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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
Further, this specific distribution leads to set2 association with plo11 component, elongating Ser2-dependent phosphorylated CTD, basically which is highly predominant over 30 ends and bodies of functional genes [56–58]. Similarly, H3K36me3 residue has also interlinked with the regulation of specific histone protein residue acetylation. Histone residue, H3K36me3, is able to recruit HDACs from active transcription regions. In yeast, H3K36me2/3 recognition by means of EAF3 complex containing bromodomain recruits the HDAC+RPD3S complex that deacetylates histones. In addition, it also prevents spurious initiation of transcription within bodies of active genes [59–61]. At the specific region of gene promoters, histone hyperacetylation and H3K4me3 might play a particular role in the regulation of transcriptional initiation from regions of transcriptional stating sites, whereby the H3K36me2/3-mediated process related with deacetylation is needed in the wake of specific active gene transcriptional machinery to prevent transcriptional initiation from inappropriate aberrant regions present within gene structure. Mutual exclusivity between the H3K36me3 and H3K4me3 may be crucial to maintain transcriptional integrity.
ChIP-seq analysis
Published in Altuna Akalin, Computational Genomics with R, 2020
We will now use normR to call peaks for the H3K36me3 histone modification, which is associated with gene bodies of expressed genes. We define the ChIP and Input files:
Aging Epigenetics
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Vasily V. Ashapkin, Lyudmila I. Kutueva, Boris F. Vanyushin
H3K36me3 is widely known to be enriched on the gene body regions of actively transcribed genes [52]. Interestingly, no large changes in genome-wide levels and distributions of H3K36me3 were found during C. elegans aging [53] confirming previous observations [48]. A still more intriguing finding was that the H3K36me3 levels do not strictly correlate with expression levels of respective genes. An inverse correlation between H3K36me3 levels and mRNA expression changes during aging was observed. Genes with a dramatic expression difference between young (D2) and old (D12) worms were marked with minimal levels of H3K36me3 in their gene bodies, irrespective of their corresponding mRNA abundance. A similar correlation was observed in D. melanogaster, suggesting a conserved mechanism for H3K36me3 in suppressing age-dependent mRNA expression variability. A global reduction in H3K36me3 levels via inactivation of the respective methyltransferase gene met-1 caused an increase in mRNA expression variability with age and shortened the life span. Thus, H3K36me3 functions to restrain gene expression variability during aging and positively affects longevity.
Ranunculus ternatus Thunb extract attenuates renal fibrosis of diabetic nephropathy via inhibiting SMYD2
Published in Pharmaceutical Biology, 2022
Weiwei Xu, Rui Peng, Siyu Chen, Congcong Wu, Xiaoxiao Wang, Ting Yu, Jiuying Jian, Ni Zhang, Siyang Zuo, Min Chen, Bing Guo, Lirong Liu
Studies have shown that SMYD2 was first identified as an H3K36-specific methyltransferase (H3K36me3) (Singh 2019). However, further studies have confirmed that SMYD2 can methylate H3K4 (H3K4ME3) or even non-histone (Abu-Farha et al. 2008; Yi et al. 2019), such as p53, STAT3 and NF-κB. NF-κB acts as a transcription factor that can be activated to induce the expression of chemokines and pro-inflammatory cytokines, leading to the recruitment and activation of immune cells. Activated immune cells in turn produce more pro-inflammatory cytokines/chemokines and growth factors, such as IL-1, IL-6, and TNF-α, which is closely related to the occurrence of DN development is closely related (Navarro-Gonzalez et al. 2011). In addition, TNF-α can also be further activated NF-κB by autocrine and/or paracrine. NF-κB plays an important role in the occurrence and development of DN by regulating the transcription of a variety of cytokines, promoting inflammatory infiltration and renal fibrosis (Li et al. 2020). Therefore, we speculated that the up-regulation of SMYD2 expression can activate various inflammatory factors and trigger the pro-fibrotic response (Figure 7).
Effect of titanium dioxide nanoparticles on histone modifications and histone modifying enzymes expression in human cell lines
Published in Nanotoxicology, 2022
Marta Pogribna, Beverly Word, Beverly Lyn-Cook, George Hammons
Histone H3 lysine 27 trimethylation (H3K27me3) has been implicated in the formation of repressive chromatin domains (Francis, Kingston, and Woodcock 2004; Ringrose, Ehret, and Paro 2004). An increase in H3K27me3 is commonly observed in human lung cancer (Langevin, Kratzke, and Kelsey 2015). High H3K27me3 expression was found in colorectal cancer tissues and was associated with more advanced stage (Carvalho et al. 2018). The expression level of H3K27me3 is elevated in patients with metachronous liver metastasis of colorectal cancer and is positively associated with tumor size and poorer survival rates (Tamagawa et al. 2013). Also, the expression levels of H3K27me3 are higher in esophageal cancers and correlate with poor prognosis for patients (He et al. 2009; Tzao et al. 2009). High levels of H3K27me3 associated with advanced clinical stage and short overall survival have also been reported in nasopharyngeal carcinoma (Cai et al. 2011a) and hepatocellular carcinoma (Cai et al. 2011b). Trimethylation of histone H3K36 (H3K36me3), an epigenetic marker associated with actively transcribed genes, is proposed to be involved in numerous biological processes, such as DNA mismatch repair, chromatin structure modulation during elongation, and stem cell regulation (McDaniel and Strahl 2017). Loss of H3K36me3 has been reported in renal cell carcinoma (Ho et al. 2016); however, increased H3K36me3 levels have been shown in prostate cancer (Yang et al. 2012) and breast cancer (Rivenbark, Coleman, and Stahl 2009). Also, H3K36me3 expression was found to positively correlate with high tumor grade and high tumor stage and to contribute to tumor recurrence and poor prognosis in hepatocellular carcinoma (Lien et al. 2018).
The relationship between histone posttranslational modification and DNA damage signaling and repair
Published in International Journal of Radiation Biology, 2019
Ajit K Sharma, Michael J. Hendzel
It has previously been reported that methylation on H3K36 plays a key role in the DDR. A wide range of KMTs can mono- and di-methylate H3K36 whereas SETD2 (KMT3A) is the only known KMT responsible for the tri-methylation on H3K36 (Wagner and Carpenter 2012). SETD2 mediates H3K36me3 and promotes genome stability by facilitating DNA resection for HR repair in human cells (Pfister et al. 2014). Depletion of SETD2 leads to decreased ATM and p53 phosphorylation, defective DNA end-resection, impaired recruitment of RPA and RAD51 and low HR efficiency after DSBs (Pfister et al. 2014). Thus, H3K36me3 is required for efficient homologous recombination repair.