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This review discusses the current model of how junctions are formed, focusing in particular on the contribution of small GTPase signalling pathways and their specific targets.
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Braga V.M.M. Epithelial cell shape: cadherins and small GTPases. Exp Cell Res. 261:2000;83-90. This review discusses the current model of how junctions are formed, focusing in particular on the contribution of small GTPase signalling pathways and their specific targets.
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Lozano, E.1
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Regulation of cadherin function by Rho and Rac: Modulation by junction maturation and cellular context
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Braga V.M.M., Del Maschio A., Machesky L.M., Dejana E. Regulation of cadherin function by Rho and Rac: modulation by junction maturation and cellular context. Mol Biol Cell. 10:1999;9-22.
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Braga, V.M.M.1
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Regulation of cell-cell adhesion by Rac and Rho small G proteins in MDCK cells
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Takaishi, K.1
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ROCK and Dia have opposing effects on adherens junctions downstream of Rho
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Inhibition of RhoA results in a reduced association of α-catenin with cadherin, thereby compromising the interaction of the complexes with the actin cytoskeleton. This is the first report to show an effect of Rho inhibition of the composition of the cadherin complex.
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Sahai E., Marshall C.J. ROCK and Dia have opposing effects on adherens junctions downstream of Rho. Nat Cell Biol. 4:2002;408-415. Inhibition of RhoA results in a reduced association of α-catenin with cadherin, thereby compromising the interaction of the complexes with the actin cytoskeleton. This is the first report to show an effect of Rho inhibition of the composition of the cadherin complex.
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Sahai, E.1
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Calcium-induced intercellular adhesion of keratinocytes does not involve accumulation of β1 integrins at cell-cell contact sites and does not involve changes in the levels or phosphorylation of the catenins
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Braga V.M.M., Najabagheri N., Watt F.M. Calcium-induced intercellular adhesion of keratinocytes does not involve accumulation of β1 integrins at cell-cell contact sites and does not involve changes in the levels or phosphorylation of the catenins. Cell Ad Com. 5:1998;137-149.
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Dynamics of cadherin/catenin complex formation: Novel protein interactions and pathways of complex assembly
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0033973134
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Selective alterations in biosynthetic and endocytic protein traffic in Madin-Darby canine epithelial cells expressing mutants of the small GTPase Rac
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Jou T.-S., Leung S.-M., Fung L.M., Ruiz W.G., Nelson W.J., Apodaca G. Selective alterations in biosynthetic and endocytic protein traffic in Madin-Darby canine epithelial cells expressing mutants of the small GTPase Rac. Mol Biol Cell. 11:2000;287-304.
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14
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0032736748
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Modulation of endocytic traffic in polarized Madin-Darby canine kidney cells by the small GTPase RhoA
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Leung S.M., Rojas R., Maples C., Flynn C., Ruiz W.G., Jou T.S., Apodaca G. Modulation of endocytic traffic in polarized Madin-Darby canine kidney cells by the small GTPase RhoA. Mol Biol Cell. 10:1999;4369-4384.
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Apodaca, G.7
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Cdc42-dependent modulation of tight junctions and membrane protein traffic in polarized Madin-Darby Canine Kidney Cells
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Rojas R., Ruiz W.G., Leung S.-M., Jou T.-S., Apodaca G. Cdc42-dependent modulation of tight junctions and membrane protein traffic in polarized Madin-Darby Canine Kidney Cells. Mol Biol Cell. 12:2001;2257-2274.
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Rojas, R.1
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16
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0035801516
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An essential role for ARF6-regulated membrane traffic in adherens junction turnover and epithelial cell migration
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This study reveals the specific effects of ARF6 activation on cadherin receptors. ARF6 activation results in cadherin receptor internalisation and junction disassembly. ARF6 exerts its role downstream of hepatocyte growth factor (HGF) and Src activation. Interestingly, junction destabilisation occurs independently of actin remodelling and lamellipodia formation. These results suggest that ARF6 is most likely to affect cadherin adhesion by interfering with receptor endocytosis.
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Palacios F., Price L., Schweitzer J., Collard J.G., D'Souza-Schorey C. An essential role for ARF6-regulated membrane traffic in adherens junction turnover and epithelial cell migration. EMBO J. 20:2001;4973-4986. This study reveals the specific effects of ARF6 activation on cadherin receptors. ARF6 activation results in cadherin receptor internalisation and junction disassembly. ARF6 exerts its role downstream of hepatocyte growth factor (HGF) and Src activation. Interestingly, junction destabilisation occurs independently of actin remodelling and lamellipodia formation. These results suggest that ARF6 is most likely to affect cadherin adhesion by interfering with receptor endocytosis.
