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10.1111/tra.12269 http://scihub22266oqcxt.onion/10.1111/tra.12269 C4440230!4440230!25690058     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Traffic 2015 ; 16 (6): 572-90 Nephropedia Template TP {{tp|p=25690058|t=2015. Microtubule Motors Power Plasma Membrane Tubulation in Clathrin-Independent Endocytosis |pdf=|usr=}}{{25690058}} gab.com Text Microtubule Motors Power Plasma Membrane Tubulation in Clathrin-Independent Endocytosis JO: Traffic http://www.kidney.de/pget.php?&tw=1&pmid=25690058 #FOAvip How the plasma membrane is bent to accommodate clathrin-independent endocytosis remains uncertain. Recent studies suggest Shiga and cholera toxin induce membrane curvature required for their uptake into clathrin-independent carriers by binding and cross-linking multiple copies of their glycosphingolipid receptors on the plasma membrane. But it remains unclear if toxin-induced sphingolipid crosslinking provides sufficient mechanical force for deforming the plasma membrane, or if host cell factors also contribute to this process. To test this, we imaged the uptake of cholera toxin B-subunit into surface-derived tubular invaginations. We found that cholera toxin mutants that bind to only one glycosphingolipid receptor accumulated in tubules, and that toxin binding was entirely dispensable for membrane tubulations to form. Unexpectedly, the driving force for tubule extension was supplied by the combination of microtubules, dynein and dynactin, thus defining a novel mechanism for generating membrane curvature during clathrin-independent endocytosis. Twit Text FOAVip Microtubule Motors Power Plasma Membrane Tubulation in Clathrin-Independent Endocytosis ????Traffic http://www.kidney.de/pget.php?&tw=1&pmid=25690058 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25690058 #FOAvip English Wikipedia <ref>{{Cite pmid|25690058}}</ref> Microtubule Motors Power Plasma Membrane Tubulation in Clathrin-Independent Endocytosis #MMPMID25690058 Day CA; Baetz NW; Copeland CA; Kraft LJ; Han B; Tiwari A; Drake KR; De Luca H; Chinnapen DJF; Davidson MW; Holmes RK; Jobling MG; Schroer TA; Lencer WI; Kenworthy AK Traffic 2015[Jun]; 16 (6): 572-90 PMID25690058show ga How the plasma membrane is bent to accommodate clathrin-independent endocytosis remains uncertain. Recent studies suggest Shiga and cholera toxin induce membrane curvature required for their uptake into clathrin-independent carriers by binding and cross-linking multiple copies of their glycosphingolipid receptors on the plasma membrane. But it remains unclear if toxin-induced sphingolipid crosslinking provides sufficient mechanical force for deforming the plasma membrane, or if host cell factors also contribute to this process. To test this, we imaged the uptake of cholera toxin B-subunit into surface-derived tubular invaginations. We found that cholera toxin mutants that bind to only one glycosphingolipid receptor accumulated in tubules, and that toxin binding was entirely dispensable for membrane tubulations to form. Unexpectedly, the driving force for tubule extension was supplied by the combination of microtubules, dynein and dynactin, thus defining a novel mechanism for generating membrane curvature during clathrin-independent endocytosis. äMicrotubule Motors Power Plasma Membrane Tubulation in Clathrin-Indepe(epmc).pdf DeepDyve Pubget Overpricing