[{"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Roblek, Marko, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research, vol. 17, no. 3, AACR, 2019, pp. 783–93, doi:10.1158/1541-7786.MCR-18-0530.","apa":"Roblek, M., Protsyuk, D., Becker, P. F., Stefanescu, C., Gorzelanny, C., Glaus Garzon, J. F., … Borsig, L. (2019). CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. AACR. https://doi.org/10.1158/1541-7786.MCR-18-0530","ama":"Roblek M, Protsyuk D, Becker PF, et al. CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. 2019;17(3):783-793. doi:10.1158/1541-7786.MCR-18-0530","short":"M. Roblek, D. Protsyuk, P.F. Becker, C. Stefanescu, C. Gorzelanny, J.F. Glaus Garzon, L. Knopfova, M. Heikenwalder, B. Luckow, S.W. Schneider, L. Borsig, Molecular Cancer Research 17 (2019) 783–793.","ieee":"M. Roblek et al., “CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis,” Molecular Cancer Research, vol. 17, no. 3. AACR, pp. 783–793, 2019.","chicago":"Roblek, Marko, Darya Protsyuk, Paul F. Becker, Cristina Stefanescu, Christian Gorzelanny, Jesus F. Glaus Garzon, Lucia Knopfova, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research. AACR, 2019. https://doi.org/10.1158/1541-7786.MCR-18-0530.","ista":"Roblek M, Protsyuk D, Becker PF, Stefanescu C, Gorzelanny C, Glaus Garzon JF, Knopfova L, Heikenwalder M, Luckow B, Schneider SW, Borsig L. 2019. CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. 17(3), 783–793."},"title":"CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis","article_processing_charge":"No","external_id":{"pmid":["30552233"],"isi":["000460099800012"]},"author":[{"first_name":"Marko","id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek","full_name":"Roblek, Marko","orcid":"0000-0001-9588-1389"},{"full_name":"Protsyuk, Darya","last_name":"Protsyuk","first_name":"Darya"},{"full_name":"Becker, Paul F.","last_name":"Becker","first_name":"Paul F."},{"first_name":"Cristina","last_name":"Stefanescu","full_name":"Stefanescu, Cristina"},{"last_name":"Gorzelanny","full_name":"Gorzelanny, Christian","first_name":"Christian"},{"first_name":"Jesus F.","full_name":"Glaus Garzon, Jesus F.","last_name":"Glaus Garzon"},{"first_name":"Lucia","last_name":"Knopfova","full_name":"Knopfova, Lucia"},{"first_name":"Mathias","full_name":"Heikenwalder, Mathias","last_name":"Heikenwalder"},{"first_name":"Bruno","last_name":"Luckow","full_name":"Luckow, Bruno"},{"full_name":"Schneider, Stefan W.","last_name":"Schneider","first_name":"Stefan W."},{"first_name":"Lubor","last_name":"Borsig","full_name":"Borsig, Lubor"}],"publication":"Molecular Cancer Research","day":"01","year":"2019","isi":1,"date_created":"2019-03-31T21:59:12Z","doi":"10.1158/1541-7786.MCR-18-0530","date_published":"2019-03-01T00:00:00Z","page":"783-793","oa":1,"publisher":"AACR","quality_controlled":"1","date_updated":"2023-08-25T08:57:01Z","department":[{"_id":"DaSi"}],"_id":"6190","status":"public","article_type":"original","type":"journal_article","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["15417786"],"eissn":["15573125"]},"volume":17,"issue":"3","pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Increased levels of the chemokine CCL2 in cancer patients are associated with poor prognosis. Experimental evidence suggests that CCL2 correlates with inflammatory monocyte recruitment and induction of vascular activation, but the functionality remains open. Here, we show that endothelial Ccr2 facilitates pulmonary metastasis using an endothelial-specific Ccr2-deficient mouse model (Ccr2ecKO). Similar levels of circulating monocytes and equal leukocyte recruitment to metastatic lesions of Ccr2ecKO and Ccr2fl/fl littermates were observed. The absence of endothelial Ccr2 strongly reduced pulmonary metastasis, while the primary tumor growth was unaffected. Despite a comparable cytokine milieu in Ccr2ecKO and Ccr2fl/fl littermates the absence of vascular permeability induction was observed only in Ccr2ecKO mice. CCL2 stimulation of pulmonary endothelial cells resulted in increased phosphorylation of MLC2, endothelial cell retraction, and vascular leakiness that was blocked by an addition of a CCR2 inhibitor. These data demonstrate that endothelial CCR2 expression is required for tumor cell extravasation and pulmonary metastasis.