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10.1091/mbc.E16-08-0564 http://scihub22266oqcxt.onion/10.1091/mbc.E16-08-0564 C5156544!5156544 !27798239     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27798239 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Mol+Biol+Cell 2016 ; 27 (25 ): 4033-4042 Nephropedia Template TP {{tp|p=27798239 |t=2016. Phosphatidylinositol 4-kinase II? negatively regulates invadopodia formation and suppresses an invasive cellular phenotype |pdf=|usr=}}{{27798239 }} gab.com Text Phosphatidylinositol 4-kinase II negatively regulates invadopodia formation and suppresses an invasive cellular phenotype JO: Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27798239 #FOAvip The type II phosphatidylinositol 4-kinase (PI4KII) enzymes synthesize the lipid phosphatidylinositol 4-phosphate (PI(4)P), which has been detected at the Golgi complex and endosomal compartments and recruits clathrin adaptors. Despite common mechanistic similarities between the isoforms, the extent of their redundancy is unclear. We found that depletion of PI4KII? and PI4KII? using small interfering RNA led to actin remodeling. Depletion of PI4KII? also induced the formation of invadopodia containing membrane type I matrix metalloproteinase (MT1-MMP). Depletion of PI4KII isoforms also differentially affected trans-Golgi network (TGN) pools of PI(4)P and post-TGN traffic. PI4KII? depletion caused increased MT1-MMP trafficking to invasive structures at the plasma membrane and was accompanied by reduced colocalization of MT1-MMP with membranes containing the endosomal markers Rab5 and Rab7 but increased localization with the exocytic Rab8. Depletion of PI4KII? was sufficient to confer an aggressive invasive phenotype on minimally invasive HeLa and MCF-7 cell lines. Mining oncogenomic databases revealed that loss of the PI4K2B allele and underexpression of PI4KII? mRNA are associated with human cancers. This finding supports the cell data and suggests that PI4KII? may be a clinically significant suppressor of invasion. We propose that PI4KII? synthesizes a pool of PI(4)P that maintains MT1-MMP traffic in the degradative pathway and suppresses the formation of invadopodia. Twit Text FOAVip Phosphatidylinositol 4-kinase II negatively regulates invadopodia formation and suppresses an invasive cellular phenotype ????Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27798239 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27798239 #FOAvip English Wikipedia <ref>{{Cite pmid|27798239 }}</ref> Phosphatidylinositol 4-kinase II? negatively regulates invadopodia formation and suppresses an invasive cellular phenotype #MMPMID27798239 Alli-Balogun GO ; Gewinner CA ; Jacobs R ; Kriston-Vizi J ; Waugh MG ; Minogue S Mol Biol Cell 2016[Dec]; 27 (25 ): 4033-4042 PMID27798239 show ga The type II phosphatidylinositol 4-kinase (PI4KII) enzymes synthesize the lipid phosphatidylinositol 4-phosphate (PI(4)P), which has been detected at the Golgi complex and endosomal compartments and recruits clathrin adaptors. Despite common mechanistic similarities between the isoforms, the extent of their redundancy is unclear. We found that depletion of PI4KII? and PI4KII? using small interfering RNA led to actin remodeling. Depletion of PI4KII? also induced the formation of invadopodia containing membrane type I matrix metalloproteinase (MT1-MMP). Depletion of PI4KII isoforms also differentially affected trans-Golgi network (TGN) pools of PI(4)P and post-TGN traffic. PI4KII? depletion caused increased MT1-MMP trafficking to invasive structures at the plasma membrane and was accompanied by reduced colocalization of MT1-MMP with membranes containing the endosomal markers Rab5 and Rab7 but increased localization with the exocytic Rab8. Depletion of PI4KII? was sufficient to confer an aggressive invasive phenotype on minimally invasive HeLa and MCF-7 cell lines. Mining oncogenomic databases revealed that loss of the PI4K2B allele and underexpression of PI4KII? mRNA are associated with human cancers. This finding supports the cell data and suggests that PI4KII? may be a clinically significant suppressor of invasion. We propose that PI4KII? synthesizes a pool of PI(4)P that maintains MT1-MMP traffic in the degradative pathway and suppresses the formation of invadopodia. |Cell Line, Tumor [MESH] |Cell Membrane/metabolism [MESH] |Cell Movement/physiology [MESH] |Endosomes/metabolism [MESH] |Extracellular Matrix/metabolism [MESH] |HeLa Cells [MESH] |Humans [MESH] |Isoenzymes [MESH] |MCF-7 Cells [MESH] |Matrix Metalloproteinase 14/metabolism [MESH] |Minor Histocompatibility Antigens/genetics/*metabolism [MESH] |Neoplasms/enzymology/pathology [MESH] |Phosphatidylinositol Phosphates/metabolism [MESH] |Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism [MESH] |Podosomes/*enzymology [MESH] |Protein Transport/physiology [MESH] |RNA, Small Interfering/administration & dosage/genetics [MESH]Phosphatidylinositol 4-kinase II? negatively regulates invadopodia for(epmc).pdf DeepDyve Pubget Overpricing