The Experts below are selected from a list of 261 Experts worldwide ranked by ideXlab platform
Naoki Mochizuki - One of the best experts on this subject based on the ideXlab platform.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon homophilic engagement of vascular endothelial cadherin (VE-cadherin) at the Cell-Cell Contacts in living Cells and that MAGI-1 is required for VE-cadherin-dependent Rap1 activation. We found that MAGI-1 localized to Cell-Cell Contacts presumably by associating with β-catenin and that MAGI-1 bound to a guanine nucleotide exchange factor for Rap1, PDZ-GEF1. Depletion of MAGI-1 suppressed the Cell-Cell Contact-induced Rap1 activation and the VE-cadherin-mediated Cell-Cell adhesion after Ca2+ switch. In addition, relocation of vinculin from Cell-extraCellular matrix Contacts to Cell-Cell Contacts after the Ca2+ switch was inhibited in MAGI-1-depleted Cells. Furthermore, inactivation of Rap1 by overexpression of Rap1GAPII impaired the VE-cadherin-dependent Cell adhesion. Collectively, MAGI-1 is important for VE-cadherin-dependent Rap1 activation upon Cell-Cell Contact. In addition, once activated, Rap1 upon Cell-Cell Contacts positively regulate the adherens junction formation by relocating vinculin that supports VE-cadherin-based Cell adhesion.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon homophilic engagement of vascular endothelial cadherin (VE-cadherin) at the Cell-Cell Contacts in living Cells and that MAGI-1 is required for VE-cadherin-dependent Rap1 activation. We found that MAGI-1 localized to Cell-Cell Contacts presumably by associating with β-catenin and that MAGI-1 bound to a guanine nucleotide exchange factor for Rap1, PDZ-GEF1. Depletion of MAGI-1 suppressed the Cell-Cell Contact-induced Rap1 activation and the VE-cadherin-mediated Cell-Cell adhesion after Ca2+ switch. In addition, relocation of vinculin from Cell-extraCellular matrix Contacts to Cell-Cell Contacts after the Ca2+ switch was inhibited in MAGI-1-depleted Cells. Furthermore, inactivation of Rap1 by overexpression of Rap1GAPII impaired the VE-cadherin-dependent Cell adhesion. Collectively, MAGI-1 is important for VE-cadherin-dependent Rap1 activation upon Cell-Cell Contact. In addition, once activated, Rap1 upon Cell-Cell Contacts positively regulate the adherens junction formation by relocating vinculin that supports VE-cadherin-based Cell adhesion.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon ho...
Gang Pei - One of the best experts on this subject based on the ideXlab platform.
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E‐Cadherin‐Mediated Cell–Cell Contact Is Critical for Induced Pluripotent Stem Cell Generation
Stem cells (Dayton Ohio), 2010Co-Authors: Taotao Chen, Detian Yuan, Bin Wei, Jing Jiang, Jiuhong Kang, Kun Ling, Lei Xiao, Gang PeiAbstract:The low efficiency of reprogramming and genomic integration of virus vectors obscure the potential application of induced pluripotent stem (iPS) Cells; therefore, identification of chemicals and cooperative factors that may improve the generation of iPS Cells will be of great value. Moreover, the Cellular mechanisms that limit the reprogramming efficiency need to be investigated. Through screening a chemical library, we found that two chemicals reported to upregulate E-cadherin considerably increase the reprogramming efficiency. Further study of the process indicated that E-cadherin is upregulated during reprogramming and the established iPS Cells possess E-cadherin-mediated Cell-Cell Contact, morphologically indistinguishable from embryonic stem (ES) Cells. Our experiments also demonstrate that overexpression of E-cadherin significantly enhances reprogramming efficiency, whereas knockdown of endogenous E-cadherin reduces the efficiency. Consistently, abrogation of Cell-Cell Contact by the inhibitory peptide or the neutralizing antibody against the extraCellular domain of E-cadherin compromises iPS Cell generation. Further mechanistic study reveals that adhesive binding activity of E-cadherin is required. Our results highlight the critical role of E-cadherin-mediated Cell-Cell Contact in reprogramming and suggest new routes for more efficient iPS Cell generation.
