Journal of signal transduction最新文献_第9页

Effect of PAR-2 Deficiency in Mice on KC Expression after Intratracheal LPS Administration. pa -2缺乏对小鼠气管内LPS处理后KC表达的影响。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-12-07 DOI: 10.1155/2011/415195

Julie C Williams, Rebecca D Lee, Claire M Doerschuk, Nigel Mackman

引用次数: 12

The Functional Crosstalk between HER2 Tyrosine Kinase and TGF-β Signaling in Breast Cancer Malignancy. 乳腺癌恶性肿瘤中HER2酪氨酸激酶与TGF-β信号的功能性串扰

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-02-24 DOI: 10.1155/2011/804236

Shizhen Emily Wang

{"title":"The Functional Crosstalk between HER2 Tyrosine Kinase and TGF-β Signaling in Breast Cancer Malignancy.","authors":"Shizhen Emily Wang","doi":"10.1155/2011/804236","DOIUrl":"https://doi.org/10.1155/2011/804236","url":null,"abstract":"Accumulating evidence indicates a functional crosstalk between the HER2 (ErbB2) tyrosine kinase and the TGF-β signaling mediated by its serine/threonine kinase receptors. In HER2-overexpressing breast cancer, this crosstalk results in increased cancer cell proliferation, survival and invasion, accelerated cancer progression and metastasis in animal models, and resistance to chemotherapy and HER2-targeted therapy. The transformed cellular context with constitutively active HER2 signaling, as a consequence of HER2 gene amplification or overexpression, converts TGF-β from a tumor suppressor to a malignancy-promoting factor. TGF-β, in turn, potentiates oncogenic HER2 signaling by inducing shedding of the ErbB ligands and clustering of HER2 with integrins. In addition, TGF-β is associated with resistance to trastuzumab, an anti-HER2 therapeutic antibody. Recent mechanistic studies indicate that TGF-β and HER2 cooperate through both Smad-dependent and independent mechanisms. Blockade of HER2:TGF-β crosstalk may significantly enhance the efficiency of conventional therapies in breast cancer patients with HER2 overexpression.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2011 ","pages":"804236"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2011/804236","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29910538","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: 44

Regulation of SRC family kinases in human cancers. SRC家族激酶在人类癌症中的调控作用。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-04-04 DOI: 10.1155/2011/865819

Banibrata Sen, Faye M Johnson

引用次数: 206

Regulation and function of syk tyrosine kinase in mast cell signaling and beyond. 酪氨酸激酶在肥大细胞信号传导及其他方面的调控和功能。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-05-12 DOI: 10.1155/2011/507291

Rodrigo Orlandini de Castro

引用次数: 22

Individual rac GTPases mediate aspects of prostate cancer cell and bone marrow endothelial cell interactions. 单个rac gtpase介导前列腺癌细胞和骨髓内皮细胞相互作用的各个方面。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-06-27 DOI: 10.1155/2011/541851

Moumita Chatterjee, Linda Sequeira, Mashariki Jenkins-Kabaila, Cara W Dubyk, Surabhi Pathak, Kenneth L van Golen

{"title":"Individual rac GTPases mediate aspects of prostate cancer cell and bone marrow endothelial cell interactions.","authors":"Moumita Chatterjee, Linda Sequeira, Mashariki Jenkins-Kabaila, Cara W Dubyk, Surabhi Pathak, Kenneth L van Golen","doi":"10.1155/2011/541851","DOIUrl":"https://doi.org/10.1155/2011/541851","url":null,"abstract":"The Rho GTPases organize the actin cytoskeleton and are involved in cancer metastasis. Previously, we demonstrated that RhoC GTPase was required for PC-3 prostate cancer cell invasion. Targeted down-regulation of RhoC led to sustained activation of Rac1 GTPase and morphological, molecular and phenotypic changes reminiscent of epithelial to mesenchymal transition. We also reported that Rac1 is required for PC-3 cell diapedesis across a bone marrow endothelial cell layer. In the current study, we queried whether Rac3 and RhoG GTPases also have a role in prostate tumor cell diapedesis. Using specific siRNAs we demonstrate roles for each protein in PC-3 and C4-2 cell adhesion and diapedesis. We have shown that the chemokine CCL2 induces tumor cell diapedesis via Rac1 activation. Here we find that RhoG partially contributes to CCL2-induced tumor cell diapedesis. We also find that Rac1 GTPase mediates tight binding of prostate cancer cells to bone marrow endothelial cells and promotes retraction of endothelial cells required for tumor cell diapedesis. Finally, Rac1 leads to β1 integrin activation, suggesting a mechanism that Rac1 can mediate tight binding with endothelial cells. Together, our data suggest that Rac1 GTPase is key mediator of prostate cancer cell-bone marrow endothelial cell interactions.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2011 ","pages":"541851"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2011/541851","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30020336","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: 23

