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Cell death and stress signaling in glycogen storage disease type I

Title
Cell death and stress signaling in glycogen storage disease type I
Authors
Kim S.Y.Bae Y.S.
Ewha Authors
배윤수김소연
SCOPUS Author ID
배윤수scopus
Issue Date
2009
Journal Title
Molecules and Cells
ISSN
1016-8478JCR Link
Citation
vol. 28, no. 3, pp. 139 - 148
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
Cell death has been traditionally classified in apoptosis and necrosis. Apoptosis, known as programmed cell death, is an active form of cell death mechanism that is tightly regulated by multiple cellular signaling pathways and requires ATP for its appropriate process. Apoptotic death plays essential roles for successful development and maintenance of normal cellular homeostasis in mammalian. In contrast to apoptosis, necrosis is classically considered as a passive cell death process that occurs rather by accident in disastrous conditions, is not required for energy and eventually induces inflammation. Regardless of different characteristics between apoptosis and necrosis, it has been well defined that both are responsible for a wide range of human diseases. Glycogen storage disease type I (GSD-I) is a kind of human genetic disorders and is caused by the deficiency of a microsomal protein, glucose-6-phosphatase-α (G6Pase-α) or glucose-6-phosphate transporter (G6PT) responsible for glucose homeostasis, leading to GSD-Ia or GSD-Ib, respectively. This review summarizes cell deaths in GSD-I and mostly focuses on current knowledge of the neutrophil apoptosis in GSD-Ib based upon ER stress and redox signaling. © The Korean Society for Molecular and Cellular Biology and Springer Netherlands 2009.
DOI
10.1007/s10059-009-0126-8
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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