scholarly journals Transcripts Targeted by the MicroRNA-16 Family Cooperatively Regulate Cell Cycle Progression

2007 ◽  
Vol 27 (6) ◽  
pp. 2240-2252 ◽  
Author(s):  
Peter S. Linsley ◽  
Janell Schelter ◽  
Julja Burchard ◽  
Miho Kibukawa ◽  
Melissa M. Martin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Control Cell ◽  
Cellular Growth ◽  
Functional Screening ◽  
Small Interfering Rnas ◽  
Cycle Progression ◽  
Mrna Targets ◽  
Microarray Profiling ◽  
The Individual

ABSTRACT microRNAs (miRNAs) are abundant, ∼21-nucleotide, noncoding regulatory RNAs. Each miRNA may regulate hundreds of mRNA targets, but the identities of these targets and the processes they regulate are poorly understood. Here we have explored the use of microarray profiling and functional screening to identify targets and biological processes triggered by the transfection of human cells with miRNAs. We demonstrate that a family of miRNAs sharing sequence identity with miRNA-16 (miR-16) negatively regulates cellular growth and cell cycle progression. miR-16-down-regulated transcripts were enriched with genes whose silencing by small interfering RNAs causes an accumulation of cells in G0/G1. Simultaneous silencing of these genes was more effective at blocking cell cycle progression than disruption of the individual genes. Thus, miR-16 coordinately regulates targets that may act in concert to control cell cycle progression.

scholarly journals Downstream of human NDR kinases: Impacting on c-myc and p21 protein stability to control cell cycle progression

Cell Cycle ◽  
2011 ◽  
Vol 10 (12) ◽  
pp. 1897-1904 ◽  
Author(s):  
Hauke Cornils ◽  
Reto S. Kohler ◽  
Alexander Hergovich ◽  
Brian A. Hemmings
Keyword(s):  
Cell Cycle ◽  
Protein Stability ◽  
Cell Cycle Progression ◽  
Control Cell ◽  
Cycle Progression ◽  
P21 Protein ◽  
Control Cell Cycle Progression

scholarly journals p73 and p63 Sustain Cellular Growth by Transcriptional Activation of Cell Cycle Progression Genes

2009 ◽  
Vol 69 (22) ◽  
pp. 8563-8571 ◽  
Author(s):  
K. Lefkimmiatis ◽  
M. F. Caratozzolo ◽  
P. Merlo ◽  
A. M. D'Erchia ◽  
B. Navarro ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcriptional Activation ◽  
Cell Cycle Progression ◽  
Cellular Growth ◽  
Cycle Progression

scholarly journals Plant hormone cytokinins control cell cycle progression and plastid replication in apicomplexan parasites

2018 ◽  
Vol 67 (1) ◽  
pp. 47-58 ◽  
Author(s):  
Syed Bilal Ahmad Andrabi ◽  
Michiru Tahara ◽  
Ryuma Matsubara ◽  
Tomoko Toyama ◽  
Hiroka Aonuma ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Plant Hormone ◽  
Control Cell ◽  
Cycle Progression ◽  
Apicomplexan Parasites ◽  
Control Cell Cycle Progression

scholarly journals HIV-1 Vif promotes the G1- to S-phase cell-cycle transition

Blood ◽  
2011 ◽  
Vol 117 (4) ◽  
pp. 1260-1269 ◽  
Author(s):  
Jiangfang Wang ◽  
Emma L. Reuschel ◽  
Jason M. Shackelford ◽  
Lauren Jeang ◽  
Debra K. Shivers ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Phase Cell ◽  
Small Interfering Rnas ◽  
Cycle Progression ◽  
Viral Infectivity Factor ◽  
G2 Phase ◽  
Regulate Cell Cycle Progression ◽  
Hiv 1

AbstractHIV-1 depends on host-cell resources for replication, access to which may be limited to a particular phase of the cell cycle. The HIV-encoded proteins Vpr (viral protein R) and Vif (viral infectivity factor) arrest cells in the G2 phase; however, alteration of other cell-cycle phases has not been reported. We show that Vif drives cells out of G1 and into the S phase. The effect of Vif on the G1-to-S transition is distinct from its effect on G2, because G2 arrest is Cullin5-dependent, whereas the G1-to-S progression is Cullin5-independent. Using mass spectrometry, we identified 2 novel cellular partners of Vif, Brd4 and Cdk9, both of which are known to regulate cell-cycle progression. We confirmed the interaction of Vif and Cdk9 by immunoprecipitation and Western blot, and showed that small interfering RNAs (siRNAs) specific for Cdk9 inhibit the Vif-mediated G1-to-S transition. These data suggest that Vif regulates early cell-cycle progression, with implications for infection and latency.

scholarly journals JAK/STAT pathway promotes Drosophila neuroblast proliferation via the direct CycE regulation

2020 ◽  
Author(s):  
Lijuan Du ◽  
Jian Wang
Keyword(s):  
Cell Cycle ◽  
Signaling Pathway ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Control Cell ◽  
Proliferative Potential ◽  
Cell Cycle Regulators ◽  
Cycle Progression ◽  
Stat Signaling ◽  
Stat Pathway

