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At fertilization mammalian eggs exhibit repetitive rises in the cytoplasmic Ca2+ concentration (Ca2+ oscillations), associated with propagating Ca2+ waves in the initial responses. The Ca2+ oscillation causes cortical granule exocytosis and resumption of second meiosis and affects later embryonic development. Recent studies using a function-blocking(More)
In this paper, we analyse the authentication protocol that has been proposed for the so called global mobility network in the October issue of the IEEE Journal on Selected Areas in Communications. Using a simple logic of authentication, we show that the protocol has aws, and we present three diierent attacks that exploit these. We correct the protocol using(More)
Mature hamster eggs exhibit repetitive increases in the intracellular Ca2+ concentration ([Ca2+]i) at fertilization, caused by inositol 1,4,5-trisphosphate (InsP3)-induced Ca2+ release (IICR) from stores. Oscillating Ca2+ rises also occurred in inseminated immature oocytes at the germinal vesicle (GV) stage but the peak [Ca2+]i of each response was about(More)
Mutations in mitochondrial DNA (mtDNA) occur at high frequency in human tumors, but whether these mutations alter tumor cell behavior has been unclear. We used cytoplasmic hybrid (cybrid) technology to replace the endogenous mtDNA in a mouse tumor cell line that was poorly metastatic with mtDNA from a cell line that was highly metastatic, and vice versa.(More)
The concentration of cytoplasmic free calcium (Ca2+) increases in various stimulated cells in a wave (Ca2+ wave) and in periodic transients (Ca2+ oscillations). These phenomena are explained by inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release (IICR) and Ca(2+)-induced Ca2+ release (CICR) from separate intracellular stores, but decisive evidence is(More)
Suppression of autophagy is always accompanied by marked accumulation of p62, a selective autophagy substrate. Because p62 interacts with the Nrf2-binding site on Keap1, which is a Cullin 3-based ubiquitin ligase adapter protein, autophagy deficiency causes competitive inhibition of the Nrf2-Keap1 interaction, resulting in stabilization of Nrf2 followed by(More)
PINK1 and Parkin were first identified as the causal genes responsible for familial forms of early-onset Parkinson's disease (PD), a prevalent neurodegenerative disorder. PINK1 encodes a mitochondrial serine/threonine protein kinase, whereas Parkin encodes an ubiquitin-protein ligase. PINK1 and Parkin cooperate to maintain mitochondrial integrity; however,(More)
Mitochondria are essential for many cellular functions such as oxidative phosphorylation and calcium homeostasis; consequently, mitochondrial dysfunction could cause many diseases, including neurological disorders. Recently, mitochondrial dynamics, such as fusion, fission, and transportation, have been visualized in living cells by using time-lapse imaging(More)
Mitochondrial DNA (mtDNA) has been proposed to be involved in respiratory function, and mtDNA mutations have been associated with aging, tumors, and various disorders, but the effects of mtDNA imported into transplants from different individuals or aged subjects have been unclear. We examined this issue by generating trans-mitochondrial tumor cells and(More)
BACKGROUND Mitochondrial DNA (mtDNA) with pathogenic mutations has been found in patients with cognitive disorders. However, little is known about whether pathogenic mtDNA mutations and the resultant mitochondrial respiration deficiencies contribute to the expression of cognitive alterations, such as impairments of learning and memory. To address this(More)