Signal transduction最新文献_第6页

TGF‐β receptors: Assembly, signalling, and disease relevance TGF - β受体:组装、信号传导和疾病相关性

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200600065

M. S. Krishnaveni, O. Eickelberg

引用次数: 3

Yin and Yang in BMP signaling: Impact on the pathology of diseases and potential for tissue regeneration BMP信号中的阴阳:对疾病病理的影响和组织再生的潜力

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200600098

A. Hartung, Christina Sieber, P. Knaus

引用次数: 17

Antioxidants and inhibitors of flavoprotein-dependent oxidases abrogate TGF-beta induction of biglycan: Evidence for a role of reactive oxygen species 黄素蛋白依赖氧化酶的抗氧化剂和抑制剂可以消除tgf - β诱导的多糖:活性氧的作用的证据

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200600100

H. Ungefroren, S. Groth, F. Fändrich

{"title":"Antioxidants and inhibitors of flavoprotein-dependent oxidases abrogate TGF-beta induction of biglycan: Evidence for a role of reactive oxygen species","authors":"H. Ungefroren, S. Groth, F. Fändrich","doi":"10.1002/SITA.200600100","DOIUrl":"https://doi.org/10.1002/SITA.200600100","url":null,"abstract":"Transforming growth factor-beta (TGF-β) in excess evokes inflammation, fibrosis, and desmoplasia in part by stimulating extracellular matrix synthesis including expression of the small leucine-rich proteoglycan biglycan (Bgn). Since TGF-β exerts some of its effects by stimulating the generation of reactive oxygen species (ROS) in cells, we investigated the possibility that ROS signaling is involved in Bgn induction by TGF-β. In pancreatic carcinoma PANC-1 cells, antioxidants (N-acetyl-L-cysteine, ascorbic acid), ROS scavengers (Tiron) and inhibitors of flavoprotein-dependent oxidases such as the ROS producing enzyme NADPH oxidase (apocynin and diphyleneiodonium) all inhibited TGF-β1-induced Bgn expression. In agreement with a role of the transcription factor NFκB in ROS cellular actions, the NFκB inhibitor pyrrolidinecarbodithiocarbamate also reduced the TGF-β effect on Bgn, while S-M-sulfate, an inhibitor of the nitric oxide-generating enzyme iNOS was ineffective in this respect. TGF-β time-dependently and moderately induced ROS production that was suppressed by diphenyleneiodonium. RT-PCR revealed that PANC-1 cells expressed various subunits of NADPH oxidase, namely p22phox, p47phox and p67phox as well as Nox isoforms 2, 4, 5 and 6, but lacked mRNA for Nox1 and 3. Blocking TGF-β-induced Bgn expression by modulating cellular redox status could have beneficial effects on fibrotic disorders caused by TGF-β hyperactivity.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"133 S2","pages":"338-344"},"PeriodicalIF":0.0,"publicationDate":"2006-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200600100","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50951195","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: 1

Updating interleukin-6 classic- and trans-signaling 更新白细胞介素-6经典和反式信号

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200600086

J. Scheller, J. Grötzinger, S. Rose-John

引用次数: 47

TGF-β/Smad-signaling in liver cells: Target genes and inhibitors of two parallel pathways 肝细胞中TGF-β/ smad信号传导:两条平行通路的靶基因和抑制剂

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200600097

K. Breitkopf, H. Weng, S. Dooley

引用次数: 9

Concentration-dependent stimulation by tissue inhibitor of metalloproteinases(TIMP)-2 of two signaling pathways in human osteosarcoma (MG-63) Cells 组织金属蛋白酶抑制剂(TIMP)-2对人骨肉瘤(MG-63)细胞两种信号通路的浓度依赖性刺激

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200500080

Ting Wang, Chihiro Kondo, K. Yamashita, M. Oguchi, K. Iwata, T. Noguchi, T. Hayakawa

{"title":"Concentration-dependent stimulation by tissue inhibitor of metalloproteinases(TIMP)-2 of two signaling pathways in human osteosarcoma (MG-63) Cells","authors":"Ting Wang, Chihiro Kondo, K. Yamashita, M. Oguchi, K. Iwata, T. Noguchi, T. Hayakawa","doi":"10.1002/SITA.200500080","DOIUrl":"https://doi.org/10.1002/SITA.200500080","url":null,"abstract":"We reported previously that tyrosine kinase (TYK) and mitogen-activated protein kinase (MAPK) play a role in TIMP-dependent growth signaling. Here we demonstrate that the activation of MAPK stimulated by TIMP-2 was sharply inhibited in MG-63 cells by PP1, a selective inhibitor of Src-family tyrosine kinases, suggesting that Src activation is possibly required for the MAPK activity in response to 1 ng/mL TIMP-2. A specific cell-permeable inhibitor of MAPK kinase (MEK), PD 98058 had an inhibitory effect on MAPK activity, indicating that MEK is an upstream effector of MAPK. By transfecting MG-63 cells with dominant-negative Ras, RasN17, and furthermore, by using a selective farnesyltransferase inhibitor, FTI-277, we found that MAPK activation stimulated by TIMP-2 was independent of Ras. We also demonstrated that the activation of MAPK in response to 1 ng/mL TIMP-2 was inhibited by a cAMP agonist, 8-bromo-cAMP. On the contrary, [3H]thymidine incorporation and the activation of MAPK, all of which were heavily suppressed by increasing the TIMP-2 concentration up to 100 ng/mL, were recovered by the addition of a cell-permeable specific PKA inhibitor, H-89. These results strongly suggest the presence of a negative crosstalk from the cAMP/PKA pathway to the TYK/MAPK one.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"2 9","pages":"280-286"},"PeriodicalIF":0.0,"publicationDate":"2006-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200500080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50950597","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: 1

