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10.1016/j.jbc.2021.100723 http://scihub22266oqcxt.onion/10.1016/j.jbc.2021.100723 33932404!8164026!33932404     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       J+Biol+Chem 2021 ; 296 (ä): 100723 Nephropedia Template TP {{tp|p=33932404|t=2021. Intrapulmonary administration of purified NEIL2 abrogates NF-kappaB-mediated inflammation |pdf=|usr=}}{{33932404}} gab.com Text Intrapulmonary administration of purified NEIL2 abrogates NF-kappaB-mediated inflammation JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=33932404 #FOAvip Aberrant or constitutive activation of nuclear factor kappa B (NF-kappaB) contributes to various human inflammatory diseases and malignancies via the upregulation of genes involved in cell proliferation, survival, angiogenesis, inflammation, and metastasis. Thus, inhibition of NF-kappaB signaling has potential for therapeutic applications in cancer and inflammatory diseases. We reported previously that Nei-like DNA glycosylase 2 (NEIL2), a mammalian DNA glycosylase, is involved in the preferential repair of oxidized DNA bases from the transcriptionally active sequences via the transcription-coupled base excision repair pathway. We have further shown that Neil2-null mice are highly sensitive to tumor necrosis factor alpha (TNFalpha)- and lipopolysaccharide-induced inflammation. Both TNFalpha and lipopolysaccharide are potent activators of NF-kappaB. However, the underlying mechanism of NEIL2's role in the NF-kappaB-mediated inflammation remains elusive. Here, we have documented a noncanonical function of NEIL2 and demonstrated that the expression of genes, such as Cxcl1, Cxcl2, Cxcl10, Il6, and Tnfalpha, involved in inflammation and immune cell migration was significantly higher in both mock- and TNFalpha-treated Neil2-null mice compared with that in the WT mice. NEIL2 blocks NF-kappaB's binding to target gene promoters by directly interacting with the Rel homology region of RelA and represses proinflammatory gene expression as determined by co-immunoprecipitation, chromatin immunoprecipitation, and electrophoretic mobility-shift assays. Remarkably, intrapulmonary administration of purified NEIL2 via a noninvasive nasal route significantly abrogated binding of NF-kappaB to cognate DNA, leading to decreased expression of proinflammatory genes and neutrophil recruitment in Neil2-null as well as WT mouse lungs. Our findings thus highlight the potential of NEIL2 as a biologic for inflammation-associated human diseases. Twit Text FOAVip Intrapulmonary administration of purified NEIL2 abrogates NF-kappaB-mediated inflammation ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=33932404 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33932404 #FOAvip English Wikipedia <ref>{{Cite pmid|33932404}}</ref> Intrapulmonary administration of purified NEIL2 abrogates NF-kappaB-mediated inflammation #MMPMID33932404 Tapryal N; Shahabi S; Chakraborty A; Hosoki K; Wakamiya M; Sarkar G; Sharma G; Cardenas VJ; Boldogh I; Sur S; Ghosh G; Hazra TK J Biol Chem 2021[Jan]; 296 (ä): 100723 PMID33932404show ga Aberrant or constitutive activation of nuclear factor kappa B (NF-kappaB) contributes to various human inflammatory diseases and malignancies via the upregulation of genes involved in cell proliferation, survival, angiogenesis, inflammation, and metastasis. Thus, inhibition of NF-kappaB signaling has potential for therapeutic applications in cancer and inflammatory diseases. We reported previously that Nei-like DNA glycosylase 2 (NEIL2), a mammalian DNA glycosylase, is involved in the preferential repair of oxidized DNA bases from the transcriptionally active sequences via the transcription-coupled base excision repair pathway. We have further shown that Neil2-null mice are highly sensitive to tumor necrosis factor alpha (TNFalpha)- and lipopolysaccharide-induced inflammation. Both TNFalpha and lipopolysaccharide are potent activators of NF-kappaB. However, the underlying mechanism of NEIL2's role in the NF-kappaB-mediated inflammation remains elusive. Here, we have documented a noncanonical function of NEIL2 and demonstrated that the expression of genes, such as Cxcl1, Cxcl2, Cxcl10, Il6, and Tnfalpha, involved in inflammation and immune cell migration was significantly higher in both mock- and TNFalpha-treated Neil2-null mice compared with that in the WT mice. NEIL2 blocks NF-kappaB's binding to target gene promoters by directly interacting with the Rel homology region of RelA and represses proinflammatory gene expression as determined by co-immunoprecipitation, chromatin immunoprecipitation, and electrophoretic mobility-shift assays. Remarkably, intrapulmonary administration of purified NEIL2 via a noninvasive nasal route significantly abrogated binding of NF-kappaB to cognate DNA, leading to decreased expression of proinflammatory genes and neutrophil recruitment in Neil2-null as well as WT mouse lungs. Our findings thus highlight the potential of NEIL2 as a biologic for inflammation-associated human diseases. |Animals[MESH] |Cell Movement[MESH] |DNA Glycosylases/*metabolism[MESH] |Gene Expression Regulation[MESH] |Inflammation/metabolism[MESH] |Lung/*metabolism/pathology[MESH] |Mice[MESH] |NF-kappa B/*metabolism[MESH]Intrapulmonary administration of purified NEIL2 abrogates NF-kappaB-me(epmc).pdf DeepDyve Pubget Overpricing