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Calcium- and integrin-binding protein 1 (CIB1) has been shown to be involved in cell spreading and migration. The signaling events regulated by CIB1 during cell migration are poorly understood. Here we found that accumulation of CIB1 at the tip of the filopodia requires an intact cytoskeleton. Depletion of CIB1 using shRNA affects formation of FAK- and phosphotyrosine-rich focal adhesions without affecting stress fiber formation. Overexpression of CIB1 results in cell migration on fibronectin and Erk1/2 MAP kinase activation. CIB1-induced cell migration is dependent upon Erk1/2 activation, since it is inhibited by the MEK-specific inhibitor PD98059. Furthermore, CIB1-induced cell migration, as well as Erk1/2 activation, is dependent on PKC, Src family kinases as well as PI-3 kinase as it is inhibited by bisindolylmaleimide 1, PP2, and wortmannin, respectively, in a dose-dependent manner. Co-expression of dominant-negative Cdc42 completely abolished CIB1-induced cell migration. Additionally, co-expression of constitutively active, but not dominant negative PAK1, a CIB1 binding protein, inhibited CIB1-induced cell migration. These results suggest that CIB1 positively regulates cell migration and is necessary for the recruitment of FAK to the focal adhesions. Furthermore, CIB1-induced cell migration is dependent on MAP kinase signaling and its function is attenuated by PAK1. 相似文献
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Shu‐Er Chow Jong‐Shyan Wang Ming‐Rung Lin Chien Lin Lee 《Journal of cellular biochemistry》2011,112(11):3459-3468
The members of Rho family are well known for their regulation of actin cytoskeleton to control cell migration. The Cip/kip members of cyclin‐dependent (CDK) inhibitors have shown to implicate in cell migration and cytoskeletal dynamics. p57kip2, a CDK inhibitor, is frequently down‐regulated in several malignancy tumors. However, its biological roles in human nasopharyngeal carcinoma (NPC) cells remained to be investigated. Here, we found p57kip2 has nuclear and cytoplasm distributions and depletion of endogenous p57kip2 did not change the cell‐cycle progression. Inhibition of cell proliferation by mitomycin C promoted FBS‐mediated cell migration and accompanied with the downregulation of ΔNp63α and p57kip2, but did not change the level of p27kip1, another CDK inhibitor. By using siRNA transfection and cell migration/invasion assays, we found that knockdown of p57kip2, but not ΔNp63α, involved in promotion of NPC cell migration and invasion via decrease of phospho‐cofilin (p‐cofilin). Treatment with Y‐27632, a specific ROCK inhibitor, we found that dysregulation of ROCK/cofilin pathway decreased p‐cofilin expression and induced cell migration. This change of p‐cofilin induced actin remodeling and pronounced increase of membrane protrusions. Further, silence of p57kip2 not only decreased the interaction between p57kip2 and LIMK‐1 assayed by immunoprecipitation but also reduced the level of phospho‐LIMK1/2. Therefore, this study indicated that dysregulation of p57kip2 promoted cell migration and invasion through modulation of LIMK/cofilin signaling and suggested this induction of inappropriate cell motility might contribute to promoting tumor cell for metastasis. J. Cell. Biochem. 112: 3459–3468, 2011. © 2011 Wiley Periodicals, Inc. 相似文献
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MicroRNA‐365 Inhibits the Proliferation of Vascular Smooth Muscle Cells by Targeting Cyclin D1
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Nanotopography Drives Stem Cell Fate Toward Osteoblast Differentiation Through α1β1 Integrin Signaling Pathway
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High‐Resolution Molecular Validation of Self‐Renewal and Spontaneous Differentiation in Clinical‐Grade Adipose‐Tissue Derived Human Mesenchymal Stem Cells
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Amel Dudakovic Emily Camilleri Scott M. Riester Eric A. Lewallen Sergiy Kvasha Xiaoyue Chen Darcie J. Radel Jarett M. Anderson Asha A. Nair Jared M. Evans Aaron J. Krych Jay Smith David R. Deyle Janet L. Stein Gary S. Stein Hee‐Jeong Im Simon M. Cool Jennifer J. Westendorf Sanjeev Kakar Allan B. Dietz Andre J. van Wijnen 《Journal of cellular biochemistry》2014,115(10):1816-1828
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