scholarly journals Erratum: Cyclin I-like (CCNI2) is a cyclin-dependent kinase 5 (CDK5) activator and is involved in cell cycle regulation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Chengcheng Liu ◽  
Xiaoyan Zhai ◽  
Bin Zhao ◽  
Yanfei Wang ◽  
Zhigang Xu
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cyclin Dependent Kinase ◽  
Cycle Regulation ◽  
Cyclin Dependent Kinase 5 ◽  
Cyclin I

scholarly journals Cyclin I-like (CCNI2) is a cyclin-dependent kinase 5 (CDK5) activator and is involved in cell cycle regulation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Chengcheng Liu ◽  
Xiaoyan Zhai ◽  
Bin Zhao ◽  
Yanfei Wang ◽  
Zhigang Xu
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Kinase Activity ◽  
Mitotic Cell ◽  
Cyclin Dependent Kinase ◽  
Cellular Events ◽  
Cycle Regulation ◽  
Cyclin Dependent Kinase 5 ◽  
Cyclin I

Abstract In contrast to conventional cyclin-dependent kinases that are important for mitotic cell division, cyclin-dependent kinase 5 (CDK5) is predominantly activated in post-mitotic cells and is involved in various cellular events. The kinase activity of CDK5 is tightly regulated by specific activators including p35, p39, and cyclin I (CCNI). Here we show that cyclin I-like (CCNI2), a homolog of CCNI, interacts with CDK5 and activates the kinase activity of CDK5. Different from CCNI, which colocalizes with CDK5 in the nuclei in transfected cells, CCNI2 mainly retains CDK5 in the cytoplasm as well as on the cell membrane. Furthermore, although the expression level of CCNI2 mRNA and CCNI2 protein do not change significantly during cell cycle, depletion of CCNI2 with siRNA affects cell cycle progression as well as cell proliferation. In conclusion, our data strongly suggest that CCNI2 is a novel CDK5 activator and is involved in cell cycle regulation.

The emerging importance of cyclin-dependent kinase inhibitors in the regulation of the plant cell cycle and related processesThis review is one of a selection of papers published in the Special Issue on Plant Cell Biology.

2006 ◽  
Vol 84 (4) ◽  
pp. 640-650 ◽  
Author(s):  
Hong Wang ◽  
Yongming Zhou ◽  
Larry C. Fowke
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Plant Cell ◽  
Cell Biology ◽  
Cell Cycle Regulation ◽  
Cellular Localization ◽  
Molecular Mechanisms ◽  
Cdk Inhibitors ◽  
Cyclin Dependent Kinase ◽  
Cycle Regulation

The cell division cycle in plants as in other eukaryotes is controlled by the cyclin-dependent kinase (CDK). This CDK paradigm determines that developmental cues and environmental signals need to impinge on the CDK complex to affect the cell cycle. An important part of understanding cell cycle regulation is to understand how CDK is regulated by various factors. In addition, there are features that set the cell cycle regulation in plants apart from that in other eukaryotes such as animals. Our knowledge of the molecular mechanisms that underlie the differences is poor. A family of plant CDK inhibitor proteins has been identified. The plant CDK inhibitors share similarity with a family of animal CDK inhibitors in a small region, while most of the sequence and the structural layout of the plant CDK inhibitors are different from the animal counterparts. Studies of plant CDK inhibitors have been performed mostly with the CDK inhibitors from Arabidopsis called ICKs (also referred to as KRPs). ICKs interact with D-type cyclins and A-type CDK. Overexpression of ICKs has been shown to affect cell division, plant growth, and morphogenesis. Studies of ICKs have also provided insightful information on the control of endoreduplication in plants. These aspects as well as cellular localization and protein regulation of ICKs are reviewed.

scholarly journals Morphogenesis signaling components influence cell cycle regulation by cyclin dependent kinase

Cell Division ◽  
2009 ◽  
Vol 4 (1) ◽  
pp. 12 ◽  
Author(s):  
Brian TD Tobe ◽  
Ana A Kitazono ◽  
Jacqueline Suen Garcia ◽  
Renee A Gerber ◽  
Brooke J Bevis ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Cyclin Dependent Kinase ◽  
Cycle Regulation ◽  
Signaling Components

ChemInform Abstract: Cyclin-Dependent Kinase Inhibitors: Useful Targets in Cell Cycle Regulation

ChemInform ◽  
2010 ◽  
Vol 31 (14) ◽  
pp. no-no
Author(s):  
Thais M. Sielecki ◽  
John F. Boylan ◽  
Pamela A. Benfield ◽  
George L. Trainor
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Kinase Inhibitors ◽  
Cyclin Dependent Kinase ◽  
Cycle Regulation

scholarly journals Silencing SHMT2 Inhibits the Progression of Oral Squamous Cell Carcinoma Through Cell Cycle Regulation