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Palacios, F.1
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17
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0036500155
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K-Ras mediates cytokine-induced formation of E-cadherin-based adherens junctions during liver development
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This is the first demonstration that K-Ras, but not H-Ras or N-Ras, has a positive effect on junction formation. This is opposed to H-Ras, whose activation destabilises junctions in epithelia. This report is interesting because of the high homology and similar targets observed for Ras family members, yet the outcome during junction assembly is very distinct.
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Matsui T., Kinoshita T., Morikawa Y., Tohya K., Katsuki M., Ito Y., Kamiya A., Miyajima A. K-Ras mediates cytokine-induced formation of E-cadherin-based adherens junctions during liver development. EMBO J. 21:2002;1021-1030. This is the first demonstration that K-Ras, but not H-Ras or N-Ras, has a positive effect on junction formation. This is opposed to H-Ras, whose activation destabilises junctions in epithelia. This report is interesting because of the high homology and similar targets observed for Ras family members, yet the outcome during junction assembly is very distinct.
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EMBO J
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Matsui, T.1
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Ito, Y.6
Kamiya, A.7
Miyajima, A.8
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18
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0033730417
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Activation of the small GTPase Rac is sufficient to disrupt cadherin-dependent cell-cell adhesion in normal human keratinocytes
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Braga V.M.M., Betson M., Li X., Lamarche-Vane N. Activation of the small GTPase Rac is sufficient to disrupt cadherin-dependent cell-cell adhesion in normal human keratinocytes. Mol Biol Cell. 11:2000;3703-3721.
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Braga, V.M.M.1
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Li, X.3
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19
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0033081407
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The Rap1 GTPase functions as a regulator of morphogenesis in vivo
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Asha H., de Ruiter N.D., Wang M., Hariharan I.K. The Rap1 GTPase functions as a regulator of morphogenesis in vivo. EMBO J. 18:1999;605-615.
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Hariharan, I.K.4
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0037083415
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Rap1 GTPase regulation of adherens junction positioning and cell adhesion
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This is the first demonstration that Rap proteins might play a role in junction organisation, without affecting the localisation of cadherins and catenins.
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Knox A.L., Brown N.H. Rap1 GTPase regulation of adherens junction positioning and cell adhesion. Science. 295:2002;1285-1288. This is the first demonstration that Rap proteins might play a role in junction organisation, without affecting the localisation of cadherins and catenins.
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Science
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Knox, A.L.1
Brown, N.H.2
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22
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0035823593
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Cadherin engagement regulates Rho family GTPases
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The effect of cadherin adhesion on the activation of Rho, Rac and Cdc42 are reported in different cell lines. The effects of cell confluence on small GTPase activation are also reported. However, conflicting results arise from the use of different cell lines.
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Noren N.K., Niessen C.M., Gumbiner B.M., Burridge K. Cadherin engagement regulates Rho family GTPases. J Biol Chem. 276:2001;33305-33308. The effect of cadherin adhesion on the activation of Rho, Rac and Cdc42 are reported in different cell lines. The effects of cell confluence on small GTPase activation are also reported. However, conflicting results arise from the use of different cell lines.
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J Biol Chem
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Noren, N.K.1
Niessen, C.M.2
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Burridge, K.4
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23
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0034994490
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Recruitment and activation of Rac1 by the formation of E-cadherin-mediated cell-cell adhesion sites
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This study demonstrates a specific activation of Rac by cadherin-dependent adhesion, in a phosphatidylinositol 3-kinase-dependent manner. No activation of Rho is observed under these experimental conditions.
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Nakagawa M., Fukata M., Yamaga M., Itoh N., Kaibuchi K. Recruitment and activation of Rac1 by the formation of E-cadherin-mediated cell-cell adhesion sites. J Cell Sci. 114:2001;1829-1838. This study demonstrates a specific activation of Rac by cadherin-dependent adhesion, in a phosphatidylinositol 3-kinase-dependent manner. No activation of Rho is observed under these experimental conditions.
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J Cell Sci
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Nakagawa, M.1
Fukata, M.2
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Itoh, N.4
Kaibuchi, K.5
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24
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0034711219
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E-cadherin-mediated cell-cell attachment activates Cdc42
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Cdc42 activation is observed in a PI3 kinase- and E-cadherin-dependent manner.
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Kim S.H., Zhigang L., Sacks D.B. E-cadherin-mediated cell-cell attachment activates Cdc42. J Biol Chem. 275:2000;36999-37005. Cdc42 activation is observed in a PI3 kinase- and E-cadherin-dependent manner.