Mos in the oocyte: how to use MAPK independently of growth factors and transcription to control meiotic divisions. 卵母细胞中的Mos:如何独立于生长因子和转录使用MAPK来控制减数分裂。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2010-12-19 DOI: 10.1155/2011/350412

Aude Dupré, Olivier Haccard, Catherine Jessus

{"title":"Mos in the oocyte: how to use MAPK independently of growth factors and transcription to control meiotic divisions.","authors":"Aude Dupré, Olivier Haccard, Catherine Jessus","doi":"10.1155/2011/350412","DOIUrl":"https://doi.org/10.1155/2011/350412","url":null,"abstract":"In many cell types, the mitogen-activated protein kinase (MAPK) also named extracellular signal-regulated kinase (ERK) is activated in response to a variety of extracellular growth factor-receptor interactions and leads to the transcriptional activation of immediate early genes, hereby influencing a number of tissue-specific biological activities, as cell proliferation, survival and differentiation. In one specific cell type however, the female germ cell, MAPK does not follow this canonical scheme. In oocytes, MAPK is activated independently of growth factors and tyrosine kinase receptors, acts independently of transcriptional regulation, plays a crucial role in controlling meiotic divisions, and is under the control of a peculiar upstream regulator, the kinase Mos. Mos was originally identified as the transforming gene of Moloney murine sarcoma virus and its cellular homologue was the first proto-oncogene to be molecularly cloned. What could be the specific roles of Mos that render it necessary for meiosis? Which unique functions could explain the evolutionary cost to have selected one gene to only serve for few hours in one very specific cell type? This review discusses the original features of MAPK activation by Mos and the roles of this module in oocytes.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2011 ","pages":"350412"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2011/350412","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29910030","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

Mitogen-Activated Protein Kinases and Reactive Oxygen Species: How Can ROS Activate MAPK Pathways? 丝裂原活化蛋白激酶和活性氧:ROS如何激活MAPK通路?

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-02-06 DOI: 10.1155/2011/792639

Yong Son, Yong-Kwan Cheong, Nam-Ho Kim, Hun-Taeg Chung, Dae Gill Kang, Hyun-Ock Pae

{"title":"Mitogen-Activated Protein Kinases and Reactive Oxygen Species: How Can ROS Activate MAPK Pathways?","authors":"Yong Son, Yong-Kwan Cheong, Nam-Ho Kim, Hun-Taeg Chung, Dae Gill Kang, Hyun-Ock Pae","doi":"10.1155/2011/792639","DOIUrl":"https://doi.org/10.1155/2011/792639","url":null,"abstract":"Mitogen-activated protein kinases (MAPKs) are serine-threonine protein kinases that play the major role in signal transduction from the cell surface to the nucleus. MAPKs, which consist of growth factor-regulated extracellular signal-related kinases (ERKs), and the stress-activated MAPKs, c-jun NH(2)-terminal kinases (JNKs) and p38 MAPKs, are part of a three-kinase signaling module composed of the MAPK, an MAPK kinase (MAP2K) and an MAPK kinase (MAP3K). MAP3Ks phosphorylate MAP2Ks, which in turn activate MAPKs. MAPK phosphatases (MKPs), which recognize the TXY amino acid motif present in MAPKs, dephosphorylate and deactivate MAPKs. MAPK pathways are known to be influenced not only by receptor ligand interactions, but also by different stressors placed on the cell. One type of stress that induces potential activation of MAPK pathways is the oxidative stress caused by reactive oxygen species (ROS). Generally, increased ROS production in a cell leads to the activation of ERKs, JNKs, or p38 MAPKs, but the mechanisms by which ROS can activate these kinases are unclear. Oxidative modifications of MAPK signaling proteins and inactivation and/or degradation of MKPs may provide the plausible mechanisms for activation of MAPK pathways by ROS, which will be reviewed in this paper.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2011 ","pages":"792639"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2011/792639","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29910537","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: 875

Receptor-tyrosine-kinase-targeted therapies for head and neck cancer. 受体酪氨酸激酶靶向治疗头颈癌。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-06-07 DOI: 10.1155/2011/982879

Lisa A Elferink, Vicente A Resto

引用次数: 23

Itk: the rheostat of the T cell response. 它是T细胞反应的变阻器。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-04-07 DOI: 10.1155/2011/297868

Juris A Grasis, Constantine D Tsoukas

引用次数: 25

Tyrosine kinase signaling in kidney glomerular podocytes. 肾小球足细胞中的酪氨酸激酶信号传导。

Journal of signal transduction Pub Date : 2011-01-01 Epub Date: 2011-05-30 DOI: 10.1155/2011/317852

Seisuke Hattori, Shoichiro Kanda, Yutaka Harita

引用次数: 20