Journal of signal transduction最新文献_第6页

Pivotal Role of AKAP12 in the Regulation of Cellular Adhesion Dynamics: Control of Cytoskeletal Architecture, Cell Migration, and Mitogenic Signaling. AKAP12在细胞粘附动力学调控中的关键作用:细胞骨架结构、细胞迁移和有丝分裂信号的控制。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-06-28 DOI: 10.1155/2012/529179

Shin Akakura, Irwin H Gelman

{"title":"Pivotal Role of AKAP12 in the Regulation of Cellular Adhesion Dynamics: Control of Cytoskeletal Architecture, Cell Migration, and Mitogenic Signaling.","authors":"Shin Akakura, Irwin H Gelman","doi":"10.1155/2012/529179","DOIUrl":"https://doi.org/10.1155/2012/529179","url":null,"abstract":"Cellular dynamics are controlled by key signaling molecules such as cAMP-dependent protein kinase (PKA) and protein kinase C (PKC). AKAP12/SSeCKS/Gravin (AKAP12) is a scaffold protein for PKA and PKC which controls actin-cytoskeleton reorganization in a spatiotemporal manner. AKAP12 also acts as a tumor suppressor which regulates cell-cycle progression and inhibits Src-mediated oncogenic signaling and cytoskeletal pathways. Reexpression of AKAP12 causes cell flattening, reorganization of the actin cytoskeleton, and the production of normalized focal adhesion structures. Downregulation of AKAP12 induces the formation of thickened, longitudinal stress fibers and the proliferation of adhesion complexes. AKAP12-null mouse embryonic fibroblasts exhibit hyperactivation of PKC, premature cellular senescence, and defects in cytokinesis, relating to the loss of PKC scaffolding activity by AKAP12. AKAP12-null mice exhibit increased cell senescence and increased susceptibility to carcinogen-induced oncogenesis. The paper describes the regulatory and scaffolding functions of AKAP12 and how it regulates cell adhesion, signaling, and oncogenic suppression.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2012 ","pages":"529179"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/529179","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30774782","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: 62

Levels of Ca(V)1.2 L-Type Ca(2+) Channels Peak in the First Two Weeks in Rat Hippocampus Whereas Ca(V)1.3 Channels Steadily Increase through Development. 大鼠海马Ca(V)1.2 l型Ca(2+)通道水平在前两周达到峰值，而Ca(V)1.3通道水平在发育过程中稳步上升。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-10-14 DOI: 10.1155/2012/597214

Audra A Kramer, Nicholas E Ingraham, Emily J Sharpe, Michelle Mynlieff

{"title":"Levels of Ca(V)1.2 L-Type Ca(2+) Channels Peak in the First Two Weeks in Rat Hippocampus Whereas Ca(V)1.3 Channels Steadily Increase through Development.","authors":"Audra A Kramer, Nicholas E Ingraham, Emily J Sharpe, Michelle Mynlieff","doi":"10.1155/2012/597214","DOIUrl":"https://doi.org/10.1155/2012/597214","url":null,"abstract":"Influx of calcium through voltage-dependent channels regulates processes throughout the nervous system. Specifically, influx through L-type channels plays a variety of roles in early neuronal development and is commonly modulated by G-protein-coupled receptors such as GABA(B) receptors. Of the four isoforms of L-type channels, only Ca(V)1.2 and Ca(V)1.3 are predominately expressed in the nervous system. Both isoforms are inhibited by the same pharmacological agents, so it has been difficult to determine the role of specific isoforms in physiological processes. In the present study, Western blot analysis and confocal microscopy were utilized to study developmental expression levels and patterns of Ca(V)1.2 and Ca(V)1.3 in the CA1 region of rat hippocampus. Steady-state expression of Ca(V)1.2 predominated during the early neonatal period decreasing by day 12. Steady-state expression of Ca(V)1.3 was low at birth and gradually rose to adult levels by postnatal day 15. In immunohistochemical studies, antibodies against Ca(V)1.2 and Ca(V)1.3 demonstrated the highest intensity of labeling in the proximal dendrites at all ages studied (P1-72). Immunohistochemical studies on one-week-old hippocampi demonstrated significantly more colocalization of GABA(B) receptors with Ca(V)1.2 than with Ca(V)1.3, suggesting that modulation of L-type calcium current in early development is mediated through Ca(V)1.2 channels.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2012 ","pages":"597214"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/597214","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31002152","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: 12

The role of bacteria in the pathogenesis of ulcerative colitis. 细菌在溃疡性结肠炎发病机制中的作用。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-04-24 DOI: 10.1155/2012/704953

