Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells

Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show that MODY3-related HNF1A mutation in patient hiPSCderived pancreatic cells decreases glucose transporter GLUT2 expression due to compromised...

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Autores principales:	Blaise Su Jun Low, Chang Siang Lim, Shirley Suet Lee Ding, Yaw Sing Tan, Natasha Hui Jin Ng, Vidhya Gomathi Krishnan, Su Fen Ang, Claire Wen Ying Neo, Chandra S. Verma, Shawn Hoon, Su Chi Lim, E. Shyong Tai, Adrian Kee Keong Teo
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/03229c3f34e24347bae20e13a756621c
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spelling	oai:doaj.org-article:03229c3f34e24347bae20e13a756621c2021-12-02T16:53:15ZDecreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells10.1038/s41467-021-22843-42041-1723https://doaj.org/article/03229c3f34e24347bae20e13a756621c2021-05-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-22843-4https://doaj.org/toc/2041-1723Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show that MODY3-related HNF1A mutation in patient hiPSCderived pancreatic cells decreases glucose transporter GLUT2 expression due to compromised DNA binding.Blaise Su Jun LowChang Siang LimShirley Suet Lee DingYaw Sing TanNatasha Hui Jin NgVidhya Gomathi KrishnanSu Fen AngClaire Wen Ying NeoChandra S. VermaShawn HoonSu Chi LimE. Shyong TaiAdrian Kee Keong TeoNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-20 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Blaise Su Jun Low Chang Siang Lim Shirley Suet Lee Ding Yaw Sing Tan Natasha Hui Jin Ng Vidhya Gomathi Krishnan Su Fen Ang Claire Wen Ying Neo Chandra S. Verma Shawn Hoon Su Chi Lim E. Shyong Tai Adrian Kee Keong Teo Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells
description	Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show that MODY3-related HNF1A mutation in patient hiPSCderived pancreatic cells decreases glucose transporter GLUT2 expression due to compromised DNA binding.
format	article
author	Blaise Su Jun Low Chang Siang Lim Shirley Suet Lee Ding Yaw Sing Tan Natasha Hui Jin Ng Vidhya Gomathi Krishnan Su Fen Ang Claire Wen Ying Neo Chandra S. Verma Shawn Hoon Su Chi Lim E. Shyong Tai Adrian Kee Keong Teo
author_facet	Blaise Su Jun Low Chang Siang Lim Shirley Suet Lee Ding Yaw Sing Tan Natasha Hui Jin Ng Vidhya Gomathi Krishnan Su Fen Ang Claire Wen Ying Neo Chandra S. Verma Shawn Hoon Su Chi Lim E. Shyong Tai Adrian Kee Keong Teo
author_sort	Blaise Su Jun Low
title	Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells
title_short	Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells
title_full	Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells
title_fullStr	Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells
title_full_unstemmed	Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells
title_sort	decreased glut2 and glucose uptake contribute to insulin secretion defects in mody3/hnf1a hipsc-derived mutant β cells
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/03229c3f34e24347bae20e13a756621c
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Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells

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