Moving on: Molecular mechanisms in TGFβ‐induced epithelial cell migration 继续:TGFβ诱导上皮细胞迁移的分子机制

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200600094

K. Giehl, A. Menke

{"title":"Moving on: Molecular mechanisms in TGFβ‐induced epithelial cell migration","authors":"K. Giehl, A. Menke","doi":"10.1002/SITA.200600094","DOIUrl":"https://doi.org/10.1002/SITA.200600094","url":null,"abstract":"TGFβ, particularly TGFβ1-3, has been shown to promote epithelial dedifferentiation or epithelial-mesenchymal transition (EMT). While inhibition of epithelial cell proliferation in response to TGFβ is mainly mediated by the well-characterised Smad-pathway and subsequent regulation of gene transcription, the molecular mechanisms leading to TGFβ-induced migration, invasion and metastasis of epithelial tumour cells are less clear. Recent results from several groups suggest that the gain of tumourigenic activity by TGFβ includes signalling by mitogen-activated protein kinases (MAP kinases), phosphatidylinositol 3-kinase (PI3-K) and Rho-GTPases. Activation of the MAP kinases extracellular signal-regulated kinase (ERK) 1 and 2, p38 as well as c-jun N-terminal kinase (JNK) has been identified as important steps in TGFβ-induced, Smad4-independent signal transduction in epithelial cells. A role of activated ERK and JNK and their association with focal complexes in TGFβ-induced cell migration and actin cytoskeleton reorganisation of carcinoma cells has been identified recently. In this review we will focus on new data about the molecular mechanisms involved in the TGFβ-induced Smad-independent regulation of epithelial cell migration.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"1 1","pages":"355-364"},"PeriodicalIF":0.0,"publicationDate":"2006-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200600094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50951120","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: 9

Recent advances in TGFβ‐regulated transcription during carcinogenesis 肿瘤发生过程中TGFβ调控转录的最新进展

Signal transduction Pub Date : 2006-08-01 DOI: 10.1002/SITA.200600093

Anita Buck, V. Ellenrieder

{"title":"Recent advances in TGFβ‐regulated transcription during carcinogenesis","authors":"Anita Buck, V. Ellenrieder","doi":"10.1002/SITA.200600093","DOIUrl":"https://doi.org/10.1002/SITA.200600093","url":null,"abstract":"The multifunctional activities of transforming growth factor-beta (TGFβ) endow it with both tumor suppressor and tumor promoting activities, depending on the stage of carcinogenesis and the cellular activation state. In early tumor stages, TGFβ inhibits epithelial cell growth through induction of apoptosis and transcriptional regulation of cell cycle controlling genes. During tumor progression, however, many cancer cells escape from TGFβ-induced growth inhibition and, instead, respond to TGFβ with increased malignancy. TGFβ stimulates tumor promotion particularly in those tumor cells in which Smad-signaling remains functional and through transcriptional regulation of gene expression. Thus, loss of sensitivity to growth inhibition by TGFβ is not synonymous with complete loss of TGFβ signaling. Rather, it suggests that tumor cells gain advantage by selective inactivation of TGFβ tumor suppressor activities while retaining its tumor promoting functions. In this review we focus on novel aspects in TGFβ signaling and transcription and in particular on the role of Smad-interacting transcription factors. We also summarize recent advances in both cytoplasmic and nuclear crosstalk mechanisms between Smad and non-Smad signaling pathways and how this interaction results in the fine-tuning of Smad-mediated transcription during cancer progression. This knowledge will help to better understand the molecular mechanisms responsible for the switch of TGFβ from a tumor suppressor to a tumor promotor.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"30 2","pages":"345-354"},"PeriodicalIF":0.0,"publicationDate":"2006-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200600093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50951108","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: 4

Oligonucleotide microarrays for studying the effects of Ras signal transduction on the genetic program 用于研究Ras信号转导对遗传程序影响的寡核苷酸微阵列

Signal transduction Pub Date : 2006-06-01 DOI: 10.1002/SITA.200600090

O. Tchernitsa, C. Sers, A. Geflitter, R. Schäfer

引用次数: 3

Protein‐protein interaction screening with the Ras‐recruitment system Ras -募集系统的蛋白-蛋白相互作用筛选

Signal transduction Pub Date : 2006-06-01 DOI: 10.1002/SITA.200600089

C. Kruse, S. Hanke, S. Vasiliev, H. Hennemann

引用次数: 5