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10.1038/cddis.2017.155 http://scihub22266oqcxt.onion/10.1038/cddis.2017.155 C5603828!5603828!28383550     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (4): e2733- Nephropedia Template TP {{tp|p=28383550|t=2017. C/EBP? LIP augments cell death by inducing osteoglycin |pdf=|usr=}}{{28383550}} gab.com Text C/EBP LIP augments cell death by inducing osteoglycin JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28383550 #FOAvip Many types of tumor cell are devoid of the extracellular matrix proteoglycan osteoglycin (Ogn), but its role in tumor biology is poorly studied. Here we show that RNAi of Ogn attenuates stress-triggered cell death, whereas its overexpression increases cell death. We found that the transcription factor C/EBP? regulates the expression of Ogn. C/EBP? is expressed as a full-length, active form (LAP) and as a truncated, dominant-negative form (LIP), and the LIP/LAP ratio is positively correlated with the extent of cell death under stress. For example, we reported that drug-resistant tumor cells lack LIP altogether, and its supplementation abolished their resistance to chemotherapy and to endoplasmic reticulum (ER) stress. Here we further show that elevated LIP/LAP ratio robustly increased Ogn expression and cell death under stress by modulating the mitogen-activated protein kinase/activator protein 1 pathway (MAPK/AP-1). Our findings suggest that LIP deficiency renders tumor cell resistant to ER stress by preventing the induction of Ogn. Twit Text FOAVip C/EBP LIP augments cell death by inducing osteoglycin ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28383550 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28383550 #FOAvip English Wikipedia <ref>{{Cite pmid|28383550}}</ref> C/EBP? LIP augments cell death by inducing osteoglycin #MMPMID28383550 Wassermann-Dozorets R; Rubinstein M Cell Death Dis 2017[Apr]; 8 (4): e2733- PMID28383550show ga Many types of tumor cell are devoid of the extracellular matrix proteoglycan osteoglycin (Ogn), but its role in tumor biology is poorly studied. Here we show that RNAi of Ogn attenuates stress-triggered cell death, whereas its overexpression increases cell death. We found that the transcription factor C/EBP? regulates the expression of Ogn. C/EBP? is expressed as a full-length, active form (LAP) and as a truncated, dominant-negative form (LIP), and the LIP/LAP ratio is positively correlated with the extent of cell death under stress. For example, we reported that drug-resistant tumor cells lack LIP altogether, and its supplementation abolished their resistance to chemotherapy and to endoplasmic reticulum (ER) stress. Here we further show that elevated LIP/LAP ratio robustly increased Ogn expression and cell death under stress by modulating the mitogen-activated protein kinase/activator protein 1 pathway (MAPK/AP-1). Our findings suggest that LIP deficiency renders tumor cell resistant to ER stress by preventing the induction of Ogn. äC/EBP? LIP augments cell death by inducing osteoglycin (epmc).pdf DeepDyve Pubget Overpricing