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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
Methylated DNA binding domain protein 2 (MBD2) coordinately silences gene expression through activation of the microRNA hsa-mir-496 promoter in breast cancer cell line.
reduced mRNA expression of MBD2 and MBD3 is implicated in gastric carcinogenesis.
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.
Thus, MBD2 and MeCP2 may mediate distinct, sequential transitions of ORN differentiation-an epigenetic mechanism that may be relevant to developmental regulation throughout the nervous system.
Gene silencing quantitatively controls the function of a developmental trans-activator: activating and silencing signals integrate to provide spatially and temporally restricted patterns of gene activity.
MBDin relieves MBD2 repression potential and reactivates transcription from methylated promoters
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