Calcium and cell cycle control

Development ◽  
1990 ◽  
Vol 108 (4) ◽  
pp. 525-542 ◽  
Author(s):  
M. Whitaker ◽  
R. Patel
Keyword(s):  
Cell Cycle ◽  
Sea Urchin ◽  
Mammalian Cells ◽  
Cell Cycle Regulation ◽  
Sea Urchins ◽  
Cell Cycle Control ◽  
Control Point ◽  
Control Cell ◽  
Free Calcium ◽  
Cycle Regulation

The cell division cycle of the early sea urchin embryo is basic. Nonetheless, it has control points in common with the yeast and mammalian cell cycles, at START, mitosis ENTRY and mitosis EXIT. Progression through each control point in sea urchins is triggered by transient increases in intracellular free calcium. The Cai transients control cell cycle progression by translational and post-translational regulation of the cell cycle control proteins pp34 and cyclin. The START Cai transient leads to phosphorylation of pp34 and cyclin synthesis. The mitosis ENTRY Cai transient triggers cyclin phosphorylation. The motosis EXIT transient causes destruction of phosphorylated cyclin. We compare cell cycle regulation by calcium in sea urchin embryos to cell cycle regulation in other eggs and oocytes and in mammalian cells.

scholarly journals Cilia and the cell cycle?

2005 ◽  
Vol 169 (5) ◽  
pp. 707-710 ◽  
Author(s):  
Lynne M. Quarmby ◽  
Jeremy D.K. Parker
Keyword(s):  
Cell Cycle ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Mammalian Cells ◽  
Cell Cycle Regulation ◽  
Polycystic Kidney ◽  
Unicellular Alga ◽  
Regulatory Relationship ◽  
Cycle Regulation ◽  
Multiple Signaling

A recent convergence of data indicating a relationship between cilia and proliferative diseases, such as polycystic kidney disease, has revived the long-standing enigma of the reciprocal regulatory relationship between cilia and the cell cycle. Multiple signaling pathways are localized to cilia in mammalian cells, and some proteins have been shown to act both in the cilium and in cell cycle regulation. Work from the unicellular alga Chlamydomonas is providing novel insights as to how cilia and the cell cycle are coordinately regulated.

scholarly journals Emerging Mechanisms of G 1 /S Cell Cycle Control by Human and Mouse Cytomegaloviruses

mBio ◽  
2021 ◽  
Author(s):  
Boris Bogdanow ◽  
Quang Vinh Phan ◽  
Lüder Wiebusch
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cell Cycle Control ◽  
Double Stranded Dna ◽  
Pathogenic Viruses ◽  
Cycle Regulation ◽  
Human And Mouse

Cytomegaloviruses (CMVs) are among the largest pathogenic viruses in mammals. To enable replication of their long double-stranded DNA genomes, CMVs induce profound changes in cell cycle regulation.

Effect of WSSV infection on cell cycle regulation, respiratory burst and cytoplasmic free calcium concentration in Penaeus vannamei

2021 ◽  
Author(s):  
Mudagandur Shashi Shekhar ◽  
Swathi Anandan ◽  
Vinaya Kumar Katneni ◽  
Ashok Kumar Jangam ◽  
Jesudhas Raymond Jani Angel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Respiratory Burst ◽  
Cell Cycle Regulation ◽  
Calcium Concentration ◽  
Free Calcium ◽  
Penaeus Vannamei ◽  
Free Calcium Concentration ◽  
Cycle Regulation ◽  
Cytoplasmic Free Calcium

scholarly journals Ubiquitin signaling in cell cycle control and tumorigenesis

2020 ◽  
Author(s):  
Fabin Dang ◽  
Li Nie ◽  
Wenyi Wei
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Kinase Inhibitors ◽  
Cell Cycle Control ◽  
Ubiquitin Ligases ◽  
E3 Ubiquitin Ligases ◽  
Cycle Progression ◽  
Precise Control ◽  
Cycle Regulation

