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Calcium signaling in cerebral artery...

Cheng, Xiaoyang.

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Calcium signaling in cerebral artery smooth muscle cells: Function of caveolin-1 in calcium ion spark coupling, and, Molecular identity and electrophysiological properties of calcium(v)1.2 channels.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Calcium signaling in cerebral artery smooth muscle cells: Function of caveolin-1 in calcium ion spark coupling, and, Molecular identity and electrophysiological properties of calcium(v)1.2 channels./
作者:	Cheng, Xiaoyang.
面頁冊數:	145 p.
附註:	Adviser: Jonathan H. Jaggar.
Contained By:	Dissertation Abstracts International67-03B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3209396
ISBN:	9780542578199

Calcium signaling in cerebral artery smooth muscle cells: Function of caveolin-1 in calcium ion spark coupling, and, Molecular identity and electrophysiological properties of calcium(v)1.2 channels.
Cheng, Xiaoyang.

Calcium signaling in cerebral artery smooth muscle cells: Function of caveolin-1 in calcium ion spark coupling, and, Molecular identity and electrophysiological properties of calcium(v)1.2 channels. - 145 p.

Adviser: Jonathan H. Jaggar.

Thesis (Ph.D.)--The University of Tennessee Health Science Center, 2006.

In vascular smooth muscle cells (SMCs), voltage-dependent Ca2+ channels (VDCCs), ryanodine-sensitive Ca2+ release channels (RyR channels), and large-conductance Ca2+-activated potassium (KCa) channels form a functional unit that regulates smooth muscle contractility. This dissertation focuses on two areas regarding Ca2+ signaling in cerebral artery SMCs: (1) the physiological function of caveolin-1 (cav-1) in the signaling between VDCCs, RyR channels, and KCa channels; (2) the molecular identity and electrophysiological properties of Cav1.2 channels, the major VDCC isoform in vascular SMCs. Using cav-1 deficient (cav-1-/-) mice, data in chapter 2 show that cav-1 ablation abolished caveolae, decreased cell capacitance, elevated Ca2+ spark frequency, and attenuated the regulation of RyR channels by VDCCs. This study suggests that cav-1 is essential for the coupling between VDCCs and RyR channels. In chapter 3, a novel 5' end sequence (exon1c) of Cav1.2 channels was discovered in rat cerebral artery SMCs and multiple Cav1.2 splice variants were cloned from cerebral arteries. A previously identified 5' end sequence (exon1b) of Ca v1.2 channels was also detected in rat cerebral artery smooth muscle cells. The novel 5' end sequence encodes a Cav1.2 alpha 1 subunit N-terminus that contains four cysteine residues. Splice variants are generated by alternative splicing at exon1b/1c, +/-9*, 21/22, 31/32, and +/-33. The function of the novel N-terminus was investigated in chapter 4 using electrophysiology of transiently transfected COS-1 cells. Data showed that the novel Cav1.2 N-terminus alters channel properties and contributes to isoform-specific regulation of Cav1.2 channel activation and inactivation by auxiliary subunits. Overall, these studies indicate that, in cerebral artery SMCs, (1) cav-1 is essential for effective communication between VDCCs and RyR channels; (2) arterial myocyte Cav1.2 channels contain a novel N-terminus that confers different regulation of channel activation and inactivation properties by auxiliary subunits; (3) multiple Cav1.2 splice variants are generated via alternative splicing at exons 1b/1c, +/-9*, 21/22, 31/32, and +/-33.

ISBN: 9780542578199Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Calcium signaling in cerebral artery smooth muscle cells: Function of caveolin-1 in calcium ion spark coupling, and, Molecular identity and electrophysiological properties of calcium(v)1.2 channels.
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245 1 0 $a Calcium signaling in cerebral artery smooth muscle cells: Function of caveolin-1 in calcium ion spark coupling, and, Molecular identity and electrophysiological properties of calcium(v)1.2 channels.
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500 $a Adviser: Jonathan H. Jaggar.
500 $a Source: Dissertation Abstracts International, Volume: 67-03, Section: B, page: 1224.
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520 $a In vascular smooth muscle cells (SMCs), voltage-dependent Ca2+ channels (VDCCs), ryanodine-sensitive Ca2+ release channels (RyR channels), and large-conductance Ca2+-activated potassium (KCa) channels form a functional unit that regulates smooth muscle contractility. This dissertation focuses on two areas regarding Ca2+ signaling in cerebral artery SMCs: (1) the physiological function of caveolin-1 (cav-1) in the signaling between VDCCs, RyR channels, and KCa channels; (2) the molecular identity and electrophysiological properties of Cav1.2 channels, the major VDCC isoform in vascular SMCs. Using cav-1 deficient (cav-1-/-) mice, data in chapter 2 show that cav-1 ablation abolished caveolae, decreased cell capacitance, elevated Ca2+ spark frequency, and attenuated the regulation of RyR channels by VDCCs. This study suggests that cav-1 is essential for the coupling between VDCCs and RyR channels. In chapter 3, a novel 5' end sequence (exon1c) of Cav1.2 channels was discovered in rat cerebral artery SMCs and multiple Cav1.2 splice variants were cloned from cerebral arteries. A previously identified 5' end sequence (exon1b) of Ca v1.2 channels was also detected in rat cerebral artery smooth muscle cells. The novel 5' end sequence encodes a Cav1.2 alpha 1 subunit N-terminus that contains four cysteine residues. Splice variants are generated by alternative splicing at exon1b/1c, +/-9*, 21/22, 31/32, and +/-33. The function of the novel N-terminus was investigated in chapter 4 using electrophysiology of transiently transfected COS-1 cells. Data showed that the novel Cav1.2 N-terminus alters channel properties and contributes to isoform-specific regulation of Cav1.2 channel activation and inactivation by auxiliary subunits. Overall, these studies indicate that, in cerebral artery SMCs, (1) cav-1 is essential for effective communication between VDCCs and RyR channels; (2) arterial myocyte Cav1.2 channels contain a novel N-terminus that confers different regulation of channel activation and inactivation properties by auxiliary subunits; (3) multiple Cav1.2 splice variants are generated via alternative splicing at exons 1b/1c, +/-9*, 21/22, 31/32, and +/-33.
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