Zobrazeno 1 - 10
of 35
pro vyhledávání: '"Lianzhi Gu"'
Autor:
An Xie, Zhen Song, Hong Liu, Anyu Zhou, Guangbin Shi, Qiongying Wang, Lianzhi Gu, Man Liu, Lai‐Hua Xie, Zhilin Qu, Samuel C. Dudley
Publikováno v:
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 7, Iss 8 (2018)
BackgroundHeart failure (HF) is associated with increased arrhythmia risk and triggered activity. Abnormal Ca2+ handling is thought to underlie triggered activity, and mitochondria participate in Ca2+ homeostasis. Methods and ResultsA model of nonisc
Externí odkaz:
https://doaj.org/article/fc176c57719242de993451f239fb0dc4
Autor:
Man Long Kwok, Geyer, Melissa, Wan Ching Chan, Shuangping Zhao, Lianzhi Gu, Fei Huang, Vogel, Steven M., Petukhov, Pavel A., Komarova, Yulia
Publikováno v:
American Journal of Respiratory Cell & Molecular Biology; Oct2023, Vol. 69 Issue 4, p391-403, 13p
Autor:
Samuel C. Dudley, Preethy Parthiban, Gyeoung Jin Kang, Elena G. Tolkacheva, Courtney Karnopp, Guangbin Shi, Anyu Zhou, Feng Feng, Lianzhi Gu, Hong Liu, Man Liu
Publikováno v:
J Clin Invest
Ischemic cardiomyopathy is associated with an increased risk of sudden death, activation of the unfolded protein response (UPR), and reductions in multiple cardiac ion channels. When activated, the protein kinase-like ER kinase (PERK) branch of the U
Autor:
Anyu Zhou, Hong Liu, Samuel C. Dudley, Guangbin Shi, Man Liu, Lianzhi Gu, Gyeoung Jin Kang, Feng Feng, Alena Talkachova, Preethy Parthiban
Publikováno v:
Circulation Research. 127
Background: Ischemic cardiomyopathy is associated with an increased risk of sudden death, activation of the unfolded protein response (UPR), and reductions in multiple cardiac ion channels and transporters. When activated, the protein kinase-like ER
Autor:
Zhen Song, Guangbin Shi, Qiongying Wang, Lianzhi Gu, Zhilin Qu, Hong Liu, An Xie, Samuel C. Dudley, Anyu Zhou, Lai-Hua Xie, Man Liu
Publikováno v:
Journal of the American Heart Association. 7
Background Heart failure (HF) is associated with increased arrhythmia risk and triggered activity. Abnormal Ca 2+ handling is thought to underlie triggered activity, and mitochondria participate in Ca 2+ homeostasis. Methods and Results A model of no
Autor:
An, Xie, Zhen, Song, Hong, Liu, Anyu, Zhou, Guangbin, Shi, Qiongying, Wang, Lianzhi, Gu, Man, Liu, Lai-Hua, Xie, Zhilin, Qu, Samuel C, Dudley
Publikováno v:
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Background Heart failure (HF) is associated with increased arrhythmia risk and triggered activity. Abnormal Ca2+ handling is thought to underlie triggered activity, and mitochondria participate in Ca2+ homeostasis. Methods and Results A model of noni
Autor:
Lianzhi Gu, Ge Gao, Anyu Zhou, J. Andrew Wasserstrom, Samuel C. Dudley, Sharlene M. Day, Adam M Noyes
Background Our previous studies showed that in ischemic and nonischemic heart failure (HF), the voltage-gated cardiac Na + channel α subunit (SCN5A) mRNA is abnormally spliced to produce two truncated transcript variants (E28C and D) that activate t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::75fcb7808f02cb7dee06d2a482471b4d
https://europepmc.org/articles/PMC5681396/
https://europepmc.org/articles/PMC5681396/
Autor:
Vikram Brahmanandam, Anish Shah, Lianzhi Gu, Mihai Raicu, Melissa Robinson Wood, Samuel C. Dudley, Alan Schwartz, Li Zhou, Srinivasan Kasturirangan, Smita I. Negi, Ankit A. Desai, Antone Tatooles, Ge Gao
Publikováno v:
Journal of the American College of Cardiology. 63(21):2261-2269
Objectives The aim of this study was to determine the association of SCN5A cardiac sodium (Na+) channel mRNA splice variants in white blood cells (WBCs) with risk of arrhythmias in heart failure (HF). Background HF is associated with upregulation of
Autor:
Guangbin Shi, Samuel C. Dudley, Anumantha G. Kanthasamy, Kai-Chien Yang, Vellareddy Anantharam, Man Liu, Lianzhi Gu
Background The reduced form of nicotinamide adenine dinucleotide (NADH) increases in cardiomyopathy, activates protein kinase C (PKC), up-regulates mitochondrial reactive oxygen species (mitoROS), and down-regulates the cardiac Na+ channel (NaV1.5).
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3de682ec1fc3491bc5227f694bde5c36
https://europepmc.org/articles/PMC5316355/
https://europepmc.org/articles/PMC5316355/
Autor:
Jianhua Zhang, Kai-Chien Yang, Man Liu, Ge Gao, Timothy J. Kamp, Samuel C. Dudley, Euy Myoung Jeong, An Xie, Lianzhi Gu, Amanda M. Herman
Publikováno v:
Circulation: Arrhythmia and Electrophysiology. 6:1018-1024
Background— Human heart failure (HF) increases alternative mRNA splicing of the type V, voltage-gated cardiac Na + channel α-subunit (SCN5A), generating variants encoding truncated, nonfunctional channels that are trapped in the endoplasmic reticu