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e cadherin mediated Cell Cell Contact is critical for induced pluripotent stem Cell generation
Stem Cells, 2010Co-Authors: Taotao Chen, Detian Yuan, Bin Wei, Jing Jiang, Jiuhong Kang, Kun Ling, Lei Xiao, Gang PeiAbstract:The low efficiency of reprogramming and genomic integration of virus vectors obscure the potential application of induced pluripotent stem (iPS) Cells; therefore, identification of chemicals and cooperative factors that may improve the generation of iPS Cells will be of great value. Moreover, the Cellular mechanisms that limit the reprogramming efficiency need to be investigated. Through screening a chemical library, we found that two chemicals reported to upregulate E-cadherin considerably increase the reprogramming efficiency. Further study of the process indicated that E-cadherin is upregulated during reprogramming and the established iPS Cells possess E-cadherin-mediated Cell-Cell Contact, morphologically indistinguishable from embryonic stem (ES) Cells. Our experiments also demonstrate that overexpression of E-cadherin significantly enhances reprogramming efficiency, whereas knockdown of endogenous E-cadherin reduces the efficiency. Consistently, abrogation of Cell-Cell Contact by the inhibitory peptide or the neutralizing antibody against the extraCellular domain of E-cadherin compromises iPS Cell generation. Further mechanistic study reveals that adhesive binding activity of E-cadherin is required. Our results highlight the critical role of E-cadherin-mediated Cell-Cell Contact in reprogramming and suggest new routes for more efficient iPS Cell generation.
Jiandong Ding - One of the best experts on this subject based on the ideXlab platform.
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Data in support of effects of Cell–Cell Contact and oxygen tension on chondrogenic differentiation of stem Cells
Data in brief, 2015Co-Authors: Bin Cao, Rong Peng, Jiandong DingAbstract:This paper presents data related to the research article entitled “Effects of Cell–Cell Contact and oxygen tension on chondrogenic differentiation of stem Cells” [1]. Three sets of micropatterns were fabricated to study the influence of the Cell–Cell Contact on the chondrogenic induction of mesenchymal stem Cells (MSCs). The basic repeat units of these micropatterns were of the same area and microisland number to guarantee the same Cell density in each culture well. Cells on these micropatterns experienced the same microenvironment except Cell–Cell Contact extent. Immunofluorescent staining and quantitative real-time polymerase chain reaction (qRT-PCR) were performed, and the data are included here.
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Effects of Cell-Cell Contact and oxygen tension on chondrogenic differentiation of stem Cells.
Biomaterials, 2015Co-Authors: Bin Cao, Rong Peng, Jiandong DingAbstract:While Cell condensation has been thought to enhance chondrogenesis, no direct evidence so far confirms that Cell-Cell Contact itself increases chondrogenic differentiation of stem Cells, since the change of Cell-Cell Contact is usually coupled with those of other Cell geometry cues and soluble factors in Cell culture. The present study semi-quantitatively examined the effect of Cell-Cell Contact in a decoupled way. We fabricated two-dimensional micropatterns with Cell-adhesive peptide arginine-glycine-aspartate (RGD) microdomains on a nonfouling poly(ethylene glycol) (PEG) hydrogel. Mesenchymal stem Cells (MSCs) were well localized on the microdomains for a long time. Based on our micropattern design, single MSCs or Cell clusters with given Cell numbers (1, 2, 3, 6 and 15) and a similar spreading area per Cell were achieved on the same substrate, thus the interference of soluble factor difference from Cell autocrine and that of Cell spreading area were ruled out. After 9-day chondrogenic induction, collagen II was stained to characterize the chondrogenic induction results; the mRNA expression levels of SOX9, collagen II, aggrecan, HIF-1α and collagen I were also detected. The statistics confirmed unambiguously that the extent of the chondrogenic differentiation increased with Cell-Cell Contact, and even a linear relation between differentiation extent and Contact extent was established within the examined range. The Cell-Cell Contact effect worked under both hypoxia (5% O2) and normoxia (21% O2) conditions, and the hypoxia condition promoted the chondrogenic induction of MSCs on adhesive microdomains more efficiently than the normoxia condition under the same Cell-Cell Contact extents.