2020 ◽  
Author(s):  
Yan Liao ◽  
Fang Wang ◽  
Yadong Zhang ◽  
Hongshi Cai ◽  
Fan Song ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Cycle Regulation ◽  
Bioinformatic Analysis ◽  
Cyclin Dependent Kinase ◽  
Cycle Regulation

Abstract Background Serine hydroxymethyltransferase 2 (SHMT2) is a vital metabolic enzyme, which catalyzes the conversion of serine to glycine in one-carbon metabolism. SHMT2 has been reported to play a crucial role in the progression of tumors, but its function in oral squamous cell carcinoma (OSCC) remains unclear.Method SHMT2 expression was analyzed using publicly-available online databases, and assessed using immunohistochemistry staining of collected clinical specimens. The correlation between SHMT2 expression and the cell cycle was predicted through bioinformatic analysis, including weighted gene co-expression network analysis and gene set enrichment analysis. After transfection with siRNA CCK8 assay, Edu staining, flow cytometry, transwell, and wound healing experiments were performed to verify the functional role of SHMT2 in vitro. A stable cell line with SHMT2 silencing was established to detect the oncogenic function of SHMT2 in vivo.Results We found that SHMT2 was up-regulated in OSCC tissues and cell lines, and high level of SHMT2 was significantly linked with a poorer clinical outcome for OSCC patients. Bioinformatic analysis found that SHMT2 was closely related with cell cycle regulation. Down-regulation of SHMT2 effectively suppressed the proliferation rate of OSCC cells, and induced the prolongation of the G1 phase of the cell cycle in vitro. Western blotting found that cell cycle-related regulators such as cyclin-dependent kinase 4 (CDK4) and cyclinD1 expression levels were increased, while the expression levels of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1 were decreased after SHMT2 knockdown. Invasive and migrative ability and epithelial mesenchymal transition were impaired by SHMT2 knockdown. Silencing SHMT2 in the HN6 cell line using short hairpin RNA impeded tumor growth in vivo.Conclusion Our findings suggested that high expression of SHMT2 in OSCC indicated low survival rates, and was associated with malignant behaviors of OSCC. SHMT2 may serve as a novel prognostic and therapeutic target of interest in OSCC.

scholarly journals Silencing SHMT2 inhibits the progression of tongue squamous cell carcinoma through cell cycle regulation

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yan Liao ◽  
Fang Wang ◽  
Yadong Zhang ◽  
Hongshi Cai ◽  
Fan Song ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Cell Cycle Regulation ◽  
Bioinformatic Analysis ◽  
Cyclin Dependent Kinase ◽  
Cycle Regulation

Abstract Background Serine hydroxymethyltransferase 2 (SHMT2) is a vital metabolic enzyme in one carbon metabolism catalyzing the conversion of serine to glycine, which has been reported to play a crucial role in the progression of tumors. However, its function in tongue squamous cell carcinoma (TSCC) remains unclear. Methods SHMT2 expression was analyzed using samples in online databases, and was assessed through immunohistochemistry staining of collected clinical specimens. The correlation between SHMT2 expression and the cell cycle was predicted through bioinformatic analysis, including weighted gene co-expression network analysis (WGCNA) and gene set enrichment analysis (GSEA). After transfection with siRNA, CCK8 assay, Edu staining, flow cytometry, trans-well assay, and wound healing experiments were performed to verify the functional role of SHMT2 in vitro. A stable cell line with SHMT2 silencing was established to detect the oncogenic function of SHMT2 in vivo. Results The expression of SHMT2 was up-regulated in TSCC tissues and cell lines compared with normal groups, and highly expressed SHMT2 significantly indicated a poorer clinical outcome for TSCC patients. Bioinformatic analysis found that high expression of SHMT2 was closely related with biologic process including cell cycle and cell cycle G1/S transition. Down regulating of SHMT2 significantly suppressed the proliferation, invasive and migrative ability of TSCC cells, and induced the prolongation of the G1 phase of the cell cycle in vitro. Furthermore, western blot showed that cell cycle-related regulators such as cyclin-dependent kinase 4 (CDK4) and cyclinD1 expression levels were decreased, while the expression levels of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1 were increased after SHMT2 knockdown. Silencing SHMT2 in the HN6 cell line using short hairpin RNA also impeded tumor growth in vivo. Conclusions Overexpression of SHMT2 in TSCC indicated low survival rates, and was associated with aggressive behaviors of TSCC. It was also found to be involved in cell cycle regulation of TSCC cells. SHMT2 may serve as a novel prognostic indicator of TSCC.

Cyclin-Dependent Kinase Inhibitors:  Useful Targets in Cell Cycle Regulation

2000 ◽  
Vol 43 (1) ◽  
pp. 1-18 ◽  
Author(s):  
Thais M. Sielecki ◽  
John F. Boylan ◽  
Pamela A. Benfield ◽  
George L. Trainor
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Kinase Inhibitors ◽  
Cyclin Dependent Kinase ◽  
Cycle Regulation
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