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This is one of two related genes encoding de novo DNA methyltransferases, which are responsible for the establishment of DNA methylation patterns in embryos.
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The aim of the present study is to investigate spatial and temporal expression levels and subcellular localizations of the DNMT1 (zeige DNMT1 Antikörper), DNMT3A, and DNMT3B (zeige DNMT3B Antikörper) proteins in the mouse germinal vesicle (GV) and metaphase II (MII) oocytes, and early embryos from 1-cell to blastocyst stages.
our Dnmt3a R878H mice have shown that leukemic cells have altered gene expression and epigenetic regulatory patterns contributing to the growth/survival advantage over WT mice.The present study found that the DNMT3A mutation contributed to hypomethylation in the gene body region of mTOR (zeige FRAP1 Antikörper) in Dnmt3aR878H/WT mice.
Knockdown of DNMT3A or DNMT1 (zeige DNMT1 Antikörper) protected neurons against mutant Htt (zeige HTT Antikörper)-induced toxicity, together demonstrating a requirement for DNMTs in mutant Htt (zeige HTT Antikörper)-triggered neuronal death and suggesting a neurodegenerative mechanism based on DNA methylation (zeige HELLS Antikörper)-mediated transcriptional repression.
Data demonstrate that DNMT3A and DNA methylation (zeige HELLS Antikörper) are key modulators of mast cell responsiveness to acute and chronic stimulation.
These data suggest that DNMT3a is required for nerve injury-induced and MBD1 (zeige DPEP1 Antikörper)-mediated epigenetic silencing of the MOR (zeige OPRM1 Antikörper) and KOR (zeige OPRK1 Antikörper) in the injured DRG. DNMT3a inhibition may serve as a promising adjuvant therapy for opioid use in neuropathic pain management.
Data show that conditional deletion of Dnmt3a and simultaneous "knock in" of Flt3ITD/+, cooperate to drive leukemia development at a faster rate than Dnmt3a loss alone.
Deletion of DNMT3a in postnatal forebrain neurons does no alter affective behavior.
Altogether, the authors demonstrate that Dnmt3a and Dnmt3b (zeige DNMT3B Antikörper) protect the epidermis from tumorigenesis and that squamous carcinomas are sensitive to inhibition of PPAR-gamma (zeige PPARG Antikörper).
Upon lysolecithin injection in the spinal cord of transgenic mice, study detected defective oligodendrocyte progenitor cells differentiation and inefficient remyelination in the DNA methyltransferase 3a null and DNA methyltransferase 1/DNA methyltransferase (zeige DNMT1 Antikörper) 3a null mice.
This is attributed in part to ineffective repression of Tcf1 (zeige HNF1A Antikörper) expression in knockout T cells, as DNMT3a localizes to the Tcf7 (zeige TCF7 Antikörper) promoter and catalyzes its de novo methylation in early effector WT CD8 (zeige CD8A Antikörper)(+) T cells. These data identify DNMT3a as a crucial regulator of CD8 (zeige CD8A Antikörper)(+) early effector cell differentiation and effector versus memory fate decisions.
This is one of two related genes encoding de novo DNA methyltransferases, which are responsible for the establishment of DNA methylation patterns in embryos. Loss of function of this gene causes developmental defects in multiple different organ systems. There is a pseudogene for this gene located on chromosome 3. Alternatively spliced transcript variants encoding multiple isoforms have been observed.
DNA (cytosine-5)-methyltransferase 3A
, DNA MTase MmuIIIA
, DNA methyltransferase MmuIIIA
, DNA methyltransferase 3A