Zobrazeno 1 - 10
of 26
pro vyhledávání: '"David R. Grubb"'
Publikováno v:
PLoS ONE, Vol 11, Iss 6, p e0158317 (2016)
Diseased myocardium from humans and experimental animal models shows heightened expression and activity of a specific subtype of phospholipase C (PLC), the splice variant PLCβ1b. Previous studies from our group showed that increasing PLCβ1b express
Externí odkaz:
https://doaj.org/article/b8940a63d5624ad68cb802d413818a75
Publikováno v:
Biochemical and Biophysical Research Communications. 461:519-524
Phospholipase Cβ1b (PLCβ1b) is an atypical splice variant of PLCβ1 that has a C-terminal proline-rich sequence instead of the PDZ-interacting motif common to other PLCβ subtypes. PLCβ1b targets to the cardiomyocyte sarcolemma through an undefine
Publikováno v:
Journal of Molecular and Cellular Cardiology. 54:19-24
Autophagy is a process that removes damaged proteins and organelles and is of particular importance in terminally differentiated cells such as cardiomyocytes, where it has primarily a protective role. We investigated the involvement of inositol(1,4,5
Publikováno v:
The FASEB Journal. 26:596-603
Activation of the heterotrimeric G protein, Gq, causes cardiomyocyte hypertrophy in vivo and in cell models. Responses to activated Gq in cardiomyocytes are mediated exclusively by phospholipase Cβ1b (PLCβ1b), because it localizes at the sarcolemma
Autor:
Peter Iliades, Jieting Luo, Elizabeth A. Woodcock, David R. Grubb, Nicola Cooley, Theresa M. Filtz, Yen Lin Yu
Publikováno v:
The FASEB Journal. 25:1040-1047
Activation of the heterotrimeric G protein Gq causes cardiomyocyte hypertrophy in vivo and in cell models. Our previous studies have shown that responses to activated Gq in cardiomyocytes are mediated exclusively by phospholipase Cβ1b (PLCβ1b), bec
Autor:
Theresa M. Filtz, Oliver Vasilevski, Jieting Luo, Elizabeth A. Woodcock, Tiffany J. McLeod-Dryden, Sundy Yang, Divya Karna, David R. Grubb, Ju Chen
Publikováno v:
Journal of Molecular and Cellular Cardiology. 45:679-684
The functional significance of the Ca2+-releasing second messenger inositol(1,4,5)trisphosphate (Ins(1,4,5)P(3), IP(3)) in the heart has been controversial. Ins(1,4,5)P(3) is generated from the precursor lipid phosphatidylinositol(4,5)bisphosphate (P
Autor:
David R. Grubb, Aya Matsumoto, Xiao-Jun Du, Xiao-Ming Gao, Julie R. McMullen, Helen Kiriazis, Elizabeth A. Woodcock
Publikováno v:
Journal of molecular and cellular cardiology. 93
The activity of phospholipase Cβ1b (PLCβ1b) is selectively elevated in failing myocardium and cardiac expression of PLCβ1b causes contractile dysfunction. PLCβ1b can be selectively inhibited by expressing a peptide inhibitor that prevents sarcole
Publikováno v:
Circulation Research. 117
The immediate downstream effector of Galpahq is the early signaling enzyme phospholipase Cbeta1b (PLCbeta1b), which is selectively elevated in failing human myocardium. When delivered to the adult mouse heart, expression of PLCbeta1b causes rapid con
Autor:
H. Qian, Xiao-Jun Du, Xiao-Ming Gao, Jieting Luo, Paul Gregorevic, Helen Kiriazis, Elizabeth A. Woodcock, Yi Ma, Bryony Crook, David R. Grubb
Publikováno v:
Journal of molecular and cellular cardiology. 84
The activity of the early signaling enzyme, phospholipase Cβ1b (PLCβ1b), is selectively elevated in diseased myocardium and activity increases with disease progression. We aimed to establish the contribution of heightened PLCβ1b activity to cardia
Autor:
David R. Grubb, Elizabeth A. Woodcock
Publikováno v:
Clinical Medicine Insights: Therapeutics, Vol 7 (2015)
Clinical Medicine Insights: Therapeutics, Vol 2015, Iss 7, Pp 11-16 (2015)
Clinical Medicine Insights: Therapeutics, Vol 2015, Iss 7, Pp 11-16 (2015)
Inotropic agents are often used to improve the contractile performance of the failing myocardium, but this is often at a cost of increased myocardial ischemia and arrhythmia. Myocyte contractility depends on the release of Ca2+from the sarcoplasmic r