1,733,661 research outputs found
Angela M. Owen July 12, 1928 - January 4, 2019
No full textAngela M. Owen passed away peacefully in Palo Alto on January 4th
Angela M. Reid, Westbrook Junior College, Class of 1962
No full textAngela M. Reid, Westbrook Junior College, Class of 1962, senior class photo. Angel lived in Bell House and majored in Liberal Arts.https://dune.une.edu/wchc_photos_students1960s/1213/thumbnail.jp
Angela M. Marconi, (1880-1971), purchased by Mrs. Howard E. Zink on May 4, 1971.
No full textDocuments regarding the double headstone for Angela M. Marconi, (1880-1971), buried with Angela M. Marconi (1878-1956), purchased by Mrs. Howard E. Zink. The marker was placed at Calvary Cemetery, Section 36 in Toledo, Ohio. The stone is made of blown mod classic letters in axed face
Regulation of store-operated calcium channel by Mitsugumin29 in skeletal muscle aging:
No full textThe 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.
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 Ca2+ signaling in skeletal muscle during exercise and aging.
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.Ph.D.Includes bibliographical references (p. 71-87)by Angela M. Thornto
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