نتایج جستجو برای: trpc3

تعداد نتایج: 533  

Journal: :The Biochemical journal 2008
Jin Seok Woo Do Han Kim Paul D Allen Eun Hui Lee

The expression of TRPC3 (canonical-type transient receptor potential cation channel type 3) is tightly regulated during skeletal muscle cell differentiation, and a functional interaction between TRPC3 and RyR1 [(ryanodine receptor type 1), an SR (sarcoplasmic reticulum) Ca2+-release channel] regulates the gain of SR Ca2+ release during EC (excitation-contraction) coupling. However, it has not b...

2010
Monu Goel William P. Schilling

Goel M, Schilling WP. Role of TRPC3 channels in ATP-induced Ca signaling in principal cells of the inner medullary collecting duct. Am J Physiol Renal Physiol 299: F225–F233, 2010. First published April 21, 2010; doi:10.1152/ajprenal.00670.2009.—The transient receptor potential channel TRPC3 is exclusively expressed in the apical membrane of principal cells of the collecting duct (CD) both in v...

2017
Bin Wang Shiqiang Xiong Shaoyang Lin Weijie Xia Qiang Li Zhigang Zhao Xing Wei Zongshi Lu Xiao Wei Peng Gao Daoyan Liu Zhiming Zhu

BACKGROUND Mitochondrial Ca2+ homeostasis is fundamental to the regulation of mitochondrial reactive oxygen species (ROS) generation and adenosine triphosphate production. Recently, transient receptor potential channel, canonical type 3 (TRPC3), has been shown to localize to the mitochondria and to play a role in maintaining mitochondrial calcium homeostasis. Inhibition of TRPC3 attenuates vasc...

2016
Naoyuki Kitajima Takuro Numaga-Tomita Masahiko Watanabe Takuya Kuroda Akiyuki Nishimura Kei Miyano Satoshi Yasuda Koichiro Kuwahara Yoji Sato Tomomi Ide Lutz Birnbaumer Hideki Sumimoto Yasuo Mori Motohiro Nishida

Reactive oxygen species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mechanotransduction during both physiological adaptation to mechanical load and maladaptive remodeling of the heart. This is despite low levels of cardiac Nox2 expression. The mechanism underlying the transition from adaptation to maladaptation remains obscure, however. We demonstrate that transient re...

2010
Jun Pu

whether TRPC3 up-regulation in aorta from SHR is associated with angiotensin II receptor (AT1R) mediate calcium influx. Methods: Blood pressure was measured using tail-cuff plethys-mography and a pressure transducer. Vasoconstriction of aortic rings was measured by organ chamber. Aortic smooth muscle cells (VSMCs) was cultured. Cytosolic calcium concentration was measured by the fluorescence te...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2008
Kathryn Smedlund Guillermo Vazquez

UNLABELLED Background- Vascular cell adhesion molecule-1 (VCAM-1) is critical in monocyte recruitment to the endothelium, a key event in development of atherosclerotic lesions. Stimulation of human coronary artery endothelial cells (HCAECs) with ATP positively modulates VCAM-1 expression and function through a mechanism involving Ca(2+) signaling. We here examined the role of Ca(2+) influx and ...

Journal: :American journal of physiology. Cell physiology 2014
Sumeet Solanki Prabhatchandra R Dube Jean-Yves Tano Lutz Birnbaumer Guillermo Vazquez

Endoplasmic reticulum (ER) stress is a prominent mechanism of macrophage apoptosis in advanced atherosclerotic lesions. Recent studies from our laboratory showed that advanced atherosclerotic plaques in Apoe(-/-) mice with bone marrow deficiency of the calcium-permeable channel Transient Receptor Potential Canonical 3 (TRPC3) are characterized by reduced areas of necrosis and fewer apoptotic ma...

2012
Kathryn Quick Jing Zhao Niels Eijkelkamp John E. Linley Francois Rugiero James J. Cox Ramin Raouf Martine Gringhuis Jane E. Sexton Joel Abramowitz Ruth Taylor Andy Forge Jonathan Ashmore Nerissa Kirkwood Corné J. Kros Guy P. Richardson Marc Freichel Veit Flockerzi Lutz Birnbaumer John N. Wood

Transient receptor potential (TRP) channels TRPC3 and TRPC6 are expressed in both sensory neurons and cochlear hair cells. Deletion of TRPC3 or TRPC6 in mice caused no behavioural phenotype, although loss of TRPC3 caused a shift of rapidly adapting (RA) mechanosensitive currents to intermediate-adapting currents in dorsal root ganglion sensory neurons. Deletion of both TRPC3 and TRPC6 caused de...

Journal: :Hypertension 2009
Daoyan Liu Dachun Yang Hongbo He Xiaoping Chen Tingbing Cao Xiaoli Feng Liqun Ma Zhidan Luo Lijuan Wang Zhencheng Yan Zhiming Zhu Martin Tepel

We tested the hypothesis that transient receptor potential canonical type 3 (TRPC3) channels are increased in vascular smooth muscle cells and aortic tissue from spontaneously hypertensive rats (SHR) compared with normotensive Wistar Kyoto rats. Expression of TRPC3 was analyzed by immunohistochemistry and Western blotting. TRPC3 gene knockdown was performed by specific small interfering RNA and...

Journal: :Cardiovascular research 2012
Sevvandi Senadheera Youngsoo Kim T Hilton Grayson Sianne Toemoe Mikhail Y Kochukov Joel Abramowitz Gary D Housley Rebecca L Bertrand Preet S Chadha Paul P Bertrand Timothy V Murphy Marianne Tare Lutz Birnbaumer Sean P Marrelli Shaun L Sandow

AIMS Microdomain signalling mechanisms underlie key aspects of artery function and the modulation of intracellular calcium, with transient receptor potential (TRP) channels playing an integral role. This study determines the distribution and role of TRP canonical type 3 (C3) channels in the control of endothelium-derived hyperpolarization (EDH)-mediated vasodilator tone in rat mesenteric artery...

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