Molecular cell biology research communications : MCBRC最新文献_第5页

Author Index for Volume 4, Number 3 第4卷第3号作者索引

Molecular cell biology research communications : MCBRC Pub Date : 2000-09-01 DOI: 10.1006/mcbr.2000.0283

引用次数: 0

IGF1 Activates PKC α-Dependent Protein Synthesis in Adult Rat Cardiomyocytes IGF1激活成年大鼠心肌细胞PKC α-依赖性蛋白合成

Molecular cell biology research communications : MCBRC Pub Date : 2000-09-01 DOI: 10.1006/mcbr.2001.0274

Anna Pecherskaya , Michele Solem

引用次数: 16

Using Neural Networks for Prediction of Subcellular Location of Prokaryotic and Eukaryotic Proteins 应用神经网络预测原核和真核蛋白的亚细胞定位

Molecular cell biology research communications : MCBRC Pub Date : 2000-09-01 DOI: 10.1006/mcbr.2001.0269

Yu-Dong Cai , Kuo-Chen Chou

引用次数: 37

PD98059 Attenuates Hydrogen Peroxide-Induced Cell Death through Inhibition of Jun N-Terminal Kinase in HT29 Cells PD98059通过抑制HT29细胞的Jun n -末端激酶减轻过氧化氢诱导的细胞死亡

Molecular cell biology research communications : MCBRC Pub Date : 2000-09-01 DOI: 10.1006/mcbr.2001.0271

Baljinder S Salh , Jason Martens , Rajinder S Hundal , Nathan Yoganathan , David Charest , Alice Mui , Antonio Gómez-Muñoz

{"title":"PD98059 Attenuates Hydrogen Peroxide-Induced Cell Death through Inhibition of Jun N-Terminal Kinase in HT29 Cells","authors":"Baljinder S Salh , Jason Martens , Rajinder S Hundal , Nathan Yoganathan , David Charest , Alice Mui , Antonio Gómez-Muñoz","doi":"10.1006/mcbr.2001.0271","DOIUrl":"10.1006/mcbr.2001.0271","url":null,"abstract":"<div><p>We have investigated the effects of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), a potent naturally occurring oxidant on cell signaling and viability in the pluripotent HT29 intestinal cell line. There was a dose-dependent reduction in cell viability upon exposure to H<sub>2</sub>O<sub>2</sub> as measured by the XTT assay. Features of apoptosis were indicated by the findings of PARP and caspase 3 cleavage, as well as changes in cell morphology using phase contrast and nuclear fragmentation using fluorescence microscopy. There was a dose-dependent increase in the activation of p45-JNK, p42/p44-ERK, and p38-HOG. Surprisingly, oxidant-induced cell injury could be attenuated by preincubation with PD98059 to 50% of untreated control cells (<em>P</em> = 0.002). This and UO126, another MEK inhibitor were ably to reproducibly inhibit p45-JNK activation induced by hydrogen peroxide. Transfection with kinase-inactive constructs of JNK and ERK revealed that the improvement in cell viability was due to inhibition of JNK and not ERK. Transient transfections with AP-1 and NF-κB luciferase reporter constructs did not reveal any transcriptional activation due to hydrogen peroxide exposure however, in both cases the basal levels of transcriptional activity were suppressed in the presence of PD98059. It is concluded that JNK mediates H<sub>2</sub>O<sub>2</sub>-induced cellular injury in the HT29 cell line, and additionally, we report for the first time that JNK activation can be inhibited by both PD98059 and UO126 at conventional doses used to inhibit MEK.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 3","pages":"Pages 158-165"},"PeriodicalIF":0.0,"publicationDate":"2000-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2001.0271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89572867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 31

Comparative Effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin on MCF-7, RL95-2, and LNCaP Cells: Role of Target Steroid Hormones in Cellular Responsiveness to CYP1A1 Induction 2,3,7,8-四氯二苯并-对二恶英对MCF-7、RL95-2和LNCaP细胞的比较效应:靶类固醇激素在细胞对CYP1A1诱导的反应性中的作用

Molecular cell biology research communications : MCBRC Pub Date : 2000-09-01 DOI: 10.1006/mcbr.2001.0275

Nihar Ranjan Jana , Shubhashishi Sarkar , Mayumi Ishizuka , Junzo Yonemoto , Chiharu Tohyama , Hideko Sone

