scholarly journals Intracellular Ca2+ Signaling in Protozoan Parasites: An Overview with a Focus on Mitochondria

2021 ◽  
Vol 22 (1) ◽  
pp. 469
Author(s):  
Pedro H. Scarpelli ◽  
Mateus F. Pecenin ◽  
Celia R. S. Garcia
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Plasmodium Falciparum ◽  
Toxoplasma Gondii ◽  
Trypanosoma Cruzi ◽  
Cell Cycle Control ◽  
Endoplasmatic Reticulum ◽  
Protozoan Parasites ◽  
Cellular Functions ◽  
Higher Eukaryotes

Ca2+ signaling has been involved in controling critical cellular functions such as activation of proteases, cell death, and cell cycle control. The endoplasmatic reticulum plays a significant role in Ca2+ storage inside the cell, but mitochondria have long been recognized as a fundamental Ca2+ pool. Protozoan parasites such as Plasmodium falciparum, Toxoplasma gondii, and Trypanosoma cruzi display a Ca2+ signaling toolkit with similarities to higher eukaryotes, including the participation of mitochondria in Ca2+-dependent signaling events. This review summarizes the most recent knowledge in mitochondrial Ca2+ signaling in protozoan parasites, focusing on the mechanism involved in mitochondrial Ca2+ uptake by pathogenic protists.

scholarly journals Role of D-GADD45 in JNK-Dependent Apoptosis and Regeneration in Drosophila

Genes ◽  
2019 ◽  
Vol 10 (5) ◽  
pp. 378 ◽  
Author(s):  
Carlos Camilleri-Robles ◽  
Florenci Serras ◽  
Montserrat Corominas
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Control ◽  
Imaginal Discs ◽  
Cellular Functions ◽  
Correct Function ◽  
Response To Stress ◽  
Wing Imaginal Discs ◽  
Harmful Effects

The GADD45 proteins are induced in response to stress and have been implicated in the regulation of several cellular functions, including DNA repair, cell cycle control, senescence, and apoptosis. In this study, we investigate the role of D-GADD45 during Drosophila development and regeneration of the wing imaginal discs. We find that higher expression of D-GADD45 results in JNK-dependent apoptosis, while its temporary expression does not have harmful effects. Moreover, D-GADD45 is required for proper regeneration of wing imaginal discs. Our findings demonstrate that a tight regulation of D-GADD45 levels is required for its correct function both, in development and during the stress response after cell death.

scholarly journals p16INK4A – Connecting Cell Cycle Control to Cell Death Regulation in Human Leukemia

10.5772/25284 ◽  
2011 ◽  
Author(s):  
Petra Obexer ◽  
Judith Hagenbuchner Markus Holzner ◽  
Michael J.
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Control ◽  
Human Leukemia

Cloning and characterisation of a Plasmodium falciparum homologue of the Ran/TC4 signal transducing GTPase involved in cell cycle control

1994 ◽  
Vol 65 (2) ◽  
pp. 331-338 ◽  
Author(s):  
Ali A. Sultan ◽  
William A. Richardson ◽  
Pietro Alano ◽  
David E. Arnot ◽  
Christian Doerig
Keyword(s):  
Cell Cycle ◽  
Plasmodium Falciparum ◽  
Cell Cycle Control

Cloning and characterisation of a Plasmodium falciparum homologue of the Ran/TC4 signal transducing GTPase involved in cell cycle control

1994 ◽  
Vol 67 (2) ◽  
pp. 339
Author(s):  
Ali A. Sultan ◽  
William A. Richardson ◽  
Pietro Alano ◽  
David E. Arnot ◽  
Christian Doerig
Keyword(s):  
Cell Cycle ◽  
Plasmodium Falciparum ◽  
Cell Cycle Control

scholarly journals P53 gene: major mutations in neoplasias and anticancer gene therapy

2012 ◽  
Vol 42 (5) ◽  
pp. 845-853 ◽  
Author(s):  
Caroline Rocha de Oliveira Lima ◽  
Rogério Elias Rabelo ◽  
Valcinir Aloísio Scalla Vulcani ◽  
Lorena Damasio Cardoso ◽  
Nicaelle Luan de Moura Sousa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Gene Therapy ◽  
Molecular Weight ◽  
Cell Death ◽  
P53 Protein ◽  
Cell Cycle Control ◽  
P53 Gene ◽  
Neoplastic Transformation ◽  
Functional Aspects