\r\n\r\nImplications: The findings provide mechanistic insight into how CCL2–CCR2 signaling in endothelial cells promotes their activation through myosin light chain phosphorylation, resulting in endothelial retraction and enhanced tumor cell migration and metastasis."}],"intvolume":" 17","month":"03","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1158/1541-7786.MCR-18-0530"}],"scopus_import":"1"},{"publisher":"eLife Sciences Publications","quality_controlled":"1","oa":1,"has_accepted_license":"1","isi":1,"year":"2019","day":"21","publication":"eLife","doi":"10.7554/eLife.45380","date_published":"2019-03-21T00:00:00Z","date_created":"2019-04-07T21:59:15Z","article_number":"e45380","citation":{"ista":"Barton NH, Hermisson J, Nordborg M. 2019. Why structure matters. eLife. 8, e45380.","chicago":"Barton, Nicholas H, Joachim Hermisson, and Magnus Nordborg. “Why Structure Matters.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.45380.","ama":"Barton NH, Hermisson J, Nordborg M. Why structure matters. eLife. 2019;8. doi:10.7554/eLife.45380","apa":"Barton, N. H., Hermisson, J., & Nordborg, M. (2019). Why structure matters. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.45380","short":"N.H. Barton, J. Hermisson, M. Nordborg, ELife 8 (2019).","ieee":"N. H. Barton, J. Hermisson, and M. Nordborg, “Why structure matters,” eLife, vol. 8. eLife Sciences Publications, 2019.","mla":"Barton, Nicholas H., et al. “Why Structure Matters.” ELife, vol. 8, e45380, eLife Sciences Publications, 2019, doi:10.7554/eLife.45380."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"last_name":"Barton","full_name":"Barton, Nicholas H","orcid":"0000-0002-8548-5240","first_name":"Nicholas H","id":"4880FE40-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Joachim","last_name":"Hermisson","full_name":"Hermisson, Joachim"},{"last_name":"Nordborg","full_name":"Nordborg, Magnus","first_name":"Magnus"}],"external_id":{"isi":["000461988300001"]},"article_processing_charge":"No","title":"Why structure matters","abstract":[{"text":"Great care is needed when interpreting claims about the genetic basis of human variation based on data from genome-wide association studies.","lang":"eng"}],"oa_version":"Published Version","scopus_import":"1","month":"03","intvolume":" 8","publication_identifier":{"eissn":["2050084X"]},"publication_status":"published","file":[{"checksum":"130d7544b57df4a6787e1263c2d7ea43","file_id":"6293","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2019_eLife_Barton.pdf","date_created":"2019-04-11T11:43:38Z","creator":"dernst","file_size":298466,"date_updated":"2020-07-14T12:47:24Z"}],"language":[{"iso":"eng"}],"volume":8,"related_material":{"link":[{"url":"https://ist.ac.at/en/news/body-height-bmi-disease-risk-co/","relation":"press_release","description":"News on IST Homepage"}]},"_id":"6230","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","date_updated":"2023-08-25T08:59:38Z","ddc":["570"],"department":[{"_id":"NiBa"}],"file_date_updated":"2020-07-14T12:47:24Z"},{"publication":"Annals of Probability","day":"01","year":"2019","isi":1,"date_created":"2019-04-07T21:59:15Z","date_published":"2019-03-01T00:00:00Z","doi":"10.1214/18-AOP1272","page":"804-834","oa":1,"quality_controlled":"1","publisher":"Institute of Mathematical Statistics","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Gerencser, Mate. “Boundary Regularity of Stochastic PDEs.” Annals of Probability, vol. 47, no. 2, Institute of Mathematical Statistics, 2019, pp. 804–34, doi:10.1214/18-AOP1272.","ama":"Gerencser M. Boundary regularity of stochastic PDEs. Annals of Probability. 