Tarnavski相关文献与解析，生知库 | 链接生命科学的每一步

Fumin Fu, Michael Pietropaolo, Lei Cui, Shilpa Pandit, Weiyan Li, Oleg Tarnavski, Suraj S Shetty, Jing Liu, Jennifer M Lussier, Yutaka Murakami, Prabhjit K Grewal, Galina Deyneko, Gordon M Turner, Andrew K P Taggart, M Gerard Waters, Shaun Coughlin, Yuichiro Adachi

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发表日期：2022

文献求助收藏

Correction for McMullen et al., "Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy"

对 McMullen 等人的文章“核糖体 S6 激酶的缺失不会减弱病理性、生理性或胰岛素样生长因子 1 受体-磷脂酰肌醇 3-激酶诱导的心脏肥大”的更正

期刊:Molecular and Cellular Biology

影响因子:2.7

doi:10.1128/MCB.00635-20

McMullen, Julie R; Shioi, Tetsuo; Zhang, Li; Tarnavski, Oleg; Sherwood, Megan C; Dorfman, Adam L; Longnus, Sarah; Pende, Mario; Martin, Kathleen A; Blenis, John; Thomas, George; Izumo, Seigo

Transcription factor GATA4 is activated but not required for insulin-like growth factor 1 (IGF1)-induced cardiac hypertrophy

转录因子 GATA4 被激活但不是胰岛素样生长因子 1 (IGF1) 诱导的心脏肥大所必需的

期刊:Journal of Biological Chemistry

影响因子:4

doi:10.1074/jbc.M111.338749

Egbert Bisping, Sadakatsu Ikeda, Miriam Sedej, Paulina Wakula, Julie R McMullen, Oleg Tarnavski, Simon Sedej, Seigo Izumo, William T Pu, Burkert Pieske

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发表日期：2012

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Gata4 is required for maintenance of postnatal cardiac function and protection from pressure overload-induced heart failure

Gata4 是维持出生后心脏功能和防止压力超负荷诱发的心力衰竭所必需的。

期刊:Proceedings of the National Academy of Sciences of the United States of America

影响因子:9.1

doi:10.1073/pnas.0602543103

Bisping, Egbert; Ikeda, Sadakatsu; Kong, Sek Won; Tarnavski, Oleg; Bodyak, Natalya; McMullen, Julie R; Rajagopal, Satish; Son, Jennifer K; Ma, Qing; Springer, Zhangli; Kang, Peter M; Izumo, Seigo; Pu, William T

Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy

核糖体S6激酶的缺失并不能减轻病理性、生理性或胰岛素样生长因子1受体-磷脂酰肌醇3-激酶诱导的心脏肥大。

期刊:Molecular and Cellular Biology

影响因子:2.7

doi:10.1128/MCB.24.14.6231-6240.2004

McMullen, Julie R; Shioi, Tetsuo; Zhang, Li; Tarnavski, Oleg; Sherwood, Megan C; Dorfman, Adam L; Longnus, Sarah; Pende, Mario; Martin, Kathleen A; Blenis, John; Thomas, George; Izumo, Seigo

Lack of authentic atrial fibrillation in commonly used murine atrial fibrillation models

常用的小鼠心房颤动模型缺乏真实的心房颤动

Correction for McMullen et al., "Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy"

对 McMullen 等人的文章“核糖体 S6 激酶的缺失不会减弱病理性、生理性或胰岛素样生长因子 1 受体-磷脂酰肌醇 3-激酶诱导的心脏肥大”的更正

Transcription factor GATA4 is activated but not required for insulin-like growth factor 1 (IGF1)-induced cardiac hypertrophy

转录因子 GATA4 被激活但不是胰岛素样生长因子 1 (IGF1) 诱导的心脏肥大所必需的

Gata4 is required for maintenance of postnatal cardiac function and protection from pressure overload-induced heart failure

Gata4 是维持出生后心脏功能和防止压力超负荷诱发的心力衰竭所必需的。

Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy

核糖体S6激酶的缺失并不能减轻病理性、生理性或胰岛素样生长因子1受体-磷脂酰肌醇3-激酶诱导的心脏肥大。