The p53 gene encodes a protein that has molecular weight of 53kD and is also called p53 protein, being constantly studied for its classic concept of "genome guardian". This gene plays a range of essential functions to ensure the cell cycle control, in addition to playing a central role in carcinogenesis. With respect to neoplasias, it prevents the neoplastic transformation through three intricate mechanisms. Depending on the extent of the mutation, different responses may be sent by p53 and those range since the disruption of the cell cycle, the correction of the mutation through the activation of repair proteins or still, the induction of senescence or cell death by apoptosis. This review aims to address the structural and functional aspects of the p53 gene and protein, and also reaffirm their participation in the carcinogenesis control, approaching their major mutations and the anticancer gene therapy involving this gene.

scholarly journals Cell cycle control of cell death in yeast

Cell Cycle ◽  
2010 ◽  
Vol 9 (20) ◽  
pp. 4052-4051 ◽  
Author(s):  
Didac Carmona-Gutierrez ◽  
Helmut Jungwirth ◽  
Tobias Eisenberg ◽  
Frank Madeo
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Control

The Role of Inducible 70-kDa Heat Shock Protein in Cell Cycle Control, Differentiation, and Apoptotic Cell Death of the Human Myeloid Leukemic HL-60 Cells

1998 ◽  
Vol 187 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Hyun-Jeong Kwak ◽  
Chang-Duk Jun ◽  
Hyun-Ock Pae ◽  
Ji-Chang Yoo ◽  
Young-Chul Park ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Apoptotic Cell ◽  
Cell Cycle Control ◽  
Apoptotic Cell Death

scholarly journals p53-mediated cell death: relationship to cell cycle control.

1993 ◽  
Vol 13 (3) ◽  
pp. 1415-1423 ◽  
Author(s):  
E Yonish-Rouach ◽  
D Grunwald ◽  
S Wilder ◽  
A Kimchi ◽  
E May ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Interleukin 6 ◽  
Cell Cycle Progression ◽  
P53 Protein ◽  
Cell Cycle Control ◽  
Growth Arrest ◽  
Leukemic Cells ◽  
Temperature Sensitive ◽  
Permissive Temperature

M1 clone S6 myeloid leukemic cells do not express detectable p53 protein. When stably transfected with a temperature-sensitive mutant of p53, these cells undergo rapid cell death upon induction of wild-type (wt) p53 activity at the permissive temperature. This process has features of apoptosis. In a number of other cell systems, wt p53 activation has been shown to induce a growth arrest. Yet, wt 53 fails to induce a measurable growth arrest in M1 cells, and cell cycle progression proceeds while viability is being lost. There exists, however, a relationship between the cell cycle and p53-mediated death, and cells in G1 appear to be preferentially susceptible to the death-inducing activity of wt p53. In addition, p53-mediated M1 cell death can be inhibited by interleukin-6. The effect of the cytokine is specific to p53-mediated death, since apoptosis elicited by serum deprivation is refractory to interleukin-6. Our data imply that p53-mediated cell death is not dependent on the induction of a growth arrest but rather may result from mutually incompatible growth-regulatory signals.

scholarly journals Rapid initiation of cell cycle reentry processes protects neurons from amyloid-β toxicity

2021 ◽  
Vol 118 (12) ◽  
pp. e2011876118
Author(s):  
Stefania Ippati ◽  
Yuanyuan Deng ◽  
Julia van der Hoven ◽  
Celine Heu ◽  
Annika van Hummel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Dynamic Process ◽  
Cell Cycle Control ◽  
Amyloid Β ◽  
Current View ◽  
Cell Cycle Reentry ◽  
Reporter Signal ◽  
Control Protein ◽  
Cycle Indicator

Neurons are postmitotic cells. Reactivation of the cell cycle by neurons has been reported in Alzheimer’s disease (AD) brains and models. This gave rise to the hypothesis that reentering the cell cycle renders neurons vulnerable and thus contributes to AD pathogenesis. Here, we use the fluorescent ubiquitination-based cell cycle indicator (FUCCI) technology to monitor the cell cycle in live neurons. We found transient, self-limited cell cycle reentry activity in naive neurons, suggesting that their postmitotic state is a dynamic process. Furthermore, we observed a diverse response to oligomeric amyloid-β (oAβ) challenge; neurons without cell cycle reentry activity would undergo cell death without activating the FUCCI reporter, while neurons undergoing cell cycle reentry activity at the time of the oAβ challenge could maintain and increase FUCCI reporter signal and evade cell death. Accordingly, we observed marked neuronal FUCCI positivity in the brains of human mutant Aβ precursor protein transgenic (APP23) mice together with increased neuronal expression of the endogenous cell cycle control protein geminin in the brains of 3-mo-old APP23 mice and human AD brains. Taken together, our data challenge the current view on cell cycle in neurons and AD, suggesting that pathways active during early cell cycle reentry in neurons protect from Aβ toxicity.

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