DNMT3L, S117_9 Host Mouse Species Reactivity IgG1 Species Reactivity Human monoclonal
- Known as:
- DNMT3L, S117_9 Host Mouse Species Reactivity IgG1 Species Reactivity Human mab
- Catalog number:
- SMC-341D
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- Stressmarq
- Gene target:
- DNMT3L S117_9 Host Mouse Species Reactivity IgG1 Human monoclonal
Related genes to: DNMT3L, S117_9 Host Mouse Species Reactivity IgG1 Species Reactivity Human monoclonal
- Gene:
- DNMT3L NIH gene
- Name:
- DNA methyltransferase 3 like
- Previous symbol:
- -
- Synonyms:
- MGC1090
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2016-06-21
- Gene:
- PRKCI NIH gene
- Name:
- protein kinase C iota
- Previous symbol:
- DXS1179E
- Synonyms:
- PKCI
- Chromosome:
- 3q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-06
- Date modifiied:
- 2016-10-05
Related products to: DNMT3L, S117_9 Host Mouse Species Reactivity IgG1 Species Reactivity Human monoclonal
Related articles to: DNMT3L, S117_9 Host Mouse Species Reactivity IgG1 Species Reactivity Human monoclonal
- DNA methyltransferase 3A (DNMT3A) and its catalytically inactive cofactor DNA methyltransferase 3-Like (DNMT3L) proteins form functional heterotetramers to deposit DNA methylation in mammalian germ cells. While both proteins have an ATRX-DNMT3-DNMT3L (ADD) domain that recognizes histone H3 tail unmethylated at lysine-4 (H3K4me0), the combined and differential roles of the domains in the two proteins have not been fully defined in vivo. Here we investigate DNA methylation landscapes in female and male germ cells derived from mice with loss-of-function amino acid substitutions in the ADD domains of DNMT3A and/or DNMT3L. Mutations in either the DNMT3A-ADD or the DNMT3L-ADD domain moderately decrease global CG methylation levels, but to different degrees, in both germ cells. Furthermore, when the ADD domains of both DNMT3A and DNMT3L lose their functions, the CG methylation levels are much more reduced, especially in oocytes, comparable to the impact of the Dnmt3a/3L knockout. In contrast, aberrant accumulation of non-CG methylation occurs at thousands of genomic regions in the double mutant oocytes and spermatozoa. These results highlight the critical role of the ADD-H3K4me0 binding in proper CG and non-CG methylation in germ cells and the various impacts of the ADD domains of the two proteins. - Source: PubMed
Publication date: 2024/04/16
Kubo NaokiUehara RyujiUemura ShuheiOhishi HiroakiShirane KenjiroSasaki Hiroyuki - Down syndrome is a well-studied aneuploidy condition in humans, which is associated with various disease phenotypes including cardiovascular, neurological, haematological and immunological disease processes. This review paper aims to discuss the research conducted on gene expression studies during fetal development. A descriptive review was conducted, encompassing all papers published on the PubMed database between September 1960 and September 2022. We found that in amniotic fluid, certain genes such as and were found to be affected, resulting in phenotypical craniofacial changes. Additionally, other genes such as , , , , and were also identified to be affected in the amniotic fluid. In the placenta, dysregulation of genes like , and was observed, which in turn affected nervous system development. In the brain, dysregulation of genes , , , , and has been shown to contribute to intellectual disability. In the cardiac tissues, dysregulated expression of genes , and was found to cause abnormalities. Furthermore, dysregulation of , , , and was observed, contributing to myeloproliferative disorders. Understanding the differential expression of genes provides insights into the genetic consequences of DS. A better understanding of these processes could potentially pave the way for the development of genetic and pharmacological therapies. - Source: PubMed
Publication date: 2024/03/04
