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10.1080/15548627.2017.1307487 http://scihub22266oqcxt.onion/10.1080/15548627.2017.1307487 C5486367!5486367!28368693     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Autophagy 2017 ; 13 (6): 1086-7 Nephropedia Template TP {{tp|p=28368693|t=2017. Galectins and TRIMs directly interact and orchestrate autophagic response to endomembrane damage |pdf=|usr=}}{{28368693}} gab.com Text Galectins and TRIMs directly interact and orchestrate autophagic response to endomembrane damage JO: Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=28368693 #FOAvip Macroautophagy/autophagy is a homeostatic process delivering cytoplasmic targets, including damaged organelles, to lysosomes for degradation; however, it is not completely understood how compromised endomembranes are recognized by the autophagic apparatus. We have described previously that the TRIM family of proteins act as receptors for selective autophagy. In this study we uncovered the property of TRIMs to directly interact with members of the family of cytosolic lectins termed galectins. Galectins patrol the cytoplasm and recognize compromised membranes. We show that TRIM16 uses LGALS3 (galectin 3) to detect damaged lysosomes and phagosomes. TRIM16 assembles the core autophagic machinery and is found in protein complexes with MTOR and TFEB, thus regulating their activity to set in motion endomembrane quality control. The TRIM16-LGALS3 system plays a key role in autophagic homeostasis of lysosomes and in the control of Mycobacterium tuberculosis in vivo. Twit Text FOAVip Galectins and TRIMs directly interact and orchestrate autophagic response to endomembrane damage ????Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=28368693 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28368693 #FOAvip English Wikipedia <ref>{{Cite pmid|28368693}}</ref> Galectins and TRIMs directly interact and orchestrate autophagic response to endomembrane damage #MMPMID28368693 Kumar S; Chauhan S; Jain A; Ponpuak M; Choi SW; Mudd M; Peters R; Mandell MA; Johansen T; Deretic V Autophagy 2017[]; 13 (6): 1086-7 PMID28368693show ga Macroautophagy/autophagy is a homeostatic process delivering cytoplasmic targets, including damaged organelles, to lysosomes for degradation; however, it is not completely understood how compromised endomembranes are recognized by the autophagic apparatus. We have described previously that the TRIM family of proteins act as receptors for selective autophagy. In this study we uncovered the property of TRIMs to directly interact with members of the family of cytosolic lectins termed galectins. Galectins patrol the cytoplasm and recognize compromised membranes. We show that TRIM16 uses LGALS3 (galectin 3) to detect damaged lysosomes and phagosomes. TRIM16 assembles the core autophagic machinery and is found in protein complexes with MTOR and TFEB, thus regulating their activity to set in motion endomembrane quality control. The TRIM16-LGALS3 system plays a key role in autophagic homeostasis of lysosomes and in the control of Mycobacterium tuberculosis in vivo. äGalectins and TRIMs directly interact and orchestrate autophagic respo(epmc).pdf DeepDyve Pubget Overpricing