International Journal of Cell Biology最新文献

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An Intimate Relationship between ROS and Insulin Signalling: Implications for Antioxidant Treatment of Fatty Liver Disease. ROS与胰岛素信号的密切关系:对脂肪肝抗氧化治疗的启示
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-02-12 DOI: 10.1155/2014/519153
Aurèle Besse-Patin, Jennifer L Estall
{"title":"An Intimate Relationship between ROS and Insulin Signalling: Implications for Antioxidant Treatment of Fatty Liver Disease.","authors":"Aurèle Besse-Patin,&nbsp;Jennifer L Estall","doi":"10.1155/2014/519153","DOIUrl":"https://doi.org/10.1155/2014/519153","url":null,"abstract":"<p><p>Oxidative stress damages multiple cellular components including DNA, lipids, and proteins and has been linked to pathological alterations in nonalcoholic fatty liver disease (NAFLD). Reactive oxygen species (ROS) emission, resulting from nutrient overload and mitochondrial dysfunction, is thought to be a principal mediator in NAFLD progression, particularly toward the development of hepatic insulin resistance. In the context of insulin signalling, ROS has a dual role, as both a facilitator and inhibitor of the insulin signalling cascade. ROS mediate these effects through redox modifications of cysteine residues affecting phosphatase enzyme activity, stress-sensitive kinases, and metabolic sensors. This review highlights the intricate relationship between redox-sensitive proteins and insulin signalling in the context of fatty liver disease, and to a larger extent, the importance of reactive oxygen species as primary signalling molecules in metabolically active cells. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"519153"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/519153","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32212717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 47
Changes in the Distribution of the α 3 Na(+)/K(+) ATPase Subunit in Heterozygous Lurcher Purkinje Cells as a Genetic Model of Chronic Depolarization during Development. α 3na (+)/K(+) atp酶亚基在杂合Lurcher Purkinje细胞中分布的变化作为发育过程中慢性去极化的遗传模型。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-02-27 DOI: 10.1155/2014/152645
Rebecca McFarland, Hadi S Zanjani, Jean Mariani, Michael W Vogel
{"title":"Changes in the Distribution of the α 3 Na(+)/K(+) ATPase Subunit in Heterozygous Lurcher Purkinje Cells as a Genetic Model of Chronic Depolarization during Development.","authors":"Rebecca McFarland,&nbsp;Hadi S Zanjani,&nbsp;Jean Mariani,&nbsp;Michael W Vogel","doi":"10.1155/2014/152645","DOIUrl":"https://doi.org/10.1155/2014/152645","url":null,"abstract":"<p><p>A common assumption of excitotoxic mechanisms in the nervous system is that the ionic imbalance resulting from overstimulation of glutamate receptors and increased Na(+) and Ca(++) influx overwhelms cellular energy metabolic systems leading to cell death. The goal of this study was to examine how a chronic Na(+) channel leak current in developing Purkinje cells in the heterozygous Lurcher mutant (+/Lc) affects the expression and distribution of the α 3 subunit of the Na(+)/K(+) ATPase pump, a key component of the homeostasis system that maintains ionic equilibrium in neurons. The expression pattern of the catalytic α 3 Na(+)/K(+) ATPase subunit was analyzed by immunohistochemistry, histochemistry, and Western Blots in wild type (WT) and +/Lc cerebella at postnatal days P10, P15, and P25 to determine if there are changes in the distribution of active Na(+)/K(+) ATPase subunits in degenerating Purkinje cells. The results suggest that the expression of the catalytic α 3 subunit is altered in chronically depolarized +/Lc Purkinje cells, although the density of active Na(+)/K(+) ATPase pumps is not significantly altered compared with WT in the cerebellar cortex at P15, and then declines from P15 to P25 in the +/Lc cerebellum as the +/Lc Purkinje cells degenerate. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"152645"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/152645","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32251488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 28
Necroptosis: molecular signalling and translational implications. 坏死性下垂:分子信号传导和翻译意义。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-01-23 DOI: 10.1155/2014/490275
Claudia Giampietri, Donatella Starace, Simonetta Petrungaro, Antonio Filippini, Elio Ziparo