Chapman Laura RRamnarine Isabela V PZemke DanMajid ArshadBell Simon M - DNA methyltransferases (Dnmts) are responsible for DNA methylation which influences patterns of gene expression and plays a crucial role in response to environmental changes. In this study, 7 LcDnmt genes were identified in the genome of large yellow croaker (Larimichthys crocea). The comprehensive analysis was conducted on gene structure, protein and location site of LcDnmts. LcDnmt proteins belonged to three groups (Dnmt1, Dnmt2, and Dnmt3) according to their conserved domains and phylogenetic analysis. Although Dnmt3 can be further divided into three sub groups (Dnmt3a, Dnmt3b, and Dnmt3l), there is no Dnmnt3l member in the large yellow croaker. Phylogenetic analysis revealed that the Dnmt family was highly conserved in teleosts. Expression patterns derived from the RNA-seq, qRT-PCR and Western blot analysis revealed that 2 LcDnmt genes (LcDnmt1 and LcDnmt3a2) significantly regulated under salinity stress in the liver, which was found to be dominantly expressed in the intestine and brain, respectively. These two genes may play an important role in the salinity stress of large yellow croaker and represent candidates for future functional analysis. Our results revealed the conservation of Dnmts during evolution and indicated a potential role of Dnmts in epigenetic regulation of response to salinity stress. - Source: PubMed
Publication date: 2024/03/05
Zhang YuChen JiaqianZheng BaoxiaoTeng JianLou ZhengjiaFeng HuijieZhao ShiqiXue Liangyi - To explore the role of Piwi protein and piRNAs in DNMT3L-mediated epigenetic inheritance. Transgenic were used to examine the effect of ectopically expressed DNMT3L on the profile of piRNAs by sequencing of small RNAs. Our previous work showed accumulation and inheritance of epimutations across multiple generations in transgenic DNMT3L . Here, we show interaction of DNMT3L with Piwi and a significant alteration in the piRNA profile across multiple generations in transgenic . In the light of its interaction with histone H1, we propose that in addition to its role of modulating core histone modifications, DNMT3L allows for inheritance of epigenetic information through its collaboration with Piwi, piRNAs and histone H1. - Source: PubMed
Publication date: 2024/03/05
Rajeev RamisettiMishra Rakesh KKhosla Sanjeev - Inhibition of protein kinase C (PKC) efficiently promoted the self-renewal of embryonic stem cells (ESCs). However, information about the function of PKC inhibition remains lacking. Here, RNA-sequencing showed that the addition of Go6983 significantly inhibited the expression of de novo methyltransferases (Dnmt3a and Dnmt3b) and their regulator Dnmt3l, resulting in global hypomethylation of DNA in mouse ESCs. Mechanistically, PR domain-containing 14 (Prdm14), a site-specific transcriptional activator, partially contributed to Go6983-mediated repression of Dnmt3 genes. Administration of Go6983 increased Prdm14 expression mainly through the inhibition of PKCδ. High constitutive expression of Prdm14 phenocopied the ability of Go6983 to maintain` mouse ESC stemness in the absence of self-renewal-promoting cytokines. In contrast, the knockdown of Prdm14 eliminated the response to PKC inhibition and substantially impaired the Go6983-induced resistance of mouse ESCs to differentiation. Furthermore, liquid chromatography-mass spectrometry profiling and Western blotting revealed low levels of Suv39h1 and Suv39h2 in Go6983-treated mouse ESCs. Suv39h enzymes are histone methyltransferases that recognize dimethylated and trimethylated histone H3K9 specifically and usually function as transcriptional repressors. Consistently, the inhibition of Suv39h1 by RNA interference or the addition of the selective inhibitor chaetocin increased Prdm14 expression. Moreover, chromatin immunoprecipitation assay showed that Go6983 treatment led to decreased enrichment of dimethylation and trimethylation of H3K9 at the Prdm14 promoter but increased RNA polymerase Ⅱ binding affinity. Together, our results provide novel insights into the pivotal association between PKC inhibition-mediated self-renewal and epigenetic changes, which will help us better understand the regulatory network of stem cell pluripotency. - Source: PubMed
Publication date: 2024/02/02
Ji JunxiangCao JianjianChen PengHuang RuYe Shou-Dong