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10.1038/cddis.2017.233 http://scihub22266oqcxt.onion/10.1038/cddis.2017.233 C5584573!5584573!28617440     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       Cell+Death+Dis 2017 ; 8 (6): e2883- Nephropedia Template TP {{tp|p=28617440|t=2017. The NF-?B1 is a key regulator of acute but not chronic renal injury |pdf=|usr=}}{{28617440}} gab.com Text The NF- B1 is a key regulator of acute but not chronic renal injury JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28617440 #FOAvip The NF-?B family of transcription factors is important for many cellular functions, in particular initiation and propagation of inflammatory and immune responses. However, recent data has suggested that different subunits of the NF-?B family can suppress the inflammatory response. NF-?B1, from the locus nf?b1, can inhibit transcription, acting as a brake to the recognised pro-inflammatory activity of other NF-?B subunits. We tested the function of NF-?B1 in an acute (nephrotoxic serum (NTS) nephritis) and a chronic (unilateral ureteric obstruction (UUO)) model of renal injury using NF-?B1 (nf?b1?/?) knockout mice. Deficiency in NF-?B1 increased the severity of glomerular injury in NTS-induced nephritis and was associated with greater proteinuria and persistent pro-inflammatory gene expression. Induction of disease in bone marrow chimeric mice demonstrated that the absence of NF-?B1 in either bone marrow or glomerular cells increased the severity of injury. Early after UUO (day 3) there was more severe histological injury in the nf?b1?/? mice but by day 10, disease severity was equivalent in wild type and nf?b1?/? mice. In conclusion, NF-?B1 modifies acute inflammatory renal injury but does not influence chronic fibrotic injury. Twit Text FOAVip The NF- B1 is a key regulator of acute but not chronic renal injury ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28617440 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28617440 #FOAvip English Wikipedia <ref>{{Cite pmid|28617440}}</ref> The NF-?B1 is a key regulator of acute but not chronic renal injury #MMPMID28617440 Fearn A; Situmorang GR; Fox C; Oakley F; Howarth R; Wilson CL; Kiosia A; Robson MG; Mann DA; Moles A; Sheerin NS Cell Death Dis 2017[Jun]; 8 (6): e2883- PMID28617440show ga The NF-?B family of transcription factors is important for many cellular functions, in particular initiation and propagation of inflammatory and immune responses. However, recent data has suggested that different subunits of the NF-?B family can suppress the inflammatory response. NF-?B1, from the locus nf?b1, can inhibit transcription, acting as a brake to the recognised pro-inflammatory activity of other NF-?B subunits. We tested the function of NF-?B1 in an acute (nephrotoxic serum (NTS) nephritis) and a chronic (unilateral ureteric obstruction (UUO)) model of renal injury using NF-?B1 (nf?b1?/?) knockout mice. Deficiency in NF-?B1 increased the severity of glomerular injury in NTS-induced nephritis and was associated with greater proteinuria and persistent pro-inflammatory gene expression. Induction of disease in bone marrow chimeric mice demonstrated that the absence of NF-?B1 in either bone marrow or glomerular cells increased the severity of injury. Early after UUO (day 3) there was more severe histological injury in the nf?b1?/? mice but by day 10, disease severity was equivalent in wild type and nf?b1?/? mice. In conclusion, NF-?B1 modifies acute inflammatory renal injury but does not influence chronic fibrotic injury. äThe NF-?B1 is a key regulator of acute but not chronic renal injury (epmc).pdf DeepDyve Pubget Overpricing