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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
Furthermore, isolated lymphocytes from type 1 diabetic patients displayed an extremely distinct profile of H3K9me2, with certain genomic regions that had increased H3K9me2 levels (SLC17A4, CXCL3, and CTLA-4) and others that had reduced levels (TNF, RARA, and CAMK4) [61]. Thus, HMNT-mediated H3K9me2-associated T cell response regulation might be related to the functional status of T cells and inflammatory disease development, including diabetes. Recently, G9a-based cell lineage-dependent specific deletion has been introduced to delineate G9a’s role in immune system cells. Three different mice strains have been generated with “floxed” G9afl/fl mice [15,62,63]. Despite that, the crossing of G9afl/fl mice with strain Cd4-Cre mice leads to the T-cell-dependent specific G9a deletion in G9aΔT mice. In addition, G9aΔT mice usually are born and develop with no observable discernable defects found in T-cell generation in lymph nodes, spleen, and thymus, suggesting that dissimilar to ES cells and HMNT inhibitors, G9a is replaceable for the proliferation of peripheral cellular naïve lymphocytes [15,64]. For in vivo/in vitro activation of T cells, G9a displayed a critically specific role in the functional regulation of T-helper cells. Despite that, consistent with G9a’s ability to strongly promote and repress gene expression, G9a-deficient lymphocytes failed to generate various cytokines, while various others overproduced [14,15]. Due to distinct differentiating conditions, G9a was needed differentially either to activate or to repress particular programs of the gene.
Anti-Inflammatory Properties of Bioactive Compounds from Medicinal Plants
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
Muhammad Imran, Abdur Rauf, Anees Ahmed Khalil, Saud Bawazeer, Seema Patel, Zafar Ali Shah
Crocin (@ 25, 50, and 100 mg/kg) and safranal (@ 0.5, 1, and 2 mg/kg) curbed edema, reduced the concentration of neutrophils, and suppressed inflammatory pain responses [25]. Treatment of crocin suppressed expression of iNOS and production of NO due to down-regulation of NF-kB activity. Crocin inducted phosphorylation of CAMK-4 (Ca2+/calmodulin-dependent protein kinase 4) and intracellular transfer of Ca2+. Further, crocin mediated suppression of iNOS expression was also retarded due to inhibition of CAMK4 [13].
Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Structural changes in dendrites and synapses require synthesis of new proteins, which implies that second messengers and some of their targets are involved in activating transcription factors, that is, proteins that control the transcription of genetic information from DNA to messenger RNA. One such ubiquitous transcription factor is the cAMP response element-binding protein (CREB) that is activated through phosphorylation by PKA, CaMKIV, a relative of CaMKII (Section 6.3.1), and other kinases that translocate to the nucleus. Dendrites have the metabolic machinery for local protein synthesis, as required for fast changes in structure and function.
Ca2+/calmodulin-dependent protein kinase IV attenuates inflammation and mitochondrial dysfunction under insulin resistance in C2C12 cells
Published in Archives of Physiology and Biochemistry, 2023
Ca2+/calmodulin-dependent protein kinase IV (CaMKIV), also known as CaMK4, was a major regulator of mitochondrial biogenesis. Skeletal muscle from CaMKIV* mice showed augmented mitochondrial DNA replication and mitochondrial biogenesis, and reduced susceptibility to fatigue during repetitive contractions (Wu et al.2002). Another study also suggests CaMKIV involved in GLUT4 (glucose transporter type 4) expression in skeletal muscle cells. CaMKIV in C2C12 myotubes increased Glut4-bound MEF2A by 70% (Smith et al.2007). Jensen et al. (2009) demonstrated CaMKIV upregulates the amount of GLUT4 mRNA by 30% in the control muscle of transgenic mice (CaMKIV-TG Cont) compared with the control muscle of wild-type mice. Of interesting, activation of MEF2A may increase the expression of GLUT4 and enhance insulin-stimulated muscle glucose uptake in CaMKIV* mice, suggesting CaMKIV as an essential regulator in glucose metabolism (Summermatter et al.2013). Moreover, muscle-specific activation of CaMKIV improves insulin-stimulated muscle glucose uptake, with increasing GLUT4 content and improvements in insulin signalling (Lee et al.2014).
New insights into the metabolism of Th17 cells
Published in Immunological Medicine, 2023
Pyruvate kinase muscle isozyme 2 (PKM2) is an enzyme that is involved in the final step of glycolysis (Figure 1). PKM2 is also a requisite for Th1 and Th17 cell differentiation. The pharmacologic inhibition of PKM2 by Shikonin or its silencing reduces Th1 and Th17 cell differentiation and ameliorates disease activity in EAE [49]. TEPP-46 has been shown to induce PKM2 tetramerization, block PKM2 nuclear translocation and inhibit Th1 and Th17 polarization as well as EAE development [50]. PKM2 translocates into the nucleus and interacts with STAT3, leading to its activation and subsequent increase in Th17 cell differentiation [51]. Interestingly PKM2 binds calcium/calmodulin-dependent protein kinase IV (CaMK4), a serine/threonine kinase [49] (Figure 1). CaMK4 is overexpressed in lupus T cells, and inhibition of CaMK4 by KN-93 ameliorates disease activity in MRL/lpr, lupus-prone mice and EAE mice [52,53]. CaMK4 enhances pyruvate kinase activity and glycolysis [49]. GLUT1 expression is increased in T cells from the patients with SLE compared to healthy controls [54]. The CaMK4 inhibitors reduce the GLUT1 expression of lupus T cells [54]. Thus, CaMK4 enhances glycolysis via the glucose transporter and PKM2.
The role of IL-17 in systemic lupus erythematosus and its potential as a therapeutic target
Published in Expert Review of Clinical Immunology, 2019
Tomohiro Koga, Kunihiro Ichinose, Atsushi Kawakami, George C. Tsokos
Compared to CaMK2 that induces NF-κB-related signals [99], CaMK4 is a multifunctional serine/threonine kinase that regulates gene expression by activating various transcription factors, including CREB (cAMP response-element binding protein) and CREM [100]. It has been suggested that the activation of CaMK4 facilitates the transcription of inflammatory cytokines and aberrant cell proliferation or migration in a wide range of immune cells [22]; therefore, the inhibition of CaMK4 may serve as a new therapeutic target for autoimmune/inflammatory diseases.