China
Africa
Explore chapters and articles related to this topic
Role of Histone Methyltransferase in Breast Cancer
Published in Meenu Gupta, Rachna Jain, Arun Solanki, Fadi Al-Turjman, Cancer Prediction for Industrial IoT 4.0: A Machine Learning Perspective, 2021
Surekha Manhas, Zaved Ahmed Khan
In non-specific innate mechanisms, the immune cells, including macrophages. However, G9a-based H3K9me2 has mostly been correlated with repressive action of the gene during intolerance of endotoxin mechanism [56–58]. Macrophages that are stimulated chronically with lipopolysaccharide presence become unresponsive when again stimulated through the H3K9me2 acquisition at the region of repressed genetic-based loci [58]. Moreover, in the condition of tolerized macrophages, enzyme G9a shows its interaction with TF ATF7 as well as various other NF-κB family members, including NF-κB1, RelA, RelB, and c-Rel [56–58]. Furthermore, it is suggested that these mentioned factors carry out G9a recruitment to specific genetic loci to deposit histone residue, H3K9me2, resulting in gene repression. During the period of endotoxin tolerance, the direct G9a role in macrophages tolerance is not tested properly.
Terpenoids in Treatment of Immunological Disease
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Avik Sarkar, Surajit Bhattacharjee
Generation of inflammatory responses in the host is dependent on both innate and adaptive immune responses. Various cells like dendritic cells, macrophages, natural killer cells and mast cells are involved in the innate immune response against inflammatory disorders, whereas, more specialized cells like B lymphocytes and T lymphocytes are responsible for the adaptive immune responses. Inflammatory responses are regulated by numerous mediators that are usually divided into two main classes as pro-inflammatory and anti-inflammatory. Host molecules like eicosanoids, cytokines and chemokines are the principal inflammatory mediators involved in the pathogenesis associated with inflammation (Turner et al., 2014). Tumour necrosis factor-alpha (TNF-α), interferon (IFN)-γ, interleukin-12 (IL-12) and IL-1α are important cytokines which exert pro-inflammatory response in multiple immune diseases. IL-1α has also been reported to exhibit anti-inflammatory activity (Schuerwegh et al., 2003). Other important cytokines include IL-6, IL-8, IL-23, IL-27 and IL-35, which are known for their inflammatory responses against various pathological conditions (Arican et al., 2005; Bobryshev et al., 2015; Casella et al., 2017). IL-10, however, is an anti-inflammatory cytokine which interferes with the functionalities of pro-inflammatory cytokines and helps maintain homeostasis (Couper et al., 2010). Amongst the eicosanoids, prostaglandin E2 (PGE2) is reported to be associated with pathological conditions resulted from heightened inflammatory responses. Phospholipase A2 (PLA2) and the cyclooxygenases (COX) are the principal enzymes involved in the formation of prostaglandins from arachidonic acid. Therefore, any abnormalities in these two groups of enzymes result in inflammatory diseases. Leukotrienes (LTs) are another group of eicosanoids involved in the inflammatory response and linked to diseases like asthma and other autoimmune disorders (O’Byrne 1997; Simopoulos 2002). Enzymes like 5-lipooxygenase (5-LOX) play a determinant role in the synthesis of LTs and are associated with the inflammatory response (Wisastra and Dekker 2014). Another enzyme that is highly associated with inflammatory conditions is nitric oxide synthase (NOS), which catalyses nitric oxide (NO) synthesis from the oxidation of the amino acid l-arginine. Like COX-2, inducible NOS (iNOS) has been reported to be one of the most crucial pro-inflammatory NOS isoforms (Soufli et al., 2016). Nuclear factor-kappa B (NF-κB) is one of the major transcription factors and is associated with regulating expression of signalling molecules that are responsible for immune and inflammatory responses (Lawrence 2009). Activation of this molecule takes place by nuclear transportation of its cytoplasmic complex, causing transcription of pro-inflammatory genes. In mammals, the NF-κB machinery comprise several members (NF-κB1 [p50/p105], NF-κB2 [p52/p100], p65 [RelA], RelB and c-Rel) which act as transactivation domains necessary for gene regulation in physiological and pathological processes associated with inflammation (Oeckinghaus and Ghosh 2009).
The ROS/NF-κB/HK2 axis is involved in the arsenic-induced Warburg effect in human L-02 hepatocytes
Published in International Journal of Environmental Health Research, 2022
Fanshuo Yin, Ying Zhang, Xin Zhang, Meichen Zhang, Zaihong Zhang, Yunyi Yin, Haili Xu, Yanmei Yang, Yanhui Gao
It is known that arsenic at low concentrations contributes to cell proliferation and malignant transformation by activating certain signal pathways that are reported to be involved in regulating the Warburg effect (Presek et al. 1988; Medda et al. 2021). The nuclear factor kappa B (NF-κB) signaling pathway is one of these pathways (Xiong et al. 2020; Quiroga et al. 2021). This pathway, the most common dysfunctional signal pathway in human cancers, also plays a regulatory role in the Warburg effect by regulating the transcription of metabolic-related genes, such as hexokinase 2 (HK2) (Kooshki et al. 2021). NF-κB is a dimeric complex composed of five subunits, namely RelA (p65), RelB, c-Rel, NF-κB1 (p105/p50), and NF-κB2. The p65 subunit, as the main functional subunit, is involved in the function of the nuclear transcription factor (Hayden and Ghosh 2004, 2008). There is evidence that arsenic at low concentrations activates the NF-κB signaling pathway (Renu et al. 2020; Tang et al. 2021) and upregulates the HK2 protein, a key enzyme of glycolysis. It can therefore be hypothesized that the NF-κB signaling pathway may participate in the arsenic-induced Warburg effect by regulating the expression of HK2.