302 Examining the role of nuclear factor kappa-B proteins in human cytokine gene expression: Comparison of type I and type III interferons

Cytokine ◽  
2008 ◽  
Vol 43 (3) ◽  
pp. 315
Author(s):  
FuiGoon Goh ◽  
Scott J.P. Thomson ◽  
Irina A. Udalova
CHEST Journal ◽  
1999 ◽  
Vol 116 ◽  
pp. 73S-74S ◽  
Author(s):  
Timothy S. Blackwell ◽  
F.E. Yull ◽  
C.-L. Chen ◽  
A. Venkatakrishnan ◽  
T.R. Blackwell ◽  
...  

2002 ◽  
Vol 112 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Sachio Takeno ◽  
Katsuhiro Hirakawa ◽  
Tsutomu Ueda ◽  
Kyosuke Furukido ◽  
Rika Osada ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Caitlin E. Murphy ◽  
Adam K. Walker ◽  
Cynthia Shannon Weickert

AbstractNeuroinflammation, particularly in the dorsolateral prefrontal cortex, is well-established in a subset of people with schizophrenia, with significant increases in inflammatory markers including several cytokines. Yet the cause(s) of cortical inflammation in schizophrenia remains unknown. Clues as to potential microenvironmental triggers and/or intracellular deficits in immunoregulation may be gleaned from looking further upstream of effector immune molecules to transcription factors that control inflammatory gene expression. Here, we focus on the ‘master immune regulator’ nuclear factor kappa B (NF-κB) and review evidence in support of NF-κB dysregulation causing or contributing to neuroinflammation in patients. We discuss the utility of ‘immune biotyping’ as a tool to analyse immune-related transcripts and proteins in patient tissue, and the insights into cortical NF-κB in schizophrenia revealed by immune biotyping compared to studies treating patients as a single, homogenous group. Though the ubiquitous nature of NF-κB presents several hurdles for drug development, targeting this key immunoregulator with novel or repurposed therapeutics in schizophrenia is a relatively underexplored area that could aid in reducing symptoms of patients with active neuroinflammation.


2001 ◽  
Vol 28 (6) ◽  
pp. 626-633 ◽  
Author(s):  
James R. Berenson ◽  
Hongjin M. Ma ◽  
Robert Vescio

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1335
Author(s):  
Marina Mostafizar ◽  
Claudia Cortes-Pérez ◽  
Wanda Snow ◽  
Jelena Djordjevic ◽  
Aida Adlimoghaddam ◽  
...  

The transcription factor nuclear factor kappa B (NF-κB) is highly expressed in almost all types of cells. NF-κB is involved in many complex biological processes, in particular in immunity. The activation of the NF-κB signaling pathways is also associated with cancer, diabetes, neurological disorders and even memory. Hence, NF-κB is a central factor for understanding not only fundamental biological presence but also pathogenesis, and has been the subject of intense study in these contexts. Under healthy physiological conditions, the NF-κB pathway promotes synapse growth and synaptic plasticity in neurons, while in glia, NF-κB signaling can promote pro-inflammatory responses to injury. In addition, NF-κB promotes the maintenance and maturation of B cells regulating gene expression in a majority of diverse signaling pathways. Given this, the protein plays a predominant role in activating the mammalian immune system, where NF-κB-regulated gene expression targets processes of inflammation and host defense. Thus, an understanding of the methodological issues around its detection for localization, quantification, and mechanistic insights should have a broad interest across the molecular neuroscience community. In this review, we summarize the available methods for the proper detection and analysis of NF-κB among various brain tissues, cell types, and subcellular compartments, using both qualitative and quantitative methods. We also summarize the flexibility and performance of these experimental methods for the detection of the protein, accurate quantification in different samples, and the experimental challenges in this regard, as well as suggestions to overcome common challenges.


Oral Diseases ◽  
2013 ◽  
Vol 20 (3) ◽  
pp. 294-300 ◽  
Author(s):  
T Arabaci ◽  
O Köse ◽  
A Kizildağ ◽  
M Albayrak ◽  
Y Çiçek ◽  
...  

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