AbstractHow neural stem cells regulate their proliferative potential and lineage diversity is a central problem in developmental neurobiology. Drosophila Mushroom bodies (MBs), centers of olfactory learning and memory, are generated by a specific set of neuroblasts (Nbs) that are born in the embryonic stage and continuously proliferate till the end of the pupal stage. Although MB presents an excellent model for studying neural stem cell proliferation, the genetic and molecular mechanisms that control the unique proliferative characteristics of the MB Nbs are largely unknown. Further, the signaling cues controlling cell cycle regulators to promote cell cycle progression in MB Nbs remain poorly understood. Here, we report that JAK/STAT signaling pathway is required for the proliferation activity and maintenance of MB Nbs. Loss of JAK/STAT activity severely reduces the later-born MB neuron types and leads to premature neuroblast termination, which can be rescued by tissue-specific overexpression of CycE and diap1. Higher JAK/STAT pathway activity in MB results in more neurons, without producing supernumerary Nbs. Furthermore, we show that JAK/STAT signaling effector Stat92E directly regulates CycE transcription in MB Nbs. Finally, MB Nb clones of loss or excess CycE phenocopy those of decreased or increased JAK/STAT signaling pathway activities. We conclude that JAK/STAT signaling controls MB Nb proliferative activity through directly regulating CycE expression to control cell cycle progression.

scholarly journals A library of yeast genomic MCM1 binding sites contains genes involved in cell cycle control, cell wall and membrane structure, and metabolism.

1994 ◽  
Vol 14 (1) ◽  
pp. 348-359 ◽  
Author(s):  
M H Kuo ◽  
E Grayhack
Keyword(s):  
Cell Cycle ◽  
Cell Wall ◽  
Binding Sites ◽  
Cell Cycle Progression ◽  
Serum Response Factor ◽  
Fusion Gene ◽  
Control Cell ◽  
Membrane Structures ◽  
Cycle Progression ◽  
Yeast Genes

The Saccharomyces cerevisiae MCM1 protein, which is essential for viability, participates in both transcription activation and repression as well as DNA replication. However, neither the full network of genes at which MCM1 acts nor whether MCM1 itself mediates a regulatory response is known. Thus far, sites of MCM1 action have been identified by chance during analysis of particular genes. To identify a more complete set of genes on which MCM1 acts, we isolated a library of yeast genomic sequences to which MCM1 binds and then identified known genes within this library. Fragments of genomic DNA, bound to bacterially expressed MCM1 protein, were collected on a nitrocellulose filter, cloned, and analyzed. This selected library contains a large number of genes. As expected, it is enriched for strong MCM1 binding sites and contains cell-type-specific genes known to require MCM1. In addition, it also includes sequences upstream (or near the 5' end) of a number of identified yeast genes that have not yet been shown to be controlled by MCM1. These include genes whose products are involved in (i) the control of cell cycle progression (CLN3, CLB2, and FAR1), (ii) synthesis and maintenance of cell wall or cell membrane structures (PMA1, PIS1, DIT1,2, and GFA1), (iii) cellular metabolism (PCK1, MET2, and CCP1), and (iv) production of a secreted glycoprotein which is heat shock inducible (HSP150). The previously unidentified MCM1 binding site in the essential PMA1 gene is required for expression of a PMA1:lacZ fusion gene, providing evidence that one site is functionally important. We speculate that MCM1 coordinates decisions about cell cycle progression with changes in cell wall integrity and metabolic activity. The presence in the library of three genes involved in cell cycle progression reinforces the idea that one of the functions of MCM1 is indeed analogous to that of the mammalian serum response factor.

scholarly journals Increased Expression of Cyclin D2 during Multiple States of Growth Arrest in Primary and Established Cells

1998 ◽  
Vol 18 (6) ◽  
pp. 3163-3172 ◽  
Author(s):  
Muthupalaniappan Meyyappan ◽  
Howard Wong ◽  
Christopher Hull ◽  
Karl T. Riabowol
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Growth Arrest ◽  
Growth Conditions ◽  
Cellular Growth ◽  
Serum Starvation ◽  
Cyclin D2 ◽  
Cycle Progression ◽  
Quiescent Cells ◽  
D2 Protein

ABSTRACT Cyclin D2 is a member of the family of D-type cyclins that is implicated in cell cycle regulation, differentiation, and oncogenic transformation. To better understand the role of this cyclin in the control of cell proliferation, cyclin D2 expression was monitored under various growth conditions in primary human and established murine fibroblasts. In different states of cellular growth arrest initiated by contact inhibition, serum starvation, or cellular senescence, marked increases (5- to 20-fold) were seen in the expression levels of cyclin D2 mRNA and protein. Indirect immunofluorescence studies showed that cyclin D2 protein localized to the nucleus in G0, suggesting a nuclear function for cyclin D2 in quiescent cells. Cyclin D2 was also found to be associated with the cyclin-dependent kinases CDK2 and CDK4 but not CDK6 during growth arrest. Cyclin D2-CDK2 complexes increased in amounts but were inactive as histone H1 kinases in quiescent cells. Transient transfection and needle microinjection of cyclin D2 expression constructs demonstrated that overexpression of cyclin D2 protein efficiently inhibited cell cycle progression and DNA synthesis. These data suggest that in addition to a role in promoting cell cycle progression through phosphorylation of retinoblastoma family proteins in some cell systems, cyclin D2 may contribute to the induction and/or maintenance of a nonproliferative state, possibly through sequestration of the CDK2 catalytic subunit.

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