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10.7554/eLife.32893 http://scihub22266oqcxt.onion/10.7554/eLife.32893 C5903866!5903866!29661273     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       eLife 2018 ; 7 (ä): ä Nephropedia Template TP {{tp|p=29661273|t=2018. IRS-1 acts as an endocytic regulator of IGF-I receptor to facilitate sustained IGF signaling |pdf=|usr=}}{{29661273}} gab.com Text IRS-1 acts as an endocytic regulator of IGF-I receptor to facilitate sustained IGF signaling JO: eLife http://www.kidney.de/pget.php?&tw=1&pmid=29661273 #FOAvip Insulin-like growth factor-I receptor (IGF-IR) preferentially regulates the long-term IGF activities including growth and metabolism. Kinetics of ligand-dependent IGF-IR endocytosis determines how IGF induces such downstream signaling outputs. Here, we find that the insulin receptor substrate (IRS)?1 modulates how long ligand-activated IGF-IR remains at the cell surface before undergoing endocytosis in mammalian cells. IRS-1 interacts with the clathrin adaptor complex AP2. IRS-1, but not an AP2-binding-deficient mutant, delays AP2-mediated IGF-IR endocytosis after the ligand stimulation. Mechanistically, IRS-1 inhibits the recruitment of IGF-IR into clathrin-coated structures; for this reason, IGF-IR avoids rapid endocytosis and prolongs its activity on the cell surface. Accelerating IGF-IR endocytosis via IRS-1 depletion induces the shift from sustained to transient Akt activation and augments FoxO-mediated transcription. Our study establishes a new role for IRS-1 as an endocytic regulator of IGF-IR that ensures sustained IGF bioactivity, independent of its classic role as an adaptor in IGF-IR signaling. Twit Text FOAVip IRS-1 acts as an endocytic regulator of IGF-I receptor to facilitate sustained IGF signaling ????eLife http://www.kidney.de/pget.php?&tw=1&pmid=29661273 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29661273 #FOAvip English Wikipedia <ref>{{Cite pmid|29661273}}</ref> IRS-1 acts as an endocytic regulator of IGF-I receptor to facilitate sustained IGF signaling #MMPMID29661273 Yoneyama Y; Lanzerstorfer P; Niwa H; Umehara T; Shibano T; Yokoyama S; Chida K; Weghuber J; Hakuno F; Takahashi SI eLife 2018[]; 7 (ä): ä PMID29661273show ga Insulin-like growth factor-I receptor (IGF-IR) preferentially regulates the long-term IGF activities including growth and metabolism. Kinetics of ligand-dependent IGF-IR endocytosis determines how IGF induces such downstream signaling outputs. Here, we find that the insulin receptor substrate (IRS)?1 modulates how long ligand-activated IGF-IR remains at the cell surface before undergoing endocytosis in mammalian cells. IRS-1 interacts with the clathrin adaptor complex AP2. IRS-1, but not an AP2-binding-deficient mutant, delays AP2-mediated IGF-IR endocytosis after the ligand stimulation. Mechanistically, IRS-1 inhibits the recruitment of IGF-IR into clathrin-coated structures; for this reason, IGF-IR avoids rapid endocytosis and prolongs its activity on the cell surface. Accelerating IGF-IR endocytosis via IRS-1 depletion induces the shift from sustained to transient Akt activation and augments FoxO-mediated transcription. Our study establishes a new role for IRS-1 as an endocytic regulator of IGF-IR that ensures sustained IGF bioactivity, independent of its classic role as an adaptor in IGF-IR signaling. äIRS-1 acts as an endocytic regulator of IGF-I receptor to facilitate s(epmc).pdf DeepDyve Pubget Overpricing