<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Roncato F</submitter><funding>German-Israeli Foundation for Scientific Research and Development</funding><pagination>166-179</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8218694</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>Microtubules (MTs) control cell shape and intracellular cargo transport. The role of MT turnover in the migration of slow-moving cells through endothelial barriers remains unclear. To irreversibly interfere with MT disassembly, we have used the MT-stabilizing agent zampanolide (ZMP) in Β16F10 melanoma as amodel of slow-moving cells. ZMP-treated B16 cells failed to follow chemotactic gradients across rigid confinements and could not generate stable sub-endothelial pseudopodia under endothelial monolayers. In vivo, ZMP-treated Β16 cells failed to extravasate though lung capillaries. In contrast to melanoma cells, the chemotaxis and transendothelial migration of ZMP-treated Tcells were largely conserved. This is afirst demonstration that MT disassembly is akey checkpoint in the directional mi</pubmed_abstract><journal>Cell adhesion &amp; migration</journal><pubmed_title>Microtubule destabilization is a critical checkpoint of chemotaxis and transendothelial migration in melanoma cells but not in T cells.</pubmed_title><pmcid>PMC8218694</pmcid><funding_grant_id>[I-1470-412.13/2018]</funding_grant_id><pubmed_authors>Yadav SK</pubmed_authors><pubmed_authors>Regev O</pubmed_authors><pubmed_authors>Roncato F</pubmed_authors><pubmed_authors>Alon R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Microtubule destabilization is a critical checkpoint of chemotaxis and transendothelial migration in melanoma cells but not in T cells.</name><description>Microtubules (MTs) control cell shape and intracellular cargo transport. The role of MT turnover in the migration of slow-moving cells through endothelial barriers remains unclear. To irreversibly interfere with MT disassembly, we have used the MT-stabilizing agent zampanolide (ZMP) in Β16F10 melanoma as amodel of slow-moving cells. ZMP-treated B16 cells failed to follow chemotactic gradients across rigid confinements and could not generate stable sub-endothelial pseudopodia under endothelial monolayers. In vivo, ZMP-treated Β16 cells failed to extravasate though lung capillaries. In contrast to melanoma cells, the chemotaxis and transendothelial migration of ZMP-treated Tcells were largely conserved. This is afirst demonstration that MT disassembly is akey checkpoint in the directional mi</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2025-04-04T10:53:24.992Z</modification><creation>2022-02-10T17:01:05.336Z</creation></dates><accession>S-EPMC8218694</accession><cross_references><pubmed>34152257</pubmed><doi>10.1080/19336918.2021.1934958</doi></cross_references></HashMap>