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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. Zusätzlich bieten wir Ihnen DNMT3A Kits (7) und viele weitere Produktgruppen zu diesem Protein an.
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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.
Compared the activity of individual DNMT3A isoforms in embryonic stem and neuronal progenitor cells and report that these isoforms differ in their genomic binding and DNA methylation (zeige HELLS Antikörper) activity at regulatory sites. We identify that the longer isoform DNMT3A1 preferentially localizes to the methylated shores of bivalent CpG island promoters in a tissue-specific manner.
Study shows that in the mouse brain during early life, the DNA methyltransferase (zeige DNMT1 Antikörper) DNMT3A preferentially binds transiently to intergenic regions and across transcribed regions of lowly expressed genes and that this binding primarily determines the pattern of DNA methylation (zeige HELLS Antikörper) at CA sequences in the adult brain.
conditional inactivation of Dnmt3a in mouse hematopoietic cells leads to an accumulation of immature progenitors in the thymus, which are less apoptotic. These data demonstrate that Dnmt3a is required for normal T-cell development, and acts as a T-ALL tumor suppressor
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