International Journal of Cell Biology最新文献_第10页

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

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, Filippo Biamonte, Graziana Esposito, Ramona Marino, Francesca Fanelli, Flavio Keller, Alessandra Micera","doi":"10.1155/2014/725928","DOIUrl":"https://doi.org/10.1155/2014/725928","url":null,"abstract":"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. ","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, Miyako Nishimoto","doi":"10.1155/2014/807013","DOIUrl":"https://doi.org/10.1155/2014/807013","url":null,"abstract":"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. ","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 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, Lakshmi R Perumalsamy, G V Shivashankar, Apurva Sarin","doi":"10.1155/2014/674753","DOIUrl":"https://doi.org/10.1155/2014/674753","url":null,"abstract":"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. ","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

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

引用次数: 125

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, Erika Carvalho, Mariana Figueiredo Rodrigues, Bruna Dos Santos Mendonça, Nivea Dias Amôedo, Franklin David Rumjanek","doi":"10.1155/2014/572097","DOIUrl":"10.1155/2014/572097","url":null,"abstract":"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. ","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

p38δ MAPK: Emerging Roles of a Neglected Isoform. p38δ MAPK:一个被忽视的异构体的新作用

International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-09-17 DOI: 10.1155/2014/272689

Carol O'Callaghan, Liam J Fanning, Orla P Barry

{"title":"p38δ MAPK: Emerging Roles of a Neglected Isoform.","authors":"Carol O'Callaghan, Liam J Fanning, Orla P Barry","doi":"10.1155/2014/272689","DOIUrl":"https://doi.org/10.1155/2014/272689","url":null,"abstract":"p38δ mitogen activated protein kinase (MAPK) is a unique stress responsive protein kinase. While the p38 MAPK family as a whole has been implicated in a wide variety of biological processes, a specific role for p38δ MAPK in cellular signalling and its contribution to both physiological and pathological conditions are presently lacking. Recent emerging evidence, however, provides some insights into specific p38δ MAPK signalling. Importantly, these studies have helped to highlight functional similarities as well as differences between p38δ MAPK and the other members of the p38 MAPK family of kinases. In this review we discuss the current understanding of the molecular mechanisms underlying p38δ MAPK activity. We outline a role for p38δ MAPK in important cellular processes such as differentiation and apoptosis as well as pathological conditions such as neurodegenerative disorders, diabetes, and inflammatory disease. Interestingly, disparate roles for p38δ MAPK in tumour development have also recently been reported. Thus, we consider evidence which characterises p38δ MAPK as both a tumour promoter and a tumour suppressor. In summary, while our knowledge of p38δ MAPK has progressed somewhat since its identification in 1997, our understanding of this particular isoform in many cellular processes still strikingly lags behind that of its counterparts. ","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"272689"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/272689","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32744544","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: 27

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, Martin Pook, Annika Trei, Toivo Maimets","doi":"10.1155/2014/280638","DOIUrl":"https://doi.org/10.1155/2014/280638","url":null,"abstract":"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. ","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

Mitochondrial stress signaling promotes cellular adaptations. 线粒体应激信号促进细胞适应。

International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-01-22 DOI: 10.1155/2014/156020

Jayne Alexandra Barbour, Nigel Turner

引用次数: 78

Lithium improves survival of PC12 pheochromocytoma cells in high-density cultures and after exposure to toxic compounds. 锂可提高高密度培养和暴露于有毒化合物后PC12嗜铬细胞瘤细胞的存活率。

International Journal of Cell Biology Pub Date : 2014-01-01 Epub Date: 2014-01-20 DOI: 10.1155/2014/135908

Cinzia Fabrizi, Stefania De Vito, Francesca Somma, Elena Pompili, Angela Catizone, Stefano Leone, Paola Lenzi, Francesco Fornai, Lorenzo Fumagalli

{"title":"Lithium improves survival of PC12 pheochromocytoma cells in high-density cultures and after exposure to toxic compounds.","authors":"Cinzia Fabrizi, Stefania De Vito, Francesca Somma, Elena Pompili, Angela Catizone, Stefano Leone, Paola Lenzi, Francesco Fornai, Lorenzo Fumagalli","doi":"10.1155/2014/135908","DOIUrl":"https://doi.org/10.1155/2014/135908","url":null,"abstract":"Autophagy is an evolutionary conserved mechanism that allows for the degradation of long-lived proteins and entire organelles which are driven to lysosomes for digestion. Different kinds of stressful conditions such as starvation are able to induce autophagy. Lithium and rapamycin are potent autophagy inducers with different molecular targets. Lithium stimulates autophagy by decreasing the intracellular myo-inositol-1,4,5-triphosphate levels, while rapamycin acts through the inhibition of the mammalian target of rapamycin (mTOR). The correlation between autophagy and cell death is still a matter of debate especially in transformed cells. In fact, the execution of autophagy can protect cells from death by promptly removing damaged organelles such as mitochondria. Nevertheless, an excessive use of the autophagic machinery can drive cells to death via a sort of self-cannibalism. Our data show that lithium (used within its therapeutic window) stimulates the overgrowth of the rat Pheochromocytoma cell line PC12. Besides, lithium and rapamycin protect PC12 cells from toxic compounds such as thapsigargin and trimethyltin. Taken together these data indicate that pharmacological activation of autophagy allows for the survival of Pheochromocytoma cells in stressful conditions such as high-density cultures and exposure to toxins. ","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":"2014 ","pages":"135908"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/135908","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32147932","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