The genetic and regulatory architecture of ERBB3-type 1 diabetes susceptibility locus
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The genetic and regulatory architecture of ERBB3-type 1 diabetes susceptibility locus. / Kaur, Simranjeet; Mirza, Aashiq H.; Brorsson, Caroline Anna; Fløyel, Tina; Størling, Joachim; Mortensen, Henrik B.; Pociot, Flemming; Hvidoere International Study Group.
In: Molecular and Cellular Endocrinology, Vol. 419, 05.01.2016, p. 83-91.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - The genetic and regulatory architecture of ERBB3-type 1 diabetes susceptibility locus
AU - Kaur, Simranjeet
AU - Mirza, Aashiq H.
AU - Brorsson, Caroline Anna
AU - Fløyel, Tina
AU - Størling, Joachim
AU - Mortensen, Henrik B.
AU - Pociot, Flemming
AU - Hvidoere International Study Group
N1 - Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
PY - 2016/1/5
Y1 - 2016/1/5
N2 - The study aimed to explore the role of ERBB3 in type 1 diabetes (T1D). We examined whether genetic variation of ERBB3 (rs2292239) affects residual β-cell function in T1D cases. Furthermore, we examined the expression of ERBB3 in human islets, the effect of ERBB3 knockdown on apoptosis in insulin-producing INS-1E cells and the genetic and regulatory architecture of the ERBB3 locus to provide insights to how rs2292239 may confer disease susceptibility. rs2292239 strongly correlated with residual β-cell function and metabolic control in children with T1D. ERBB3 locus associated lncRNA (NONHSAG011351) was found to be expressed in human islets. ERBB3 was expressed and down-regulated by pro-inflammatory cytokines in human islets and INS-1E cells; knockdown of ERBB3 in INS-1E cells decreased basal and cytokine-induced apoptosis. Our data suggests an important functional role of ERBB3 and its potential regulators in the β-cells and may constitute novel targets to prevent β-cell destruction in T1D.
AB - The study aimed to explore the role of ERBB3 in type 1 diabetes (T1D). We examined whether genetic variation of ERBB3 (rs2292239) affects residual β-cell function in T1D cases. Furthermore, we examined the expression of ERBB3 in human islets, the effect of ERBB3 knockdown on apoptosis in insulin-producing INS-1E cells and the genetic and regulatory architecture of the ERBB3 locus to provide insights to how rs2292239 may confer disease susceptibility. rs2292239 strongly correlated with residual β-cell function and metabolic control in children with T1D. ERBB3 locus associated lncRNA (NONHSAG011351) was found to be expressed in human islets. ERBB3 was expressed and down-regulated by pro-inflammatory cytokines in human islets and INS-1E cells; knockdown of ERBB3 in INS-1E cells decreased basal and cytokine-induced apoptosis. Our data suggests an important functional role of ERBB3 and its potential regulators in the β-cells and may constitute novel targets to prevent β-cell destruction in T1D.
KW - Journal Article
KW - Research Support, N.I.H., Extramural
KW - Research Support, Non-U.S. Gov't
U2 - 10.1016/j.mce.2015.10.002
DO - 10.1016/j.mce.2015.10.002
M3 - Journal article
C2 - 26450151
VL - 419
SP - 83
EP - 91
JO - Molecular and Cellular Endocrinology
JF - Molecular and Cellular Endocrinology
SN - 0303-7207
ER -
ID: 178487913