Ca2+ signaling, genes and the cell cycle

Machaca, Khaled

doi:10.1016/j.ceca.2010.10.003

Cited by 58 publications

(29 citation statements)

References 135 publications

(141 reference statements)

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“…For example, the ability of certain EGTA injections to block 1-MA-induced oocyte maturation has been attributed to possible toxic effects of the particular experimental protocol that was used (Picard and Doree, 1983). Similarly, the fact that BAPTA-loaded Xenopus oocytes fail to mature may not be due to calcium chelation, but rather to the sequestration of such transition metals as zinc (Machaca, 2011). Conversely, in cases where calcium chelators fail to block GVBD, the chelator treatment should also be demonstrated as actually preventing a pre-GVBD calcium rise.…”

Section: Discussionmentioning

confidence: 99%

“…promote, progesterone-induced maturation in Xenopus (Sun and Machaca, 2004), it has been concluded that calcium transients are not required for GVBD in frog oocytes (Machaca, 2011). Alternatively, in spite of findings that follicle-enclosed mouse oocytes can undergo GVBD independently of calcium signals (Mehlmann et al, 2006), calcium is still viewed as a key stimulator of GVBD in mammals (e.g.…”

Section: Nemerteans (Ribbon Worms)mentioning

confidence: 99%

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Calcium signals and oocyte maturation in marine invertebrates

Deguchi¹,

Takeda²,

Stricker³

2015

Int. J. Dev. Biol.

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In various oocytes and eggs of animals, transient elevations in cytoplasmic calcium ion concentrations are known to regulate key processes during fertilization and the completion of meiosis. However, whether or not calcium transients also help to reinitiate meiotic progression at the onset of oocyte maturation remains controversial. This article summarizes reports of calcium signals playing essential roles during maturation onset (=germinal vesicle breakdown, GVBD) in several kinds of marine invertebrate oocytes. Conversely, other data from the literature, as well as previously unpublished findings for jellyfish oocytes, fail to support the view that calcium signals are required for GVBD. In addition to assessing the effects of calcium transients on GVBD in marine invertebrate oocytes, the ability of maturing oocytes to enhance their calcium-releasing capabilities after GVBD is also reviewed. Furthermore, possible explanations are proposed for the contradictory results that have been obtained regarding calcium signals during oocyte maturation in marine invertebrates.

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Section: Discussionmentioning

confidence: 99%

Section: Nemerteans (Ribbon Worms)mentioning

confidence: 99%

Calcium signals and oocyte maturation in marine invertebrates

Deguchi¹,

Takeda²,

Stricker³

2015

Int. J. Dev. Biol.

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“…Changes in the spatial distribution and concentration of Ca 2+ in the cytoplasm constitute a very important intracellular signalling pathway in cellular physiology, including cell proliferation [257]. Ca 2+ is an activator of some PKCs, and at the same time PKC-dependent phosphorylation reactions change the spatiotemporal pattern of cellular Ca 2+ responses.…”

Section: Protein Kinase Cmentioning

confidence: 99%

Protein Kinases and Phosphatases in the Control of Cell Fate

et al. 2011

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Protein phosphorylation controls many aspects of cell fate and is often deregulated in pathological conditions. Several recent findings have provided an intriguing insight into the spatial regulation of protein phosphorylation across different subcellular compartments and how this can be finely orchestrated by specific kinases and phosphatases. In this review, the focus will be placed on (i) the phosphoinositide 3-kinase (PI3K) pathway, specifically on the kinases Akt and mTOR and on the phosphatases PP2a and PTEN, and on (ii) the PKC family of serine/threonine kinases. We will look at general aspects of cell physiology controlled by these kinases and phosphatases, highlighting the signalling pathways that drive cell division, proliferation, and apoptosis.

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“…[19,20] Furthermore, during cell release, target cells are exposed to nonphysiologic levels of calcium chelating agents which may initiate unwanted signaling cascades within the target cells, and have the potential to alter the observed cell phenotype and proliferation state. [21–23] …”

Section: Introductionmentioning

confidence: 99%

Biopolymer System for Cell Recovery from Microfluidic Cell Capture Devices

Shah

Nakamura³

et al. 2012

Anal. Chem.

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Microfluidic systems for affinity-based cell isolation have emerged as a promising approach for the isolation of specific cells from complex matrices (i.e., circulating tumor cells in whole blood). However, these technologies remain limited by the lack of reliable methods for the innocuous recovery of surface captured cells. Here, we present a biofunctional sacrificial hydrogel coating for microfluidic chips that enables the highly efficient release of isolated cells (99% ± 1%) following gel dissolution. This covalently crosslinked alginate biopolymer system is stable in a wide variety of physiologic solutions (including EDTA treated whole blood) and may be rapidly degraded via backbone cleavage with alginate lyase. The capture and release of EpCAM expressing cancer cells using this approach was found to have no significant effect on cell viability or proliferative potential and recovered cells were demonstrated to be compatible with downstream immunostaining and FISH analysis.

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Ca2+ signaling, genes and the cell cycle

Cited by 58 publications

References 135 publications

Calcium signals and oocyte maturation in marine invertebrates

Calcium signals and oocyte maturation in marine invertebrates

Protein Kinases and Phosphatases in the Control of Cell Fate

Biopolymer System for Cell Recovery from Microfluidic Cell Capture Devices

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