The Regulation of NF-κB Subunits by Phosphorylation

نویسندگان

  • Frank Christian
  • Emma L. Smith
  • Ruaidhrí J. Carmody
چکیده

The NF-κB transcription factor is the master regulator of the inflammatory response and is essential for the homeostasis of the immune system. NF-κB regulates the transcription of genes that control inflammation, immune cell development, cell cycle, proliferation, and cell death. The fundamental role that NF-κB plays in key physiological processes makes it an important factor in determining health and disease. The importance of NF-κB in tissue homeostasis and immunity has frustrated therapeutic approaches aimed at inhibiting NF-κB activation. However, significant research efforts have revealed the crucial contribution of NF-κB phosphorylation to controlling NF-κB directed transactivation. Importantly, NF-κB phosphorylation controls transcription in a gene-specific manner, offering new opportunities to selectively target NF-κB for therapeutic benefit. This review will focus on the phosphorylation of the NF-κB subunits and the impact on NF-κB function.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

VGB3 Induces Apoptosis by Inhibiting Phosphorylation of NF-κB p65 at Serine 536 in the Human Umbilical Vein Endothelial Cells

Background and objectives: Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) inhibition results in an increase in apoptosis. It has been demonstrated that NF-κB subunit p65 phosphorylation at the IκB kinase phosphorylation site serine 536 (Ser536) is essential for the NF-κB nuclear translocation and activation. Therefore, NF-κB can be downregulated by suppressing its phosph...

متن کامل

The effects of adenosine injection after of brain ischemia reperfusion injury on gene expression of NF-kB/p65 and activity level of ROS in male Wistar rats

Background: Unit of p65 is one of the subunits of NF-κB and its phosphorylation by stress oxidative causes activation of NF-κB. The aim of present study was to investigate the effects of adenosine injection after brain ischemia reperfusion injury on gene expression of NF-κB /p65 and Reactive Oxygen Species (ROS) in hippocampus tissue of male wistar rats. Methods: 40 male wistar rats were rando...

متن کامل

The effect of down-regulation of CCL5 on lipopolysaccharide-induced WI-38 fibroblast injury: a potential role for infantile pneumonia

Objective(s): Aberrant expression of CCL5 has been found in several kinds of inflammatory diseases, and the roles of CCL5 in these diseases have also been reported. However, the role of CCL5 in infantile pneumonia is still unclear. Thus, the function and acting mechanism of CCL5 in the in vitro model of infantile pneumonia were researched in this study. Materials and Methods: Human fetal lung f...

متن کامل

Monascin ameliorate inflammation in the lipopolysaccharide-induced BV-2 microglial cells via suppressing the NF-κB/p65 pathway

Objective(s): The pathophysiology of neurodegenerative diseases is complicated, in which inflammatory reactions play a vital role. Microglia cells activation, an essential process of neuroinflammation, can produce neurotoxic molecules and neurotrophic factors, which aggravate inflammation and neuronal injury. Monascin, a major component of red yeast rice, is an azaphil...

متن کامل

Salidroside regulates the expressions of IL-6 and defensins in LPS-activated intestinal epithelial cells through NF-κB/MAPK and STAT3 pathways

Objective(s): To reveal the detailed mechanism underlying the functions of salidroside on the inflammation of intestinal epithelial cells during IBD.Materials and Methods: Quantitative real-time PCR was employed to assess the expression of IL-6, IL-10, and α-defensins 5 and 6. ELISA assay was performed to measure the secretion of IL-6 and IL-10. MTT assay was used to determine the cell viabilit...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 5  شماره 

صفحات  -

تاریخ انتشار 2016