Maiko Sasaki, Jan-Michael A Klapproth

{"title":"The role of bacteria in the pathogenesis of ulcerative colitis.","authors":"Maiko Sasaki, Jan-Michael A Klapproth","doi":"10.1155/2012/704953","DOIUrl":"https://doi.org/10.1155/2012/704953","url":null,"abstract":"Factors implicated in the pathophysiology of ulcerative colitis (UC) are an abnormal immune response, defect in intestinal epithelial barrier function, and gut microbiota. Currently, it is unclear whether specific bacterial strains are responsible for the induction of intestinal inflammation, but increased bacterial tissue invasion has been described in affected UC patients. Further, a quantitative and qualitative microbial imbalance in UC, defined as dysbiosis, has been characterized by an increase in Rhodococcus spp., Shigella spp., and Escherichia spp., but a decrease in certain Bacteroides spp.. More specifically, Campylobacter spp., Enterobacteriae, and enterohepatic Helicobacter were more prevalent in tissue sample from UC patients subjected to molecular detection methods, but not controls. In addition, serologic testing identified Fusobacterim varium as a potential contributor to the intestinal inflammation in UC. Interestingly, in-situ hybridization studies have shown anti-inflammatory Lactobacillus spp. and Pediococcus spp. were absent in samples from subjects affected by UC. Therefore, dysbiosis is a factor in the pathogenesis of UC.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2012 ","pages":"704953"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/704953","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30637948","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: 78

Regulation of adherens junction dynamics by phosphorylation switches. 磷酸化开关对粘附体连接动力学的调节。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-07-12 DOI: 10.1155/2012/125295

Cristina Bertocchi, Megha Vaman Rao, Ronen Zaidel-Bar

引用次数: 56

Focal adhesion kinases in adhesion structures and disease. 黏附结构和疾病中的局灶性黏附激酶。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-07-19 DOI: 10.1155/2012/296450

Pierre P Eleniste, Angela Bruzzaniti

引用次数: 29

Increased Cell-Matrix Adhesion upon Constitutive Activation of Rho Proteins by Cytotoxic Necrotizing Factors from E. Coli and Y. Pseudotuberculosis. 大肠杆菌和假结核杆菌的细胞毒性坏死因子对Rho蛋白的本构激活增加了细胞-基质的粘附。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-07-05 DOI: 10.1155/2012/570183

Martin May, Tanja Kolbe, Tianbang Wang, Gudula Schmidt, Harald Genth

{"title":"Increased Cell-Matrix Adhesion upon Constitutive Activation of Rho Proteins by Cytotoxic Necrotizing Factors from E. Coli and Y. Pseudotuberculosis.","authors":"Martin May, Tanja Kolbe, Tianbang Wang, Gudula Schmidt, Harald Genth","doi":"10.1155/2012/570183","DOIUrl":"https://doi.org/10.1155/2012/570183","url":null,"abstract":"Cytotoxic necrotizing factors (CNFs) encompass a class of autotransporter toxins produced by uropathogenic E. coli (CNF1) or Y. pseudotuberculosis (CNFy). CNF toxins deamidate and thereby constitutively activate RhoA, Rac1, and Cdc42. In this study, the effects of CNF1 on cell-matrix adhesion are analysed using functional cell-adhesion assays. CNF1 strongly increased cell-matrix binding of suspended Hela cells and decreased the susceptibly of cells to trypsin-induced cell detachment. Increased cell-matrix binding was also observed upon treatment of Hela cells with isomeric CNFy, that specifically deamidates RhoA. Increased cell-matrix binding thus appears to depend on RhoA deamidation. In contrast, increased cell spreading was specifically observed upon CNF1 treatment, suggesting that it rather depended on Rac1/Cdc42 deamidation. Increased cell-matrix adhesion is further presented to result in reduced cell migration of adherent cells. In contrast, migration of suspended cells was not affected upon treatment with CNF1 or CNFy. CNF1 and CNFy thus reduced cell migration specifically under the condition of pre-established cell-matrix adhesion.","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2012 ","pages":"570183"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/570183","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30787666","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: 18

The role of phosphoinositide 3-kinase signaling in intestinal inflammation. 磷酸肌肽3-激酶信号在肠道炎症中的作用。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-04-09 DOI: 10.1155/2012/358476

Catherine M Cahill, Jack T Rogers, W Allan Walker

引用次数: 18

Protein-tyrosine kinase signaling in the biological functions associated with sperm. 与精子相关的生物学功能中的蛋白酪氨酸激酶信号。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-11-11 DOI: 10.1155/2012/181560

Takashi W Ijiri, A K M Mahbub Hasan, Ken-Ichi Sato

引用次数: 28

Oxidative stress, mitochondrial dysfunction, and aging. 氧化应激，线粒体功能障碍和衰老。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2011-10-02 DOI: 10.1155/2012/646354

Hang Cui, Yahui Kong, Hong Zhang

引用次数: 831

The Role of p38 MAPK and Its Substrates in Neuronal Plasticity and Neurodegenerative Disease. p38 MAPK及其底物在神经元可塑性和神经退行性疾病中的作用。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-06-25 DOI: 10.1155/2012/649079

Sônia A L Corrêa, Katherine L Eales

引用次数: 0