{"title":"Comparative Effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin on MCF-7, RL95-2, and LNCaP Cells: Role of Target Steroid Hormones in Cellular Responsiveness to CYP1A1 Induction","authors":"Nihar Ranjan Jana , Shubhashishi Sarkar , Mayumi Ishizuka , Junzo Yonemoto , Chiharu Tohyama , Hideko Sone","doi":"10.1006/mcbr.2001.0275","DOIUrl":"10.1006/mcbr.2001.0275","url":null,"abstract":"A study was conducted to investigate whether target hormones affect 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible gene expression, using as an experimental model system three human cancer cell lines, breast (MCF-7), uterine (RL95-2), and prostate (LNCaP). Exposure to TCDD induced the CYP1A1 gene in all three cell lines. MCF-7 and RL95-2 cells showed more than 15- and 10-fold induction of EROD (7-ethoxyresorufin O-deethylase) activity, respectively, compared with the less responsive LNCaP cells. Surprisingly, however, TCDD-induced reporter gene activity driven by a single XRE element was similar in RL95-2 and LNCaP cells. The steady-state levels of expression of aryl hydrocarbon receptor (AhR) and aryl hydrocarbon receptor nuclear translocator (ARNT) were similar in all three cell lines. Expression of the CYP1B1 and PAI-2 genes was induced by TCDD in MCF-7 and RL95-2, but not in LNCaP, cells. Transient coexpression of estradiol receptor-alpha (ER-alpha) with a TCDD-responsive reporter plasmid and subsequent TCDD treatment increased responsiveness to TCDD in RL95-2 and LNCaP cells. Treatment with AZA-C, a DNA methyltransferase inhibitor, enhanced responsiveness to TCDD, in terms of EROD activity in LNCaP cells, but not in MCF-7 and RL95-2 cells, suggesting that DNA methylation in the CpG dinucleotide within the XRE core sequence is another factor involved in silencing of CYP1A1 in LNCaP cells. TCDD markedly inhibited E(2)- or testosterone-induced reporter gene activities in all three cell lines. Conversely, these target hormones inhibited TCDD-induced EROD activity in the three cell lines. These findings suggest that TCDD and the target steroid hormones negatively regulate each other's activity.","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 3","pages":"Pages 174-180"},"PeriodicalIF":0.0,"publicationDate":"2000-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2001.0275","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83441795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 42

Cloning and Expression of the Mouse PIP49 (Pancreatitis Induced Protein 49) mRNA Which Encodes a New Putative Transmembrane Protein Activated in the Pancreas with Acute Pancreatitis 小鼠PIP49(胰腺炎诱导蛋白49)mRNA的克隆和表达，该mRNA编码一种在急性胰腺炎中激活的新跨膜蛋白

Molecular cell biology research communications : MCBRC Pub Date : 2000-09-01 DOI: 10.1006/mcbr.2000.0277

Amina Azizi Samir , Alejandro Ropolo , Daniel Grasso , Richard Tomasini , Jean-Charles Dagorn , Nelson Dusetti , Juan L. Iovanna , Maria Inea Vaccaro

引用次数: 10

Distinct Mechanisms of Inhibition of Interleukin-6-Induced Stat3 Signaling by TGF-β and α-Thrombin in CCL39 Cells TGF-β和α-凝血酶抑制白细胞介素-6诱导的CCL39细胞Stat3信号通路的不同机制

Molecular cell biology research communications : MCBRC Pub Date : 2000-09-01 DOI: 10.1006/mcbr.2001.0272

