日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human β-cardiac myosin allosterically

肥厚型心肌病突变Y115H和E497D通过变构作用破坏人β-心肌肌球蛋白的折叠状态。

Nandwani, Neha; Bhowmik, Debanjan; Glaser, Camille; Childers, Matthew Carter; Goluguri, Rama Reddy; Dawood, Aminah; Regnier, Michael; Houdusse, Anne; Spudich, James A; Ruppel, Kathleen M

A FRET assay to monitor different structural states of human β-cardiac myosin including the interacting-heads motif

利用FRET检测法监测人β-心肌肌球蛋白的不同结构状态,包括相互作用头部基序。

Goluguri, Rama Reddy; Guhathakurta, Piyali; Nandwani, Neha; Dawood, Aminah; Yokota, Seiji; Roopnarine, Osha; Thomas, David D; Ruppel, Kathleen M; Spudich, James A

The G256E HCM mutation prolongs relaxation via altered nucleotide handling

G256E HCM突变通过改变核苷酸处理延长舒张期。

Kao, Kerry Yvonne; Childers, Matthew Carter; Pathak, Divya; Goluguri, Rama Reddy; McMillen, Timothy S; Ruppel, Kathleen M; Spudich, James A; Regnier, Michael

Incomplete-penetrant hypertrophic cardiomyopathy MYH7 G256E mutation causes hypercontractility and elevated mitochondrial respiration

MYH7 G256E 突变导致不完全外显的肥厚型心肌病,引起心肌收缩力增强和线粒体呼吸增强。

Lee, Soah; Vander Roest, Alison S; Blair, Cheavar A; Kao, Kerry; Bremner, Samantha B; Childers, Matthew C; Pathak, Divya; Heinrich, Paul; Lee, Daniel; Chirikian, Orlando; Mohran, Saffie E; Roberts, Brock; Smith, Jacqueline E; Jahng, James W; Paik, David T; Wu, Joseph C; Gunawardane, Ruwanthi N; Ruppel, Kathleen M; Mack, David L; Pruitt, Beth L; Regnier, Michael; Wu, Sean M; Spudich, James A; Bernstein, Daniel

Reassessing the unifying hypothesis for hypercontractility caused by myosin mutations in hypertrophic cardiomyopathy

重新评估肥厚型心肌病中肌球蛋白突变引起的过度收缩的统一假说

Spudich, James A; Nandwani, Neha; Robert-Paganin, Julien; Houdusse, Anne; Ruppel, Kathleen M

One must reconstitute the functions of interest from purified proteins

必须从纯化的蛋白质中重建目标功能。

Spudich, James A

From amoeboid myosin to unique targeted medicines for a genetic cardiac disease

从变形虫样肌球蛋白到针对遗传性心脏病的独特靶向药物

Spudich, James A

Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin allosterically

肥厚型心肌病突变Y115H和E497D通过变构作用破坏人β-心肌肌球蛋白的折叠状态。

Nandwani, Neha; Bhowmik, Debanjan; Childers, Matthew C; Goluguri, Rama Reddy; Dawood, Aminah; Regnier, Michael; Spudich, James A; Ruppel, Kathleen M

Motility Assay to Probe the Calcium Sensitivity of Myosin and Regulated Thin Filaments

运动性分析用于探测肌球蛋白和调节性细丝的钙敏感性

Liu, Chao; Ruppel, Kathleen M; Spudich, James A

A FRET assay to quantitate levels of the human β-cardiac myosin interacting heads motif based on its near-atomic resolution structure.

基于接近原子分辨率结构的FRET检测方法,可定量分析人类β-心肌肌球蛋白相互作用头部基序的水平

Goluguri Rama Reddy, Guhathakurta Piyali, Nandwani Neha, Dawood Aminah, Yakota Seiji, Roopnarine Osha, Thomas David D, Spudich James A, Ruppel Kathleen M