Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
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.
Showing 10 out of 10 products:
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
These data demonstrate that haploinsufficiency for Dnmt3a alters hematopoiesis and predisposes mice (and probably humans) to myeloid malignancies by a mechanism that is not yet clear.
Loss of DNMT3A expression is associated with development of malignancy.
confirm the transformation potential of DNMT3A(R882H) Tet2 (zeige TET2 Antikörper)(-/-) progenitors and represent the first cooperative model in mice involving Tet2 (zeige TET2 Antikörper) inactivation driving lymphoid malignancies
overexpression of Dnmt3a partially rescued the impairment of adipogenesis induced by AP2alpha (zeige TFAP2A Antikörper) knockdown.
These data show that DNMT3a plays an important role in regulating embryonic cardiomyocyte gene expression, morphology and function.
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