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the regulation of stem Cell differentiation by Cell Cell Contact on micropatterned material surfaces
Biomaterials, 2010Co-Authors: Jian Tang, Rong Peng, Jiandong DingAbstract:Abstract Using the material technique recently developed by us, we prepared a micropattern on poly(ethylene glycol) (PEG) hydrogel to keep background resistant to Cell adhesion for a long time, which made examination of differentiation of localized stem Cells available. Our micropattern designed in this paper prevented or ensured Contact between Cells adhering in arginine-glycine-aspartic acid (RGD) microdomains, and thus afforded a unique way to study the effects of Cell-Cell Contact on the lineage differentiation of stem Cells while ruling out the interference of soluble factors or Cell seeding concentration etc. As demonstration, mesenchymal stem Cells derived from rats were examined in this study, and both osteogenic and adipogenic differentiations were found to be regulated by Cell-Cell Contact. Isolated Cells exhibited less significant differentiation than paired or aggregated Cells. For those stem Cells in Contact, the extent of differentiation was fairly linearly related to the extent of Contact characterized by coordination number. Additionally, we revealed the existence of some unknown cues besides gap junction responsible for such effects of Cell-Cell Contact.
Atsuko Sakurai - One of the best experts on this subject based on the ideXlab platform.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon homophilic engagement of vascular endothelial cadherin (VE-cadherin) at the Cell-Cell Contacts in living Cells and that MAGI-1 is required for VE-cadherin-dependent Rap1 activation. We found that MAGI-1 localized to Cell-Cell Contacts presumably by associating with β-catenin and that MAGI-1 bound to a guanine nucleotide exchange factor for Rap1, PDZ-GEF1. Depletion of MAGI-1 suppressed the Cell-Cell Contact-induced Rap1 activation and the VE-cadherin-mediated Cell-Cell adhesion after Ca2+ switch. In addition, relocation of vinculin from Cell-extraCellular matrix Contacts to Cell-Cell Contacts after the Ca2+ switch was inhibited in MAGI-1-depleted Cells. Furthermore, inactivation of Rap1 by overexpression of Rap1GAPII impaired the VE-cadherin-dependent Cell adhesion. Collectively, MAGI-1 is important for VE-cadherin-dependent Rap1 activation upon Cell-Cell Contact. In addition, once activated, Rap1 upon Cell-Cell Contacts positively regulate the adherens junction formation by relocating vinculin that supports VE-cadherin-based Cell adhesion.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon homophilic engagement of vascular endothelial cadherin (VE-cadherin) at the Cell-Cell Contacts in living Cells and that MAGI-1 is required for VE-cadherin-dependent Rap1 activation. We found that MAGI-1 localized to Cell-Cell Contacts presumably by associating with β-catenin and that MAGI-1 bound to a guanine nucleotide exchange factor for Rap1, PDZ-GEF1. Depletion of MAGI-1 suppressed the Cell-Cell Contact-induced Rap1 activation and the VE-cadherin-mediated Cell-Cell adhesion after Ca2+ switch. In addition, relocation of vinculin from Cell-extraCellular matrix Contacts to Cell-Cell Contacts after the Ca2+ switch was inhibited in MAGI-1-depleted Cells. Furthermore, inactivation of Rap1 by overexpression of Rap1GAPII impaired the VE-cadherin-dependent Cell adhesion. Collectively, MAGI-1 is important for VE-cadherin-dependent Rap1 activation upon Cell-Cell Contact. In addition, once activated, Rap1 upon Cell-Cell Contacts positively regulate the adherens junction formation by relocating vinculin that supports VE-cadherin-based Cell adhesion.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon ho...
Keisuke Sako - One of the best experts on this subject based on the ideXlab platform.