{"title":"Necroptosis: molecular signalling and translational implications.","authors":"Claudia Giampietri,&nbsp;Donatella Starace,&nbsp;Simonetta Petrungaro,&nbsp;Antonio Filippini,&nbsp;Elio Ziparo","doi":"10.1155/2014/490275","DOIUrl":"https://doi.org/10.1155/2014/490275","url":null,"abstract":"<p><p>Necroptosis is a form of programmed necrosis whose molecular players are partially shared with apoptotic cell death. Here we summarize what is known about molecular signalling of necroptosis, particularly focusing on fine tuning of FLIP and IAP proteins in the apoptosis/necroptosis balance. We also emphasize necroptosis involvement in physiological and pathological conditions, particularly in the regulation of immune homeostasis. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"490275"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/490275","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32168820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 60
Formation and regulation of mitochondrial membranes. 线粒体膜的形成和调控。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-01-22 DOI: 10.1155/2014/709828
Laila Cigana Schenkel, Marica Bakovic
{"title":"Formation and regulation of mitochondrial membranes.","authors":"Laila Cigana Schenkel,&nbsp;Marica Bakovic","doi":"10.1155/2014/709828","DOIUrl":"https://doi.org/10.1155/2014/709828","url":null,"abstract":"<p><p>Mitochondrial membrane phospholipids are essential for the mitochondrial architecture, the activity of respiratory proteins, and the transport of proteins into the mitochondria. The accumulation of phospholipids within mitochondria depends on a coordinate synthesis, degradation, and trafficking of phospholipids between the endoplasmic reticulum (ER) and mitochondria as well as intramitochondrial lipid trafficking. Several studies highlight the contribution of dietary fatty acids to the remodeling of phospholipids and mitochondrial membrane homeostasis. Understanding the role of phospholipids in the mitochondrial membrane and their metabolism will shed light on the molecular mechanisms involved in the regulation of mitochondrial function and in the mitochondrial-related diseases. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"709828"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/709828","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32160893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 121
Characterization of NGF, trkA (NGFR) , and p75 (NTR) in Retina of Mice Lacking Reelin Glycoprotein. 缺乏Reelin糖蛋白小鼠视网膜中NGF、trkA (NGFR)和p75 (NTR)的表征。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-01-30 DOI: 10.1155/2014/725928
Bijorn Omar Balzamino, Filippo Biamonte, Graziana Esposito, Ramona Marino, Francesca Fanelli, Flavio Keller, Alessandra Micera
{"title":"Characterization of NGF, trkA (NGFR) , and p75 (NTR) in Retina of Mice Lacking Reelin Glycoprotein.","authors":"Bijorn Omar Balzamino,&nbsp;Filippo Biamonte,&nbsp;Graziana Esposito,&nbsp;Ramona Marino,&nbsp;Francesca Fanelli,&nbsp;Flavio Keller,&nbsp;Alessandra Micera","doi":"10.1155/2014/725928","DOIUrl":"https://doi.org/10.1155/2014/725928","url":null,"abstract":"<p><p>Both Reelin and Nerve Growth Factor (NGF) exert crucial roles in retinal development. Retinogenesis is severely impaired in E-reeler mice, a model of Reelin deficiency showing specific Green Fluorescent Protein expression in Rod Bipolar Cells (RBCs). Since no data are available on Reelin and NGF cross-talk, NGF and trkA(NGFR)/ p75(NTR) expression was investigated in retinas from E-reeler versus control mice, by confocal microscopy, Western blotting, and real time PCR analysis. A scattered increase of NGF protein was observed in the Ganglion Cell Layer and more pronounced in the Inner Nuclear Layer (INL). A selective increase of p75(NTR) was detected in most of RBCs and in other cell subtypes of INL. On the contrary, a slight trend towards a decrease was detected for trkA(NGFR), albeit not significant. Confocal data were validated by Western blot and real time PCR. Finally, the decreased trkA(NGFR)/ p75(NTR) ratio, representative of p75(NTR) increase, significantly correlated with E-reeler versus E-control. These data indicate that NGF-trkA(NGFR)/ p75(NTR) is affected in E-reeler retina and that p75(NTR) might represent the main NGF receptor involved in the process. This first NGF-trkA(NGFR)/ p75(NTR) characterization suggests that E-reeler might be suitable for exploring Reelin-NGF cross-talk, representing an additional information source in those pathologies characterized by retinal degeneration. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"725928"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/725928","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32174101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
Matrix gla protein binds to fibronectin and enhances cell attachment and spreading on fibronectin. 基质玻璃蛋白与纤维连接蛋白结合,增强细胞在纤维连接蛋白上的附着和扩散。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-08-21 DOI: 10.1155/2014/807013
Satoru Ken Nishimoto, Miyako Nishimoto