2019;47(2):804-834. doi:10.1214/18-AOP1272","apa":"Gerencser, M. (2019). Boundary regularity of stochastic PDEs. Annals of Probability. Institute of Mathematical Statistics. https://doi.org/10.1214/18-AOP1272","short":"M. Gerencser, Annals of Probability 47 (2019) 804–834.","ieee":"M. Gerencser, “Boundary regularity of stochastic PDEs,” Annals of Probability, vol. 47, no. 2. Institute of Mathematical Statistics, pp. 804–834, 2019.","chicago":"Gerencser, Mate. “Boundary Regularity of Stochastic PDEs.” Annals of Probability. Institute of Mathematical Statistics, 2019. https://doi.org/10.1214/18-AOP1272.","ista":"Gerencser M. 2019. Boundary regularity of stochastic PDEs. Annals of Probability. 47(2), 804–834."},"title":"Boundary regularity of stochastic PDEs","external_id":{"arxiv":["1705.05364"],"isi":["000459681900005"]},"article_processing_charge":"No","author":[{"id":"44ECEDF2-F248-11E8-B48F-1D18A9856A87","first_name":"Mate","last_name":"Gerencser","full_name":"Gerencser, Mate"}],"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["00911798"]},"volume":47,"issue":"2","oa_version":"Preprint","abstract":[{"text":"The boundary behaviour of solutions of stochastic PDEs with Dirichlet boundary conditions can be surprisingly—and in a sense, arbitrarily—bad: as shown by Krylov[ SIAM J. Math. Anal.34(2003) 1167–1182], for any α>0 one can find a simple 1-dimensional constant coefficient linear equation whose solution at the boundary is not α-Hölder continuous.We obtain a positive counterpart of this: under some mild regularity assumptions on the coefficients, solutions of semilinear SPDEs on C1 domains are proved to be α-Hölder continuous up to the boundary with some α>0.","lang":"eng"}],"intvolume":" 47","month":"03","main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1705.05364"}],"scopus_import":"1","date_updated":"2023-08-25T08:59:11Z","department":[{"_id":"JaMa"}],"_id":"6232","status":"public","type":"journal_article"},{"oa_version":"Published Version","pmid":1,"abstract":[{"text":"Gravitropism is an adaptive response that orients plant growth parallel to the gravity vector. Asymmetric\r\ndistribution of the phytohormone auxin is a necessary prerequisite to the tropic bending both in roots and\r\nshoots. During hypocotyl gravitropic response, the PIN3 auxin transporter polarizes within gravity-sensing\r\ncells to redirect intercellular auxin fluxes. First gravity-induced PIN3 polarization to the bottom cell mem-\r\nbranes leads to the auxin accumulation at the lower side of the organ, initiating bending and, later, auxin\r\nfeedback-mediated repolarization restores symmetric auxin distribution to terminate bending. Here, we per-\r\nformed a forward genetic screen to identify regulators of both PIN3 polarization events during gravitropic\r\nresponse. We searched for mutants with defective PIN3 polarizations based on easy-to-score morphological\r\noutputs of decreased or increased gravity-induced hypocotyl bending. We identified the number of\r\nhypocotyl reduced bending (hrb) and hypocotyl hyperbending (hhb) mutants, revealing that reduced bending corre-\r\nlated typically with defective gravity-induced PIN3 relocation whereas all analyzed hhb mutants showed\r\ndefects in the second, auxin-mediated PIN3 relocation. Next-generation sequencing-aided mutation map-\r\nping identified several candidate genes, including SCARECROW and ACTIN2, revealing roles of endodermis\r\nspecification and actin cytoskeleton in the respective gravity- and auxin-induced PIN polarization events.\r\nThe hypocotyl gravitropism screen thus promises to provide novel insights into mechanisms underlying cell\r\npolarity and plant adaptive development.","lang":"eng"}],"intvolume":" 98","month":"06","scopus_import":"1","language":[{"iso":"eng"}],"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","checksum":"ad3b5e270b67ba2a45f894ce3be27920","file_id":"6304","creator":"dernst","file_size":1383100,"date_updated":"2020-07-14T12:47:25Z","file_name":"2019_PlantJournal_Rakusov.pdf","date_created":"2019-04-15T09:38:43Z"}],"publication_status":"published","publication_identifier":{"issn":["0960-7412"],"eissn":["1365-313x"]},"ec_funded":1,"issue":"6","volume":98,"_id":"6262","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","ddc":["580"],"date_updated":"2023-08-25T10:11:03Z","file_date_updated":"2020-07-14T12:47:25Z","department":[{"_id":"JiFr"}],"oa":1,"quality_controlled":"1","publisher":"Wiley","publication":"The