Derivation and characterization of two human induced pluripotent stem cell lines (NUIGi004-A) and (NUIGi012-A) from two patients with LQT2 disease

Min Liu; Ning Ge; Jianhua Zhang; Meimei Yang; Fan Yang; Janusz Krawczyk; Deirdre Ward; Veronica McInerney; Timothy O'Brien; Sanbing Shen; Terence Prendiville

doi:10.1016/j.scr.2021.102555

Derivation and characterization of two human induced pluripotent stem cell lines (NUIGi004-A) and (NUIGi012-A) from two patients with LQT2 disease

Min Liu
, Ning Ge
, Jianhua Zhang
, Meimei Yang
, Fan Yang
, Janusz Krawczyk
, Deirdre Ward
, Veronica McInerney
, Timothy O'Brien
, Sanbing Shen
, Terence Prendiville

Medicine

Research output: Contribution to a Journal (Peer & Non Peer) › Article › peer-review

1 Citation (Scopus)

Abstract

Long QT syndrome type 2 (LQT2) is associated with KCNH2, which encodes the α subunit of the ion channel that controls the K⁺ current in the heart. Mutations of KCNH2 cause loss of Kv11.1 channel function by disrupting subunit folding, assembly, or trafficking of the channel to the cell surface. Here we generated two induced pluripotent stem cell (iPSC) lines from two patients carrying mutation in KCNH2 gene. These iPSCs express the pluripotent markers and have the capacity of differentiation into other cell types. These patient-derived iPSCs are useful for investigating the disease pathology and identifying the therapeutic target.

Original language	English
Article number	102555
Journal	Stem Cell Research
Volume	56
DOIs	https://doi.org/10.1016/j.scr.2021.102555
Publication status	Published - Oct 2021

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10.1016/j.scr.2021.102555

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title = "Derivation and characterization of two human induced pluripotent stem cell lines (NUIGi004-A) and (NUIGi012-A) from two patients with LQT2 disease",

abstract = "Long QT syndrome type 2 (LQT2) is associated with KCNH2, which encodes the α subunit of the ion channel that controls the K+ current in the heart. Mutations of KCNH2 cause loss of Kv11.1 channel function by disrupting subunit folding, assembly, or trafficking of the channel to the cell surface. Here we generated two induced pluripotent stem cell (iPSC) lines from two patients carrying mutation in KCNH2 gene. These iPSCs express the pluripotent markers and have the capacity of differentiation into other cell types. These patient-derived iPSCs are useful for investigating the disease pathology and identifying the therapeutic target.",

author = "Min Liu and Ning Ge and Jianhua Zhang and Meimei Yang and Fan Yang and Janusz Krawczyk and Deirdre Ward and Veronica McInerney and Timothy O'Brien and Sanbing Shen and Terence Prendiville",

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year = "2021",

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doi = "10.1016/j.scr.2021.102555",

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T1 - Derivation and characterization of two human induced pluripotent stem cell lines (NUIGi004-A) and (NUIGi012-A) from two patients with LQT2 disease

AU - Liu, Min

AU - Ge, Ning

AU - Zhang, Jianhua

AU - Yang, Meimei

AU - Yang, Fan

AU - Krawczyk, Janusz

AU - Ward, Deirdre

AU - McInerney, Veronica

AU - O'Brien, Timothy

AU - Shen, Sanbing

AU - Prendiville, Terence

PY - 2021/10

Y1 - 2021/10

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AB - Long QT syndrome type 2 (LQT2) is associated with KCNH2, which encodes the α subunit of the ion channel that controls the K+ current in the heart. Mutations of KCNH2 cause loss of Kv11.1 channel function by disrupting subunit folding, assembly, or trafficking of the channel to the cell surface. Here we generated two induced pluripotent stem cell (iPSC) lines from two patients carrying mutation in KCNH2 gene. These iPSCs express the pluripotent markers and have the capacity of differentiation into other cell types. These patient-derived iPSCs are useful for investigating the disease pathology and identifying the therapeutic target.

UR - https://www.scopus.com/pages/publications/85116712955

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DO - 10.1016/j.scr.2021.102555

M3 - Article

C2 - 34628246

AN - SCOPUS:85116712955

SN - 1873-5061

VL - 56

JO - Stem Cell Research

JF - Stem Cell Research

M1 - 102555

ER -

Derivation and characterization of two human induced pluripotent stem cell lines (NUIGi004-A) and (NUIGi012-A) from two patients with LQT2 disease

Abstract

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