observed in this mutant mouse."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.org/dc/terms/identifier | "doi:10.1677/joe-09-0198"xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/author | "Welsh M."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/author | "Jansson L."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/author | "Akerblom B."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/author | "Barg S."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/author | "Mokhtari D."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/author | "Calounova G."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/name | "J Endocrinol"xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/pages | "271-279"xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/title | "Impaired glucose homeostasis in Shb-/- mice."xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://purl.uniprot.org/core/volume | "203"xsd:string |
| http://purl.uniprot.org/citations/19696098 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19696098 |
| http://purl.uniprot.org/citations/19696098 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19696098 |
| http://purl.uniprot.org/uniprot/#_Q6PD21-mappedCitation-19696098 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19696098 |
| http://purl.uniprot.org/uniprot/Q6PD21 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/19696098 |