Matches in SemOpenAlex for { <https://semopenalex.org/work/W2110940443> ?p ?o ?g. }
- W2110940443 endingPage "240" @default.
- W2110940443 startingPage "219" @default.
- W2110940443 abstract "Since NF-<TEX>${kappa}B$</TEX> has been identified as a transcription factor associated with immune cell activation, groups of researchers have dedicated to reveal detailed mechanisms of nuclear factor of <TEX>${kappa}B$</TEX> (NF-<TEX>${kappa}B$</TEX>) in inflammatory signaling for decades. The various molecular components of NF-<TEX>${kappa}B$</TEX> transcription factor pathway have been being evaluated as important therapeutic targets due to their roles in diverse human diseases including inflammation, cystic fibrosis, sepsis, rheumatoid arthritis, cancer, atherosclerosis, ischemic injury, myocardial infarction, osteoporosis, transplantation rejection, and neurodegeneration. With regards to new drugs directly or indirectly modulating the NF-<TEX>${kappa}B$</TEX> pathway, FDA recently approved a proteasome inhibitor bortezomib for the treatment of multiple myeloma. Many pharmaceutical companies have been trying to develop new drugs to inhibit various kinases in the NF-<TEX>${kappa}B$</TEX> signaling pathway for many therapeutic applications. However, a gene knock-out study for <TEX>$IKK{beta}$</TEX> in the NF-<TEX>${kappa}B$</TEX> pathway has given rise to controversies associated with efficacy as therapeutics. Mice lacking hepatocyte <TEX>$IKK{beta}$</TEX> accelerated cancer instead of preventing progress of cancer. However, it is clear that pharmacological inhibition of <TEX>$IKK{beta}$</TEX> appears to be beneficial to reduce HCC. This article will update issues of the NF-<TEX>${kappa}B$</TEX> pathway and inhibitors regulating this pathway." @default.
- W2110940443 created "2016-06-24" @default.
- W2110940443 creator A5051751690 @default.
- W2110940443 creator A5074403516 @default.
- W2110940443 date "2009-07-31" @default.
- W2110940443 modified "2023-10-15" @default.
- W2110940443 title "NF-κB and Therapeutic Approach" @default.
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