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Our data indicates that VHL changes the behavior of MTs dependent on their subcellular localization implying a role for VHL in cellular processes such as migration, polarization, and cell cell interactions.
APC localisation to the plus ends of growing microtubules is well established [33], [42] and is linked to its role in cell migration, polarization and microtubule stability [23].
Microtubules have long been a target for cancer therapy given their critical and diverse cellular functions in intracellular transport and metabolism, as well as cell shape, signaling, migration, polarization and division [ 1].
The LINC complex plays roles in many cellular processes, and is involved not only in controlling nuclear size, shape, and structure, but also in cell migration, polarization, and differentiation 5. Abnormalities of LINC complex and nuclear lamina proteins are associated with many human diseases.
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Building the complex architecture of tubular organs is a highly dynamic process that involves cell migration, polarization, shape changes, adhesion to neighboring cells and the extracellular matrix, physicochemical characteristics of the extracellular matrix and reciprocal signaling with the mesenchyme.
Neuron migration can also be described by the distinct yet integrated steps of classic cell migration models: polarization and protrusion, attachment at the cell front, forward movement of the cell body, and detachment with retraction at the cell rear [13], [14], [15], [16].
We conclude that onco-Dbl has a potentially important, previously unreported, capacity to dramatically alter epithelial cell migration, replication, polarization and differentiation and to induce vascularization of an epithelial tissue.
The ras-related Rho GTPases are known to play pivotal roles in a broad range of cytoskeletal activities that are required for cell migration, cell polarization and cytoskeletal rearrangements [8], [9], [10].
Osteoclast migration, adhesion, polarization, and resorption are very much coupled processes.
Thymocytes express multiple Rac1/2 GEFs [ 77], in which the deletion of Dock2 resulting in similar defects in migration, actin polarization, and Rac GTPase activation seen in the Rac1/Rac2-deficient thymocytes [ 78].
DOI: http://dx.doi.org/10.7554/eLife.05279.019 10.7554/eLiFigure79.020 Figure 4 figure supplement 2. PGCs extend filopodia in the direction of migration prior to polarization and actual onset of migration.
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