Abstract Cell cycle progression is a tightly regulated process by which DNA replicates and cell reproduces. The major driving force underlying cell cycle progression is the sequential activation of cyclin-dependent kinases (CDKs), which is achieved in part by the ubiquitin-mediated proteolysis of their cyclin partners and kinase inhibitors (CKIs). In eukaryotic cells, two families of E3 ubiquitin ligases, anaphase-promoting complex/cyclosome and Skp1-Cul1-F-box protein complex, are responsible for ubiquitination and proteasomal degradation of many of these CDK regulators, ensuring cell cycle progresses in a timely and precisely regulated manner. In the past couple of decades, accumulating evidence have demonstrated that the dysregulated cell cycle transition caused by inefficient proteolytic control leads to uncontrolled cell proliferation and finally results in tumorigenesis. Based upon this notion, targeting the E3 ubiquitin ligases involved in cell cycle regulation is expected to provide novel therapeutic strategies for cancer treatment. Thus, a better understanding of the diversity and complexity of ubiquitin signaling in cell cycle regulation will shed new light on the precise control of the cell cycle progression and guide anticancer drug development.

scholarly journals CDKs family -a glimpse into the past and present: from cell cycle control to current biological functions

2020 ◽  
Vol 5 (1) ◽  
pp. 1-9
Author(s):  
Muzna Shah ◽  
Muhammad Fazal Hussain Qureshi ◽  
Danish Mohammad ◽  
Mahira Lakhani ◽  
Tabinda Urooj ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cells ◽  
Cell Cycle Progression ◽  
Cell Cycle Control ◽  
Cell Renewal ◽  
Catalytic Subunits ◽  
Cyclin Dependent Kinases ◽  
Stem Cell Renewal ◽  
Cyclin Protein ◽  
Cycle Regulation

Cyclin-dependent kinases (CDKs) are the catalytic subunits or protein kinases characterized by separate subunit “cyclin” that are essential for their enzymatic activity. CDKs play important roles in the control of cell cycle progression, cell division, neuronal function, epigenetic regulation, metabolism, stem cell renewal and transcription. However, they can accomplish some of these tasks independently, without binding with cyclin protein or kinase activity. Thus, so far, twenty different CDKs and cyclins have been reported in mammalian cells. The evolutionary expansion of the CDK family in mammals led to the division of CDKs into three cell-cycle-related subfamilies (Cdk1, Cdk4 and Cdk5) and five transcriptional subfamilies (Cdk7, Cdk8, Cdk9, Cdk11 and Cdk20). In this review, we summarizes that how CDKs are traditionally involve their latest revelations, their functional diversity beyond cell cycle regulation and their impact on development of disease in mammals.  

scholarly journals Three independent forms of regulation affect expression of HO, CLN1 and CLN2 during the cell cycle of Saccharomyces cerevisiae.

Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1015-1024 ◽  
Author(s):  
L Breeden ◽  
G Mikesell
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Normal Cell ◽  
Cell Cycle Regulation ◽  
Cell Cycle Control ◽  
G1 Cyclins ◽  
Affect Expression ◽  
Cdc28 Kinase ◽  
Cycle Regulation ◽  
Normal Cell Cycle

Abstract The G1 cyclins (CLNs) bind to and activate the CDC28 kinase during the G1 to S transition in Saccharomyces cerevisiae. Two G1 cyclins are regulated at the RNA level so that their RNAs peak at the G1/S boundary. In this report we show that the cell cycle regulation of CLN1 and CLN2 is partially determined by the restricted expression of SW14, a known trans-activator of SCB elements. When SWI4 is constitutively expressed or deleted, cell cycle regulation of CLN1/2 is reduced but not eliminated. In the absence of SwI6, another known regulator of both SCB and MCB elements, cell cycle regulation of the CLNs is also reduced, and the Start-dependence of HO transcription is eliminated. This indicates that SwI6 also plays an important role in the normal cell cycle regulation of all three promoters. When both SwI6 activity and the transcriptional regulation of SW14 are eliminated, cell cycle regulation is further reduced, indicating that these are two independent pathways of regulation. However, a twofold fluctuation in transcript levels still persists under these conditions. This reveals a third source of cell cycle control, which could affect SwI4 activity post-transcriptionally, or reflect the existence of another unidentified regulator of these promoters.

Sign in / Sign up

Export Citation Format

Share Document