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Kim, S.H.1
Zhigang, L.2
Sacks, D.B.3
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25
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Mechanisms of cold-induced platelet actin assembly
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Hoffmeister K.M., Falet H., Toker A., Barkalow K.L., Stossel T.P., Hartwig J.H. Mechanisms of cold-induced platelet actin assembly. J Biol Chem. 276:2001;24751-24759.
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Hoffmeister, K.M.1
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Barkalow, K.L.4
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Hartwig, J.H.6
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26
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The small GTPases Rho and Rac are required for the establishment of cadherin-dependent cell-cell contacts
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Braga V.M.M., Machesky L.M., Hall A., Hotchin N.A. The small GTPases Rho and Rac are required for the establishment of cadherin-dependent cell-cell contacts. J Cell Biol. 137:1997;1421-1431.
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Effects of regulated expression of mutant RhoA and Rac1 small GTPases on the development of epithelial (MDCK) cell polarity
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0037033804
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Fyn tyrosine kinase is a downstream mediator of Rho/PRK2 function in keratinocyte cell-cell adhesion
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Calautti E., Grossi M., Mammucari C., Aoyama Y., Pirro M., Ono Y., Li J., Dotto G.P. Fyn tyrosine kinase is a downstream mediator of Rho/PRK2 function in keratinocyte cell-cell adhesion. J Cell Biol. 156:2002;137-148.
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Calautti, E.1
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Dotto, G.P.8
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29
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0036226067
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VE-Cadherin regulates endothelial actin activating Rac and increasing membrane association of Tiam
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The expression of VE-cadherin in VE-cadherin null cells results in Rac activation, and Rho inhibition. Interestingly, there is a remarkable induction of stress-fibres, which is not dependent on Rho function.
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Lampugnani M.G., Zanetti A., Breviario F., Balconi G., Orsenigo F., Corada M., Spagnuolo R., Betson M., Braga V., Dejana E. VE-Cadherin regulates endothelial actin activating Rac and increasing membrane association of Tiam. Mol Biol Cell. 13:2002;1175-1189. The expression of VE-cadherin in VE-cadherin null cells results in Rac activation, and Rho inhibition. Interestingly, there is a remarkable induction of stress-fibres, which is not dependent on Rho function.
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Lampugnani, M.G.1
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Spagnuolo, R.7
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+-ATPase activity is required for formation of tight junctions, desmosomes, and induction of polarity in epithelial cells
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+ ATPase leads to inhibition of Rho activity, and prevents the formation of desmosomes and tight junctions.
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Rajasekaran, S.A.1
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+-ATPase β-subunit is required for epithelial polarization, suppression of invasion, and cell motility
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Protein kinase C activation upregulates intercellular adhesion of α-catenin-negative human colon cancer variants via induction of desmosomes
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van Hengel J., Gohon L., Bruyneel E., Vermeulen S., Cornelissen M., Mareel M., van Roy F. Protein kinase C activation upregulates intercellular adhesion of α-catenin-negative human colon cancer variants via induction of desmosomes. J Cell Biol. 137:1997;1103-1116.
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Cytoskeletal involvement in the modulation of cell-cell junctions by the protein kinase inhibitor H-7
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Different effects of protein kinase inhibitors on the localization of junctional proteins at cell-cell contact sites
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Atypical protein kinase C is involved in the evolutionarily conserved PAR protein complex and plays a critical role in establishing epithelia-specific junctional structures
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An interesting study, in which the role of atypical protein kinase Cλ during tight-junction assembly and function is investigated using a dominant-negative approach. As no drug treatments were used, this is the first report in which a specific role for atypical protein kinase C was clearly observed.
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Suzuki A., Yamanaka T., Hirose T., Manabe N., Mizuno K., Shimizu M., Akimoto K., Izumi Y., Ohnishi T., Ohno S. Atypical protein kinase C is involved in the evolutionarily conserved PAR protein complex and plays a critical role in establishing epithelia-specific junctional structures. J Cell Biol. 152:2001;1183-1196. An interesting study, in which the role of atypical protein kinase Cλ during tight-junction assembly and function is investigated using a dominant-negative approach. As no drug treatments were used, this is the first report in which a specific role for atypical protein kinase C was clearly observed.
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J Cell Biol
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Suzuki, A.1
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Izumi, Y.8
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Assembly of epithelial tight junctions is negatively regulated by Par6
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The authors present the unexpected result that Par6 activation appears to inhibit tight junction morphology and function.
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Gao L., Joberty G., Macara I.G. Assembly of epithelial tight junctions is negatively regulated by Par6. Curr Biol. 12:2002;221-225. The authors present the unexpected result that Par6 activation appears to inhibit tight junction morphology and function.
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CDC-42 controls early cell polarity and spindle orientation in C. elegans
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