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10.1172/JCI87105 http://scihub22266oqcxt.onion/10.1172/JCI87105 C5127665!5127665!27797340     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 126 (12): 4537-53 Nephropedia Template TP {{tp|p=27797340|t=ä. Sorting protein VPS33B regulates exosomal autocrine signaling to mediate hematopoiesis and leukemogenesis |pdf=|usr=}}{{27797340}} gab.com Text Sorting protein VPS33B regulates exosomal autocrine signaling to mediate hematopoiesis and leukemogenesis JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27797340 #FOAvip Certain secretory proteins are known to be critical for maintaining the stemness of stem cells through autocrine signaling. However, the processes underlying the biogenesis, maturation, and secretion of these proteins remain largely unknown. Here we demonstrate that many secretory proteins produced by hematopoietic stem cells (HSCs) undergo exosomal maturation and release that is controlled by vacuolar protein sorting protein 33b (VPS33B). Deletion of VPS33B in either mouse or human HSCs resulted in impaired exosome maturation and secretion as well as loss of stemness. Additionally, VPS33B deficiency led to a dramatic delay in leukemogenesis. Exosomes purified from either conditioned medium or human plasma could partially rescue the defects of HSCs and leukemia-initiating cells (LICs). VPS33B co-existed in exosomes with GDI2, VPS16B, FLOT1, and other known exosome markers. Mechanistically, VPS33B interacted with the GDI2/RAB11A/RAB27A pathway to regulate the trafficking of secretory proteins as exosomes. These findings reveal an essential role for VPS33B in exosome pathways in HSCs and LICs. Moreover, they shed light on the understanding of vesicle trafficking in other stem cells and on the development of improved strategies for cancer treatment. Twit Text FOAVip Sorting protein VPS33B regulates exosomal autocrine signaling to mediate hematopoiesis and leukemogenesis ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27797340 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27797340 #FOAvip English Wikipedia <ref>{{Cite pmid|27797340}}</ref> Sorting protein VPS33B regulates exosomal autocrine signaling to mediate hematopoiesis and leukemogenesis #MMPMID27797340 Gu H; Chen C; Hao X; Wang C; Zhang X; Li Z; Shao H; Zeng H; Yu Z; Xie L; Xia F; Zhang F; Liu X; Zhang Y; Jiang H; Zhu J; Wan J; Wang C; Weng W; Xie J; Tao M; Zhang CC; Liu J; Chen GQ; Zheng J J Clin Invest ä[]; 126 (12): 4537-53 PMID27797340show ga Certain secretory proteins are known to be critical for maintaining the stemness of stem cells through autocrine signaling. However, the processes underlying the biogenesis, maturation, and secretion of these proteins remain largely unknown. Here we demonstrate that many secretory proteins produced by hematopoietic stem cells (HSCs) undergo exosomal maturation and release that is controlled by vacuolar protein sorting protein 33b (VPS33B). Deletion of VPS33B in either mouse or human HSCs resulted in impaired exosome maturation and secretion as well as loss of stemness. Additionally, VPS33B deficiency led to a dramatic delay in leukemogenesis. Exosomes purified from either conditioned medium or human plasma could partially rescue the defects of HSCs and leukemia-initiating cells (LICs). VPS33B co-existed in exosomes with GDI2, VPS16B, FLOT1, and other known exosome markers. Mechanistically, VPS33B interacted with the GDI2/RAB11A/RAB27A pathway to regulate the trafficking of secretory proteins as exosomes. These findings reveal an essential role for VPS33B in exosome pathways in HSCs and LICs. Moreover, they shed light on the understanding of vesicle trafficking in other stem cells and on the development of improved strategies for cancer treatment. äSorting protein VPS33B regulates exosomal autocrine signaling to media(epmc).pdf DeepDyve Pubget Overpricing