Plant Journal","day":"01","year":"2019","isi":1,"has_accepted_license":"1","date_created":"2019-04-09T08:46:44Z","date_published":"2019-06-01T00:00:00Z","doi":"10.1111/tpj.14301","page":"1048-1059","project":[{"_id":"25716A02-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"282300","name":"Polarity and subcellular dynamics in plants"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Rakusová, Hana, Huibin Han, Petr Valošek, and Jiří Friml. “Genetic Screen for Factors Mediating PIN Polarization in Gravistimulated Arabidopsis Thaliana Hypocotyls.” The Plant Journal. Wiley, 2019. https://doi.org/10.1111/tpj.14301.","ista":"Rakusová H, Han H, Valošek P, Friml J. 2019. Genetic screen for factors mediating PIN polarization in gravistimulated Arabidopsis thaliana hypocotyls. The Plant Journal. 98(6), 1048–1059.","mla":"Rakusová, Hana, et al. “Genetic Screen for Factors Mediating PIN Polarization in Gravistimulated Arabidopsis Thaliana Hypocotyls.” The Plant Journal, vol. 98, no. 6, Wiley, 2019, pp. 1048–59, doi:10.1111/tpj.14301.","short":"H. Rakusová, H. Han, P. Valošek, J. Friml, The Plant Journal 98 (2019) 1048–1059.","ieee":"H. Rakusová, H. Han, P. Valošek, and J. Friml, “Genetic screen for factors mediating PIN polarization in gravistimulated Arabidopsis thaliana hypocotyls,” The Plant Journal, vol. 98, no. 6. Wiley, pp. 1048–1059, 2019.","apa":"Rakusová, H., Han, H., Valošek, P., & Friml, J. (2019). Genetic screen for factors mediating PIN polarization in gravistimulated Arabidopsis thaliana hypocotyls. The Plant Journal. Wiley. https://doi.org/10.1111/tpj.14301","ama":"Rakusová H, Han H, Valošek P, Friml J. Genetic screen for factors mediating PIN polarization in gravistimulated Arabidopsis thaliana hypocotyls. The Plant Journal. 2019;98(6):1048-1059. doi:10.1111/tpj.14301"},"title":"Genetic screen for factors mediating PIN polarization in gravistimulated Arabidopsis thaliana hypocotyls","article_processing_charge":"Yes (via OA deal)","external_id":{"isi":["000473644100008"],"pmid":["30821050"]},"author":[{"first_name":"Hana","full_name":"Rakusová, Hana","last_name":"Rakusová"},{"id":"31435098-F248-11E8-B48F-1D18A9856A87","first_name":"Huibin","last_name":"Han","full_name":"Han, Huibin"},{"first_name":"Petr","id":"3CDB6F94-F248-11E8-B48F-1D18A9856A87","last_name":"Valošek","full_name":"Valošek, Petr"},{"full_name":"Friml, Jiří","orcid":"0000-0002-8302-7596","last_name":"Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jiří"}]},{"oa_version":"Submitted Version","abstract":[{"lang":"eng","text":"Cell-cell and cell-glycocalyx interactions under flow are important for the behaviour of circulating cells in blood and lymphatic vessels. However, such interactions are not well understood due in part to a lack of tools to study them in defined environments. Here, we develop a versatile in vitro platform for the study of cell-glycocalyx interactions in well-defined physical and chemical settings under flow. Our approach is demonstrated with the interaction between hyaluronan (HA, a key component of the endothelial glycocalyx) and its cell receptor CD44. We generate HA brushes in situ within a microfluidic device, and demonstrate the tuning of their physical (thickness and softness) and chemical (density of CD44 binding sites) properties using characterisation with reflection interference contrast microscopy (RICM) and application of polymer theory. We highlight the interactions of HA brushes with CD44-displaying beads and cells under flow. Observations of CD44+ beads on a HA brush with RICM enabled the 3-dimensional trajectories to be generated, and revealed interactions in the form of stop and go phases with reduced rolling velocity and reduced distance between the bead and the HA brush, compared to uncoated beads. Combined RICM and bright-field microscopy of CD44+ AKR1 T-lymphocytes revealed complementary information about the dynamics of cell rolling and cell morphology, and highlighted the formation of tethers and slings, as they interacted with a HA brush under flow. This platform can readily incorporate more complex models of the glycocalyx, and should permit the study of how mechanical and biochemical factors are orchestrated to enable highly selective blood cell-vessel wall interactions under flow."