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10.1371/journal.pone.0140378 http://scihub22266oqcxt.onion/10.1371/journal.pone.0140378 C4605505!4605505!26465598     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (10): ä Nephropedia Template TP {{tp|p=26465598|t=2015. A Cilia Independent Role of Ift88/Polaris during Cell Migration |pdf=|usr=}}{{26465598}} gab.com Text A Cilia Independent Role of Ift88/Polaris during Cell Migration JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26465598 #FOAvip Ift88 is a central component of the intraflagellar transport (Ift) complex B, essential for the building of cilia and flagella from single cell organisms to mammals. Loss of Ift88 results in the absence of cilia and causes left-right asymmetry defects, disordered Hedgehog signaling, and polycystic kidney disease, all of which are explained by aberrant ciliary function. In addition, a number of extraciliary functions of Ift88 have been described that affect the cell-cycle, mitosis, and targeting of the T-cell receptor to the immunological synapse. Similarly, another essential ciliary molecule, the kinesin-2 subunit Kif3a, which transports Ift-B in the cilium, affects microtubule (MT) dynamics at the leading edge of migrating cells independently of cilia. We now show that loss of Ift88 impairs cell migration irrespective of cilia. Ift88 is required for the polarization of migrating MDCK cells, and Ift88 depleted cells have fewer MTs at the leading edge. Neither MT dynamics nor MT nucleation are dependent on Ift88. Our findings dissociate the function of Ift88 from Kif3a outside the cilium and suggest a novel extraciliary function for Ift88. Future studies need to address what unifying mechanism underlies the different extraciliary functions of Ift88. Twit Text FOAVip A Cilia Independent Role of Ift88/Polaris during Cell Migration ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26465598 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26465598 #FOAvip English Wikipedia <ref>{{Cite pmid|26465598}}</ref> A Cilia Independent Role of Ift88/Polaris during Cell Migration #MMPMID26465598 Boehlke C; Janusch H; Hamann C; Powelske C; Mergen M; Herbst H; Kotsis F; Nitschke R; Kuehn EW PLoS One 2015[]; 10 (10): ä PMID26465598show ga Ift88 is a central component of the intraflagellar transport (Ift) complex B, essential for the building of cilia and flagella from single cell organisms to mammals. Loss of Ift88 results in the absence of cilia and causes left-right asymmetry defects, disordered Hedgehog signaling, and polycystic kidney disease, all of which are explained by aberrant ciliary function. In addition, a number of extraciliary functions of Ift88 have been described that affect the cell-cycle, mitosis, and targeting of the T-cell receptor to the immunological synapse. Similarly, another essential ciliary molecule, the kinesin-2 subunit Kif3a, which transports Ift-B in the cilium, affects microtubule (MT) dynamics at the leading edge of migrating cells independently of cilia. We now show that loss of Ift88 impairs cell migration irrespective of cilia. Ift88 is required for the polarization of migrating MDCK cells, and Ift88 depleted cells have fewer MTs at the leading edge. Neither MT dynamics nor MT nucleation are dependent on Ift88. Our findings dissociate the function of Ift88 from Kif3a outside the cilium and suggest a novel extraciliary function for Ift88. Future studies need to address what unifying mechanism underlies the different extraciliary functions of Ift88. äA Cilia Independent Role of Ift88/Polaris during Cell Migration (epmc).pdf DeepDyve Pubget Overpricing