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An Effective Feedback Loop between Cell-Cell Contact Duration and Morphogen Signaling Determines Cell Fate
Developmental cell, 2017Co-Authors: Vanessa Barone, Keisuke Sako, Mateusz Sikora, Moritz Lang, S. F. Gabriel Krens, Saurabh J. Pradhan, Shayan Shamipour, Călin C. Guet, Carl-philipp HeisenbergAbstract:Cell-Cell Contact formation constitutes an essential step in evolution, leading to the differentiation of specialized Cell types. However, remarkably little is known about whether and how the interplay between Contact formation and fate specification affects development. Here, we identify a positive feedback loop between Cell-Cell Contact duration, morphogen signaling, and mesendoderm Cell-fate specification during zebrafish gastrulation. We show that long-lasting Cell-Cell Contacts enhance the competence of prechordal plate (ppl) progenitor Cells to respond to Nodal signaling, required for ppl Cell-fate specification. We further show that Nodal signaling promotes ppl Cell-Cell Contact duration, generating a positive feedback loop between ppl Cell-Cell Contact duration and Cell-fate specification. Finally, by combining mathematical modeling and experimentation, we show that this feedback determines whether anterior axial mesendoderm Cells become ppl or, instead, turn into endoderm. Thus, the interdependent activities of Cell-Cell signaling and Contact formation control fate diversification within the developing embryo.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon homophilic engagement of vascular endothelial cadherin (VE-cadherin) at the Cell-Cell Contacts in living Cells and that MAGI-1 is required for VE-cadherin-dependent Rap1 activation. We found that MAGI-1 localized to Cell-Cell Contacts presumably by associating with β-catenin and that MAGI-1 bound to a guanine nucleotide exchange factor for Rap1, PDZ-GEF1. Depletion of MAGI-1 suppressed the Cell-Cell Contact-induced Rap1 activation and the VE-cadherin-mediated Cell-Cell adhesion after Ca2+ switch. In addition, relocation of vinculin from Cell-extraCellular matrix Contacts to Cell-Cell Contacts after the Ca2+ switch was inhibited in MAGI-1-depleted Cells. Furthermore, inactivation of Rap1 by overexpression of Rap1GAPII impaired the VE-cadherin-dependent Cell adhesion. Collectively, MAGI-1 is important for VE-cadherin-dependent Rap1 activation upon Cell-Cell Contact. In addition, once activated, Rap1 upon Cell-Cell Contacts positively regulate the adherens junction formation by relocating vinculin that supports VE-cadherin-based Cell adhesion.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon homophilic engagement of vascular endothelial cadherin (VE-cadherin) at the Cell-Cell Contacts in living Cells and that MAGI-1 is required for VE-cadherin-dependent Rap1 activation. We found that MAGI-1 localized to Cell-Cell Contacts presumably by associating with β-catenin and that MAGI-1 bound to a guanine nucleotide exchange factor for Rap1, PDZ-GEF1. Depletion of MAGI-1 suppressed the Cell-Cell Contact-induced Rap1 activation and the VE-cadherin-mediated Cell-Cell adhesion after Ca2+ switch. In addition, relocation of vinculin from Cell-extraCellular matrix Contacts to Cell-Cell Contacts after the Ca2+ switch was inhibited in MAGI-1-depleted Cells. Furthermore, inactivation of Rap1 by overexpression of Rap1GAPII impaired the VE-cadherin-dependent Cell adhesion. Collectively, MAGI-1 is important for VE-cadherin-dependent Rap1 activation upon Cell-Cell Contact. In addition, once activated, Rap1 upon Cell-Cell Contacts positively regulate the adherens junction formation by relocating vinculin that supports VE-cadherin-based Cell adhesion.
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magi 1 is required for rap1 activation upon Cell Cell Contact and for enhancement of vascular endothelial cadherin mediated Cell adhesion
Molecular Biology of the Cell, 2005Co-Authors: Atsuko Sakurai, Akiko Yamagishi, Keisuke Sako, Yoshikazu Nakaoka, Michitaka Masuda, Shigetomo Fukuhara, Yuji Kamioka, Naoki MochizukiAbstract:Rap1 is a small GTPase that regulates adherens junction maturation. It remains elusive how Rap1 is activated upon Cell-Cell Contact. We demonstrate for the first time that Rap1 is activated upon ho...