{"title":"Matrix gla protein binds to fibronectin and enhances cell attachment and spreading on fibronectin.","authors":"Satoru Ken Nishimoto,&nbsp;Miyako Nishimoto","doi":"10.1155/2014/807013","DOIUrl":"https://doi.org/10.1155/2014/807013","url":null,"abstract":"<p><p>Background. Matrix Gla protein (MGP) is a vitamin K-dependent, extracellular matrix protein. MGP is a calcification inhibitor of arteries and cartilage. However MGP is synthesized in many tissues and is especially enriched in embryonic tissues and in cancer cells. The presence of MGP in those instances does not correlate well with the calcification inhibitory role. This study explores a potential mechanism for MGP to bind to matrix proteins and alter cell matrix interactions. Methods. To determine whether MGP influences cell behavior through interaction with fibronectin, we studied MGP binding to fibronectin, the effect of MGP on fibronectin mediated cell attachment and spreading and immunolocalized MGP and fibronectin. Results. First, MGP binds to fibronectin. The binding site for MGP is in a specific fibronectin fragment, called III1-C or anastellin. The binding site for fibronectin is in a MGP C-terminal peptide comprising amino acids 61-77. Second, MGP enhances cell attachment and cell spreading on fibronectin. MGP alone does not promote cell adhesion. Third, MGP is present in fibronectin-rich regions of tissue sections. Conclusions. MGP binds to fibronectin. The presence of MGP increased cell-fibronectin interactions. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"807013"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/807013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32659299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
The Mitochondrial Aminoacyl tRNA Synthetases: Genes and Syndromes. 线粒体氨酰基tRNA合成酶:基因和综合征。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-02-04 DOI: 10.1155/2014/787956
Daria Diodato, Daniele Ghezzi, Valeria Tiranti
{"title":"The Mitochondrial Aminoacyl tRNA Synthetases: Genes and Syndromes.","authors":"Daria Diodato,&nbsp;Daniele Ghezzi,&nbsp;Valeria Tiranti","doi":"10.1155/2014/787956","DOIUrl":"https://doi.org/10.1155/2014/787956","url":null,"abstract":"<p><p>Mitochondrial respiratory chain (RC) disorders are a group of genetically and clinically heterogeneous diseases. This is because protein components of the RC are encoded by both mitochondrial and nuclear genomes and are essential in all cells. In addition, the biogenesis and maintenance of mitochondria, including mitochondrial DNA (mtDNA) replication, transcription, and translation, require nuclear-encoded genes. In the past decade, a growing number of syndromes associated with dysfunction of mtDNA translation have been reported. This paper reviews the current knowledge of mutations affecting mitochondrial aminoacyl tRNAs synthetases and their role in the pathogenic mechanisms underlying the different clinical presentations. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"787956"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/787956","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32184244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 125
The linker histone h1.2 is an intermediate in the apoptotic response to cytokine deprivation in T-effectors. 连接蛋白h1.2是t效应物中细胞因子剥夺导致凋亡反应的中间物。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-02-13 DOI: 10.1155/2014/674753
Megha Garg, Lakshmi R Perumalsamy, G V Shivashankar, Apurva Sarin
{"title":"The linker histone h1.2 is an intermediate in the apoptotic response to cytokine deprivation in T-effectors.","authors":"Megha Garg,&nbsp;Lakshmi R Perumalsamy,&nbsp;G V Shivashankar,&nbsp;Apurva Sarin","doi":"10.1155/2014/674753","DOIUrl":"https://doi.org/10.1155/2014/674753","url":null,"abstract":"<p><p>Tissue homeostasis is a dynamic process involving proliferation and the removal of redundant or damaged cells. This is exemplified in the coordinated deletion-triggered by limiting trophic factors/cytokines in the extracellular milieu-of differentiated T cells overproduced during the mammalian immune response. However, mechanisms by which extracellular cues are perceived and transduced as apoptotic triggers remain incompletely understood. T-effectors are dependent on cytokines for survival and undergo apoptosis following cytokine withdrawal. Here we report that leptomycin B (LMB), an inhibitor of nuclear export machinery, protected T-effectors from apoptosis implicating a nuclear intermediate in the apoptotic pathway. Evidence is presented that the linker histone H1.2 localizes to the cytoplasm, by a mechanism sensitive to regulation by LMB, to activate apoptotic signaling culminating in nuclear and mitochondrial damage in T-effectors in response to cytokine deprivation. H1.2 is detected in a complex with the proapoptotic mitochondrial resident Bak and its subcellular localization regulated by Jun-N-terminal kinase (JNK), an intermediate in the apoptotic cascade in T-effectors. These data suggest that metabolic stressors may impinge on H1.2 dynamics favoring its activity at the mitochondrion, thereby functioning as a molecular switch for T-effector apoptosis. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"674753"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/674753","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32225502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