Jagadambika J. Gunaje, G. Jayarama Bhat

{"title":"Distinct Mechanisms of Inhibition of Interleukin-6-Induced Stat3 Signaling by TGF-β and α-Thrombin in CCL39 Cells","authors":"Jagadambika J. Gunaje, G. Jayarama Bhat","doi":"10.1006/mcbr.2001.0272","DOIUrl":"10.1006/mcbr.2001.0272","url":null,"abstract":"<div><p>We previously demonstrated that exposure of CCL39 lung fibroblast cells to α-thrombin inhibits interleukin-6 (IL-6)-induced tyrosine phosphorylation of Stat3 (signal transducers and activators of transcription-3) protein via a mitogen-activated protein (MAP)-kinase dependent mechanism. In the present study, we investigated the mechanism of regulation of IL-6-induced signaling by transforming growth factor-β (TGF-β) and compared this to α-thrombin-mediated inhibition. We demonstrate that exposure of CCL39 cells to TGF-β completely inhibits IL-6-induced Stat3 tyrosine phosphorylation and gp130 gene expression. However, in contrast to α-thrombin, TGF-β-mediated inhibition did not require activation of the MAP kinase pathway. Also, unlike α-thrombin, TGF-β-mediated inhibition requires synthesis of new proteins. Interestingly, TGF-β and α-thrombin both inhibit IL-6-induced expression of gp130 mRNA levels. These results demonstrate that although the end effects are the same, α-thrombin and TGF-β utilize distinct mechanisms to inhibit IL-6-induced Stat3 signaling.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 3","pages":"Pages 151-157"},"PeriodicalIF":0.0,"publicationDate":"2000-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2001.0272","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51527308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Autocrine Phosphorylation of p70S6k in Response to Acute Stretch in Myotubes p70S6k自分泌磷酸化对肌管急性拉伸的反应

Molecular cell biology research communications : MCBRC Pub Date : 2000-08-01 DOI: 10.1006/mcbr.2000.0257

Keith Baar , Carol E. Torgan , William E. Kraus , Karyn Esser

引用次数: 42

Differential Requirement for the Stress-Activated Protein Kinase/c-Jun NH2-Terminal Kinase in RNA Damage-Induced Apoptosis in Primary and in Immortalized Fibroblasts 原代和永生化成纤维细胞RNA损伤诱导凋亡中应激激活蛋白激酶/c-Jun nh2末端激酶的差异需求

Molecular cell biology research communications : MCBRC Pub Date : 2000-08-01 DOI: 10.1006/mcbr.2000.0266

Mihail S Iordanov , John Wong , Dianne L Newton , Susanna M Rybak , Robert K Bright , Richard A Flavell , Roger J Davis , Bruce E Magun

{"title":"Differential Requirement for the Stress-Activated Protein Kinase/c-Jun NH2-Terminal Kinase in RNA Damage-Induced Apoptosis in Primary and in Immortalized Fibroblasts","authors":"Mihail S Iordanov , John Wong , Dianne L Newton , Susanna M Rybak , Robert K Bright , Richard A Flavell , Roger J Davis , Bruce E Magun","doi":"10.1006/mcbr.2000.0266","DOIUrl":"10.1006/mcbr.2000.0266","url":null,"abstract":"<div><p>Onconase, an anticancer ribonuclease, damages cellular tRNA and causes caspase-dependent apoptosis in targeted cells (M. S. Iordanov, O. P. Ryabinina, J. Wong, T. H. Dinh, D. L. Newton, S. M. Rybak, and B. E. Magun. <em>Cancer Res.</em> 60, 1983–1994, 2000). The proapoptotic action of onconase depends on its RNase activity, but the molecular mechanisms leading to RNA damage-induced caspase activation are completely unknown. In this study, we have investigated whether onconase activates two signal-transduction pathways commonly stimulated by conventional chemo- and radiotherapy, namely the stress-activated protein kinase (SAPK) cascade and the pathway leading to the activation of nuclear factor-kappa B (NF-κB). We found that, in all cell types tested, onconase is a potent activator of SAPK1 (JNK1 and JNK2) and SAPK2 (p38 MAP kinase), but that it is incapable of activating NF-κB. Inhibition of p38 MAP kinase activity with a pharmacological inhibitor, SB203580, demonstrated that p38 MAP kinase is not required for onconase cytotoxicity. Using explanted fibroblasts from mice that contain targeted disruption of both <em>jnk1</em> and <em>jnk2</em> alleles, we found that JNKs are important mediators of onconase-induced cytotoxicity. Surprisingly, following the immortalization of these same cells with human papilloma virus (HPV16) gene products E6 and E7, additional proapoptotic pathways (exclusive of JNK) were provoked by onconase. Our results demonstrate that onconase may activate proapoptotic pathways in tumor cells that are not able to be accessed in normal cells. These results present the possibility that the cytotoxic activity of onconase in normal cells may be reduced by blocking the activity of JNKs.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 2","pages":"Pages 122-128"},"PeriodicalIF":0.0,"publicationDate":"2000-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0266","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91003861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 33

Author Index for Volume 4, Number 2 第4卷第2号作者索引

Molecular cell biology research communications : MCBRC Pub Date : 2000-08-01 DOI: 10.1006/mcbr.2001.0268

引用次数: 0