}],"month":"05","file":[{"file_name":"2018_MatrixBiology_Davies.pdf","date_created":"2020-05-14T09:02:07Z","file_size":4444339,"date_updated":"2020-07-14T12:47:27Z","creator":"dernst","file_id":"7825","checksum":"790878cd78bfc54a147ddcc7c8f286a0","content_type":"application/pdf","relation":"main_file","access_level":"open_access"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0945-053X"]},"publication_status":"published","volume":"78-79","_id":"6297","status":"public","article_type":"original","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"ddc":["570"],"date_updated":"2023-08-25T10:11:28Z","department":[{"_id":"MaLo"}],"file_date_updated":"2020-07-14T12:47:27Z","publisher":"Elsevier","quality_controlled":"1","oa":1,"day":"01","publication":"Matrix Biology","has_accepted_license":"1","isi":1,"year":"2019","doi":"10.1016/j.matbio.2018.12.002","date_published":"2019-05-01T00:00:00Z","date_created":"2019-04-11T20:55:01Z","page":"47-59","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Davies HS, Baranova NS, El Amri N, Coche-Guérente L, Verdier C, Bureau L, Richter RP, Débarre D. 2019. An integrated assay to probe endothelial glycocalyx-blood cell interactions under flow in mechanically and biochemically well-defined environments. Matrix Biology. 78–79, 47–59.","chicago":"Davies, Heather S., Natalia S. Baranova, Nouha El Amri, Liliane Coche-Guérente, Claude Verdier, Lionel Bureau, Ralf P. Richter, and Delphine Débarre. “An Integrated Assay to Probe Endothelial Glycocalyx-Blood Cell Interactions under Flow in Mechanically and Biochemically Well-Defined Environments.” Matrix Biology. Elsevier, 2019. https://doi.org/10.1016/j.matbio.2018.12.002.","ieee":"H. S. Davies et al., “An integrated assay to probe endothelial glycocalyx-blood cell interactions under flow in mechanically and biochemically well-defined environments,” Matrix Biology, vol. 78–79. Elsevier, pp. 47–59, 2019.","short":"H.S. Davies, N.S. Baranova, N. El Amri, L. Coche-Guérente, C. Verdier, L. Bureau, R.P. Richter, D. Débarre, Matrix Biology 78–79 (2019) 47–59.","apa":"Davies, H. S., Baranova, N. S., El Amri, N., Coche-Guérente, L., Verdier, C., Bureau, L., … Débarre, D. (2019). An integrated assay to probe endothelial glycocalyx-blood cell interactions under flow in mechanically and biochemically well-defined environments. Matrix Biology. Elsevier. https://doi.org/10.1016/j.matbio.2018.12.002","ama":"Davies HS, Baranova NS, El Amri N, et al. An integrated assay to probe endothelial glycocalyx-blood cell interactions under flow in mechanically and biochemically well-defined environments. Matrix Biology. 2019;78-79:47-59. doi:10.1016/j.matbio.2018.12.002","mla":"Davies, Heather S., et al. “An Integrated Assay to Probe Endothelial Glycocalyx-Blood Cell Interactions under Flow in Mechanically and Biochemically Well-Defined Environments.” Matrix Biology, vol. 78–79, Elsevier, 2019, pp. 47–59, doi:10.1016/j.matbio.2018.12.002."},"title":"An integrated assay to probe endothelial glycocalyx-blood cell interactions under flow in mechanically and biochemically well-defined environments","author":[{"first_name":"Heather S.","last_name":"Davies","full_name":"Davies, Heather S."},{"last_name":"Baranova","orcid":"0000-0002-3086-9124","full_name":"Baranova, Natalia S.","first_name":"Natalia S.","id":"38661662-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Nouha","full_name":"El Amri, Nouha","last_name":"El Amri"},{"last_name":"Coche-Guérente","full_name":"Coche-Guérente, Liliane","first_name":"Liliane"},{"first_name":"Claude","last_name":"Verdier","full_name":"Verdier, Claude"},{"full_name":"Bureau, Lionel","last_name":"Bureau","first_name":"Lionel"},{"first_name":"Ralf P.","full_name":"Richter, Ralf P.","last_name":"Richter"},{"first_name":"Delphine","full_name":"Débarre, Delphine","last_name":"Débarre"}],"external_id":{"isi":["000468707600005"]},"article_processing_charge":"No"}]