東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Regulation of store-operated calcium...

Rutgers The State University of New Jersey - New Brunswick., Graduate School - New Brunswick.

FindBook

Google Book

Amazon

博客來

Regulation of store-operated calcium entry in skeletal muscle health and aging.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Regulation of store-operated calcium entry in skeletal muscle health and aging./
作者:	Thornton, Angela M.
面頁冊數:	103 p.
附註:	Advisers: Jianjie Ma; Marco A. DePaula Brotto.
Contained By:	Dissertation Abstracts International70-03B.
標題:	Biology, Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3350144
ISBN:	9781109072440

Regulation of store-operated calcium entry in skeletal muscle health and aging.
Thornton, Angela M.

Regulation of store-operated calcium entry in skeletal muscle health and aging. - 103 p.

Advisers: Jianjie Ma; Marco A. DePaula Brotto.

Thesis (Ph.D.)--Rutgers The State University of New Jersey - New Brunswick, 2009.

The study of store-operated Ca2+ channel entry (SOCE) and its role in muscle contractility in young and aged skeletal muscle necessitates a thorough knowledge of the Ca2+ signaling from the sarcoplasmic reticulum (SR) that activates SOCE. Yet, all of the molecular components involved have yet to be fully elucidated, as neither T-tubule voltage sensors, nor SR ryanodine receptor Ca2+ channels, together or independently, are necessary or sufficient for the establishment of a close association between the T-tubule and SR membranes. Therefore, other protein components must be involved for the formation of triad junctional complexes.

ISBN: 9781109072440Subjects--Topical Terms:

1017816
Biology, Physiology.

Regulation of store-operated calcium entry in skeletal muscle health and aging.
LDR:03069nmm 2200313 a 45 001 886681
005 20101007
008 101007s2009 ||||||||||||||||| ||eng d
020 $a 9781109072440
035 $a (UMI)AAI3350144
035 $a AAI3350144
040 $a UMI $c UMI
100 1 $a Thornton, Angela M. $3 1058390
245 1 0 $a Regulation of store-operated calcium entry in skeletal muscle health and aging.
300 $a 103 p.
500 $a Advisers: Jianjie Ma; Marco A. DePaula Brotto.
500 $a Source: Dissertation Abstracts International, Volume: 70-03, Section: B, page: 1523.
502 $a Thesis (Ph.D.)--Rutgers The State University of New Jersey - New Brunswick, 2009.
520 $a The study of store-operated Ca2+ channel entry (SOCE) and its role in muscle contractility in young and aged skeletal muscle necessitates a thorough knowledge of the Ca2+ signaling from the sarcoplasmic reticulum (SR) that activates SOCE. Yet, all of the molecular components involved have yet to be fully elucidated, as neither T-tubule voltage sensors, nor SR ryanodine receptor Ca2+ channels, together or independently, are necessary or sufficient for the establishment of a close association between the T-tubule and SR membranes. Therefore, other protein components must be involved for the formation of triad junctional complexes.
520 $a Mitsugumin29 (MG29), a protein localized to the triad junction, may function as a structural component involved in the coupling between the SR and T-tubule, as abnormalities in both T-tubule and SR membranes have been reported in mg29(-/-) mice. In addition, muscles from these mice share many morphological and functional characteristics with muscle from aged mice, including increased susceptibility to fatigue, defective SR Ca2+ release and defective SOC function. Either of these may be responsible for the altered Ca 2+ signaling in skeletal muscle during exercise and aging.
520 $a Our data suggests that SOCE is not merely important for skeletal muscle function in aging; but, it is also required for maintenance of Ca2+ signaling during repetitive stimulation under intensive muscle activity (i.e., fatigue) in the healthy state. In addition, we propose that SOCE diminishes with age, contributing to the age-associated muscle weakness. Finally, we find that while SOCE is a functional marker of muscle performance in aging, MG29 is a molecular marker, as SOCE is compromised in aged wild type mice through the decreased expression of MG29. Therefore, mg29(-/-) mice can serve as an appropriate model for the study of skeletal muscle aging. Through this project, we have begun to understand the physiological function of SOCE and MG29 and their contribution to muscle contractility in both young and aged mice.
590 $a School code: 0190.
650 4 $a Biology, Physiology. $3 1017816
650 4 $a Engineering, Biomedical. $3 1017684
690 $a 0541
690 $a 0719
710 2 $a Rutgers The State University of New Jersey - New Brunswick. $b Graduate School - New Brunswick. $3 1019196
773 0 $t Dissertation Abstracts International $g 70-03B.
790 $a 0190
790 1 0 $a Brotto, Marco A. DePaula, $e advisor
790 1 0 $a Ma, Jianjie, $e advisor
791 $a Ph.D.
792 $a 2009
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3350144