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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 (9) und und viele weitere Produktgruppen zu diesem Protein an.
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individual pain vulnerability may be inherent mostly in the emotional/affective component of chronic pain and remain consistent in different aspects of negative emotion, in which adaptive changes in the function of DNA methyltransferase 3a for DNA methylation (zeige HELLS Antikörper) in central amygdala may play an important role.
Taken together, these data demonstrate that adipose Dnmt3a is a novel epigenetic mediator of insulin (zeige INS Antikörper) resistance in vitro and in vivo.
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).
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
, DNA (cytosine-5-)-methyltransferase 6