PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. indoleacetic acid 51-54 insulin Homo sapiens 43-50 13910496-0 1962 Quantitative effects of glucose, sulfonylureas, salicylate, and indole-3-acetic acid on the secretion of insulin activity into pancreatic venous blood. indoleacetic acid 64-84 insulin Homo sapiens 105-112 13634074-0 1959 Plasma insulin activity in human diabetes during hypoglycemic response to tolbutamide and indole-3-acetic acid. indoleacetic acid 90-110 insulin Homo sapiens 7-14 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. indoleacetic acid 51-54 insulin Homo sapiens 141-148 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. indoleacetic acid 51-54 insulin Homo sapiens 141-148 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. indoleacetic acid 129-132 insulin Homo sapiens 43-50 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. indoleacetic acid 129-132 insulin Homo sapiens 141-148 32308449-3 2020 IAS pathogenesis involves the formation of insulin-IAA complexes that induce glycemic alterations with a double-phase mechanism: IAA prevent insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia. indoleacetic acid 129-132 insulin Homo sapiens 141-148 17059894-2 2007 IAA affinity was measured by competitive binding using constant amounts of Tyr14A [125I] human insulin and increasing quantities of unlabeled human insulin. indoleacetic acid 0-3 insulin Homo sapiens 95-102 25583753-7 2015 During follow-up, good responders to anti-CD3 treatment (i.e., IAA(+) participants with relatively preserved beta-cell function [>= 25% of healthy control subjects]) experienced a less pronounced insulin-induced rise in I(A)A and lower insulin needs. indoleacetic acid 63-66 insulin Homo sapiens 199-206 25583753-7 2015 During follow-up, good responders to anti-CD3 treatment (i.e., IAA(+) participants with relatively preserved beta-cell function [>= 25% of healthy control subjects]) experienced a less pronounced insulin-induced rise in I(A)A and lower insulin needs. indoleacetic acid 63-66 insulin Homo sapiens 239-246 23835325-6 2013 The risk-associated insulin gene rs689 A/A genotypes were more frequent in children with IAA as the first autoantibody compared with the other children (P = 0.002). indoleacetic acid 89-92 insulin Homo sapiens 20-27 17059894-2 2007 IAA affinity was measured by competitive binding using constant amounts of Tyr14A [125I] human insulin and increasing quantities of unlabeled human insulin. indoleacetic acid 0-3 insulin Homo sapiens 148-155 10047433-7 1999 IAA was more frequently detected in insulin-requiring patients (40%vs. indoleacetic acid 0-3 insulin Homo sapiens 36-43 16010521-4 2005 METHODS: IAA affinity was determined by competitive binding to 125I-insulin with increasing concentrations of cold insulin and with cold proinsulin in sera from 46 IAA-positive children identified in the Karlsburg Type 1 Diabetes Risk Study of a Normal Schoolchild Population in north-eastern Germany. indoleacetic acid 9-12 insulin Homo sapiens 68-75 16010521-4 2005 METHODS: IAA affinity was determined by competitive binding to 125I-insulin with increasing concentrations of cold insulin and with cold proinsulin in sera from 46 IAA-positive children identified in the Karlsburg Type 1 Diabetes Risk Study of a Normal Schoolchild Population in north-eastern Germany. indoleacetic acid 9-12 insulin Homo sapiens 115-122 16010521-4 2005 METHODS: IAA affinity was determined by competitive binding to 125I-insulin with increasing concentrations of cold insulin and with cold proinsulin in sera from 46 IAA-positive children identified in the Karlsburg Type 1 Diabetes Risk Study of a Normal Schoolchild Population in north-eastern Germany. indoleacetic acid 9-12 insulin Homo sapiens 137-147 16010521-8 2005 IAA affinity was significantly higher in samples with proinsulin reactive IAA (p<0.0001). indoleacetic acid 0-3 insulin Homo sapiens 54-64 10073003-5 1997 Only in this group, the levels of IAA varied with increased amount of unlabeled insulin (P < 0.01). indoleacetic acid 34-37 insulin Homo sapiens 80-87 10073003-6 1997 Should similar events be confronted, it is advisable to increase the amount of unlabeled insulin in IAA radioimmunoassay on purpose to avoid missed diagnosis. indoleacetic acid 100-103 insulin Homo sapiens 89-96 3046970-8 1988 After total insulin extraction of IAA samples, there was a significant fall in mean I1 + 3 to 134 +/- 55.4 mU/L (P less than .001), but the control value was unchanged. indoleacetic acid 34-37 insulin Homo sapiens 12-19 3046970-9 1988 IAA can significantly falsify insulin measurement, and care must be taken in the interpretation of insulin-release tests when IAA is present. indoleacetic acid 0-3 insulin Homo sapiens 30-37 3046970-9 1988 IAA can significantly falsify insulin measurement, and care must be taken in the interpretation of insulin-release tests when IAA is present. indoleacetic acid 126-129 insulin Homo sapiens 99-106 1478247-2 1992 Maximal specific insulin binding was 7.8 (1.5; SE) pmol l-1 for IAA and 28.1 (6.7) pmol l-1 for IBA (P < 0.01), and the binding capacity of the high affinity class of IAA 0.01 (0.003) nmol l-1, as compared with 0.19 (0.08) nmol l-1 for the corresponding IBA class (P < 0.01). indoleacetic acid 64-67 insulin Homo sapiens 17-24