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anti-Human MBD2 Antibodies:
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Human Polyclonal MBD2 Primary Antibody for ELISA, WB - ABIN543196
Fujita, Fujii, Aratani, Amano, Fukamizu, Nakajima: Antithetic effects of MBD2a on gene regulation. in Molecular and cellular biology 2003
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Human Polyclonal MBD2 Primary Antibody for IHC (p), IHC - ABIN188691
Tan, Nakielny: Control of the DNA methylation system component MBD2 by protein arginine methylation. in Molecular and cellular biology 2006
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Human Polyclonal MBD2 Primary Antibody for IHC, WB - ABIN2779675
Xing, Stewart, Gu, Lu, Spitz, Wu: Expression of methylation-related genes is associated with overall survival in patients with non-small cell lung cancer. in British journal of cancer 2008
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Human Polyclonal MBD2 Primary Antibody for IHC, ELISA - ABIN334432
Auriol, Billard, Magdinier, Dante: Specific binding of the methyl binding domain protein 2 at the BRCA1-NBR2 locus. in Nucleic acids research 2005
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Human Polyclonal MBD2 Primary Antibody for ICC, IF - ABIN257102
Kim, Kwak, Weitz: Specificity in circadian clock feedback from targeted reconstitution of the NuRD corepressor. in Molecular cell 2014
we conclude that disruption of MBD2 can inhibit the proliferation of CML-BP cells in vivo and in vitro. Given the striking effect in CML blast crisis cell lines, we believe that targeting MBD2 could be a candidate therapeutic strategy for CML-BP patients.
IL-6 treatment downregulated wild-type TP53 protein and induced mRNA and protein expression of the epigenetic reader methyl CpG binding domain protein 2 (MBD2), specifically the alternative mRNA splicing variant MBD2_v2.
In Notch1-driven T-cell acute lymphoblastic leukemia (T-ALL), MBD2 was required for the progression and maintenance of leukemia. The results define essential roles for MBD2 in lymphopoiesis and T-ALL and suggest MBD2 as a candidate therapeutic target in T-ALL.
Suggest that reduced MBD2 expression could contribute to chronic airway inflammation in COPD.
knockdown of MBD2 by siRNA attenuated vancomycin-induced apoptosis, caspase activity, and the expression of BAX and cleaved caspase 3.
CpG and methylation-dependent DNA binding and dynamics of the MBD2 protein at the single-molecule level have been reported.
Results show that MBD2 mediates epigenetic silencing of Htra1.
MBD2 has a critical role in 'rewriting' the cancer methylome at specific regulatory regions.
MBD2 expression was elevated in HCC tissue, which suggesting MBD2 as a candidate prognostic marker of HCC.
downregulation of miR-221 inhibits cell migration and invasion at least partially through targeting MBD2 in the human OSCC cell line UM1.
Specifically, methyl-CpG-binding domain protein 2 (MBD2) is revealed to be recruited to DNA damage sites after laser microirradiation, which was mediated through MBD domain and MBD2 C-terminus.
MBD2 targets short interspersed nuclear elements, but does not exclude RNA Polymerase III.
The dynamics of MBD2 deposition across methylated DNA regions was associated with the oncogenic transformation of human mammary cells.
Data suggest that MBD2 binds primarily at highly methylated regions, with a strong preference for CpG islands and highlights that MBD2 binding sites display increased methylation in primary breast cancer tissues as compared to normal mammary cells.
Biophysical analyses show that the MBD2IDR is an intrinsically disordered region (IDR). However, despite this inherent disorder, MBD2IDR increases the overall binding affinity of MBD2 for methylated DNA.
This study investigates the genetic association between methyl-CpG-binding domain (MBD) gene polymorphisms and schizophrenia.
alternatively spliced isoforms support pluripotency of stem cells
The methylated-DNA binding protein MBD2 enhances NGFI-A (egr-1)-mediated transcriptional activation of the glucocorticoid receptor.
These data point to a potential new approach in targeting the DNA methylation machinery by combination of MBD2 and DNMT inhibitors.
MBD2 seems to play a selective role in gene repression depending on the CpG content of the promoter region
Environmental interactions within the intestine can alter DNA methylation patterns, and Mbd2 may play a key role in determining whether these interactions are anti- or pro-tumourigenic.
MBD2-mediated Th17 differentiation in severe asthma is associated with impaired SOCS3 expression.
Mbd2-CP2c functional loop drives adult-type globin gene expression and erythroid differentiation of erythroid cells.
MBD2 Regulates Th17 Cell Differentiation and Experimental Severe Asthma by Affecting IRF4 Expression
It has been shown that chromatin localization of Mbd2 and Mbd3 is highly overlapping, and both proteins are interdependent for chromatin association.
Loss of Mbd2 resulted in impaired implementation of above DNA methylation changes associated with altered energy homeostasis, which then protected mice from HFD-induced obesity and insulin resistance.
Mbd2 has a key role regulating expression of a range of genes that are associated with optimal dendritic cell activation and function.
methyl-CpG-binding domain protein 2 (MBD2), an epigenetic regulator, controls autoimmunity and EAE through T-bet/Hlx.
miR-290/371-Mbd2-Myc circuit regulates glycolytic metabolism to promote pluripotency.
these findings suggest that CpG methylation and MBD2 are involved in altering Scn3a expression during postnatal development and seizure condition.
Data suggest that methyl-CpG binding domain protein 2 (MBD2) gene knockout may lead to accumulation of more deposits on the Bruch's membrane (BM) and influence the pathogenesis of age-related macular degeneration (AMD).
In metastatic colorectal cancer cells, reduced levels of miR-221* and miR-224 increase levels of MBD2, thereby decreasing expression of the metastasis suppressor maspin.
Mbd2 has a key role in promoting the Treg-specific demethylation region demethylation, Foxp3 expression, and Treg-suppressive function.
Our results strengthen the possibility that MeCP2 and MBD2 direct interactions could crosslink chromatin fibers and therefore give novel insight into the molecular mechanism of MBD mediated global heterochromatin architecture.
Loss of methyl-CpG-binding domain protein 2 enhances endothelial angiogenesis and protects mice against hind-limb ischemic injury.
DNA methylases (DNMT1, 3a and 3b) and a putative demethylase (MBD2) were differently modulated by one-carbon metabolism in Alzheimer's disease models.
DNA methylation is the major modification of eukaryotic genomes and plays an essential role in mammalian development. Human proteins MECP2, MBD1, MBD2, MBD3, and MBD4 comprise a family of nuclear proteins related by the presence in each of a methyl-CpG binding domain (MBD). Each of these proteins, with the exception of MBD3, is capable of binding specifically to methylated DNA. MECP2, MBD1 and MBD2 can also repress transcription from methylated gene promoters. The protein encoded by this gene may function as a mediator of the biological consequences of the methylation signal. It is also reported that the this protein functions as a demethylase to activate transcription, as DNA methylation causes gene silencing. Two transcript variants encoding different isoforms have been found for this gene.
methyl-CpG binding domain protein 2
, methyl-CpG-binding domain protein 2
, methyl-CpG-binding protein MBD2
, methyl-CpG binding protein MBD2