Methyl jasmonate: putative mechanisms of action on cancer cells cycle, metabolism, and apoptosis. 茉莉酸甲酯:癌症细胞周期、代谢和凋亡的假定作用机制。
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-02-06 DOI: 10.1155/2014/572097
Italo Mario Cesari, Erika Carvalho, Mariana Figueiredo Rodrigues, Bruna Dos Santos Mendonça, Nivea Dias Amôedo, Franklin David Rumjanek
{"title":"Methyl jasmonate: putative mechanisms of action on cancer cells cycle, metabolism, and apoptosis.","authors":"Italo Mario Cesari,&nbsp;Erika Carvalho,&nbsp;Mariana Figueiredo Rodrigues,&nbsp;Bruna Dos Santos Mendonça,&nbsp;Nivea Dias Amôedo,&nbsp;Franklin David Rumjanek","doi":"10.1155/2014/572097","DOIUrl":"10.1155/2014/572097","url":null,"abstract":"<p><p>Methyl jasmonate (MJ), an oxylipid that induces defense-related mechanisms in plants, has been shown to be active against cancer cells both in vitro and in vivo, without affecting normal cells. Here we review most of the described MJ activities in an attempt to get an integrated view and better understanding of its multifaceted modes of action. MJ (1) arrests cell cycle, inhibiting cell growth and proliferation, (2) causes cell death through the intrinsic/extrinsic proapoptotic, p53-independent apoptotic, and nonapoptotic (necrosis) pathways, (3) detaches hexokinase from the voltage-dependent anion channel, dissociating glycolytic and mitochondrial functions, decreasing the mitochondrial membrane potential, favoring cytochrome c release and ATP depletion, activating pro-apoptotic, and inactivating antiapoptotic proteins, (4) induces reactive oxygen species mediated responses, (5) stimulates MAPK-stress signaling and redifferentiation in leukemia cells, (6) inhibits overexpressed proinflammatory enzymes in cancer cells such as aldo-keto reductase 1 and 5-lipoxygenase, and (7) inhibits cell migration and shows antiangiogenic and antimetastatic activities. Finally, MJ may act as a chemosensitizer to some chemotherapics helping to overcome drug resistant. The complete lack of toxicity to normal cells and the rapidity by which MJ causes damage to cancer cells turn MJ into a promising anticancer agent that can be used alone or in combination with other agents. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"572097"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/572097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32191692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 79
Assessment of the Potential of CDK2 Inhibitor NU6140 to Influence the Expression of Pluripotency Markers NANOG, OCT4, and SOX2 in 2102Ep and H9 Cells. CDK2抑制剂NU6140对多能性标志物NANOG、OCT4和SOX2在2102Ep和H9细胞中表达的影响
International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-11-17 DOI: 10.1155/2014/280638
Ade Kallas, Martin Pook, Annika Trei, Toivo Maimets
{"title":"Assessment of the Potential of CDK2 Inhibitor NU6140 to Influence the Expression of Pluripotency Markers NANOG, OCT4, and SOX2 in 2102Ep and H9 Cells.","authors":"Ade Kallas,&nbsp;Martin Pook,&nbsp;Annika Trei,&nbsp;Toivo Maimets","doi":"10.1155/2014/280638","DOIUrl":"https://doi.org/10.1155/2014/280638","url":null,"abstract":"<p><p>As cyclin-dependent kinases (CDKs) regulate cell cycle progression and RNA transcription, CDKs are attractive targets for creating cancer cell treatments. In this study we investigated the effects of the small molecular agent NU6140 (inhibits CDK2 and cyclin A interaction) on human embryonic stem (hES) cells and embryonal carcinoma-derived (hEC) cells via the expression of transcription factors responsible for pluripotency. A multiparameter flow cytometric method was used to follow changes in the expression of NANOG, OCT4, and SOX2 together in single cells. Both hES and hEC cells responded to NU6140 treatment by induced apoptosis and a decreased expression of NANOG, OCT4, and SOX2 in surviving cells. A higher sensitivity to NU6140 application in hES than hEC cells was detected. NU6140 treatment arrested hES and hEC cells in the G2 phase and inhibited entry into the M phase as evidenced by no significant increase in histone 3 phosphorylation. When embryoid bodies (EBs) formed from NU6104 treated hES cells were compared to EBs from untreated hES cells differences in ectodermal, endodermal, and mesodermal lineages were found. The results of this study highlight the importance of CDK2 activity in maintaining pluripotency of hES and hEC cells and in differentiation of hES cells. </p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"280638"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/280638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32882094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
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