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Study have demonstrated that MBD3/ NuRD inhibits formation of liver induced cancer stem cells (iCSCs). In addition, MBD3 suppression induces c-JUN, resulting in the induction of pluripotent genes in iCSCs.
Suggest that MBD3 exerts influences on both active and silenced genes in glioma cells.
MBD3 inhibits epithelial-mesenchymal transition in pancreatic cancer cells probably via TGF-beta/Smad signaling and may be a candidate for diagnostics and prognosis of pancreatic cancer.
Overexpression of MBD3 is associated with neoplasms.
Insufficient MBD3 induced by small interfering RNA (siRNA) was found to result in a global DNA hypermethylation as well as increased methylation in the promoter CpG islands (CGIs) of a number of cell cycle related genes.
This study investigates the genetic association between methyl-CpG-binding domain (MBD) gene polymorphisms and schizophrenia.
These data suggest that MBD3, and by extension the NuRD complex, may have multiple roles in fine tuning expression for both active and silent genes, representing an important step in defining regulatory mechanisms
reduced mRNA expression of MBD2 and MBD3 is implicated in gastric carcinogenesis.
MBD3 is enriched at active promoters, whereas MBD2 is bound at methylated promoters and enriched at exon sequences of active genes.
These factors lead to a binding affinity hierarchy of p66alpha for the different MBD2 homologues (MBD2 approximately MBD3 > MBD3L1 approximately MBD3L2).
MBD3 mutations are not responsible for ICR1 hypomethylation in Silver-Russell syndrome.
MBD3 is highly expressed in glioblastome multiforme compared to astrocytoma and anaplastic astrocytoma
interaction with two highly related p66 proteins
localization in Aurora-A-positive centrosomes in M phase
MBD3L2 interacts with MBD3 and components of the NuRD complex and can oppose MBD2-MeCP1-mediated methylation silencing
MBD3 assembles into mutually exclusive distinct Mi-2/NuRD-like complex, called MBD3/NuRD.
This is the first demonstration that MBD3 is involved in inducing and maintaining the demethylated state of a specific promoter.
data demonstrate a causal relationship between MBD3 and DNA demethylation of genomic targets in cells.
Study demonstrates a direct role of the MBD3, a subunit of nucleosome remodeling and deacetylase corepressor complex complex in aberrant gene repression and transmission of epigenetic repressive marks in acute promyelocytic leukemia.
These findings collectively support a role for MBD3 in cell cycle progression and cell death as a modulator of HDAC-mediated transcription.
It has been shown that chromatin localization of Mbd2 and Mbd3 is highly overlapping, and both proteins are interdependent for chromatin association.
controls lymphoid cell fate and inhibits tumorigenesis by repressing a B cell transcriptional program
Smek/Mbd3 interaction regulates neuronal gene expression and neuronal differentiation during cortical development.
This work revealed the critical function of miR-134-Mbd3 axis on regulating reprogramming and pluripotency of induced pluripotent stem cells derived from the neural progenitor cells.
Cigarette smoke induces proteosomal-mediated degradation of Mbd-3 in embryonic orofacial cells.
Although MBD3/NuRD is not required for neural stem cell lineage commitment, it is required to repress inappropriate transcription in progenitor cells and neurons to facilitate appropriate cell lineage choice and differentiation programmes.
overexpression facilitates NANOG-mediated reprogramming in neural stem cells
Data indicate an association of ovarian stimulation with a downregulation of mRNAs encoding the base excision repair proteins APEX1 and POLB as well as the 5-methyl-CpG-binding domain protein MBD3 in individual morula embryos.
cyclin-dependent kinase 2-associated protein 1 (CDK2AP1), an essential gene for early embryonic development, plays a role in pluripotency of ESC by engaging MBD3 to the promoter region of Wnt signaling genes
Study finds that Mbd3 and Brg1 antagonistically regulate a common set of genes by regulating promoter nucleosome occupancy; furthermore, both Mbd3 and Brg1 play key roles in the biology of 5-hydroxymethylcytosine.
the transactivation domain of c-Jun recruits Mbd3/NuRD to AP-1 target genes to mediate gene repression, and this repression is relieved by JNK-mediated c-Jun N-terminal phosphorylation
Mbd3 helps restrict ES cells from differentiating towards the trophectoderm lineage and is an important epigenetic player in maintaining full pluripotency of mouse ES cells
MBD3 protein is differentially expressed in principal neurons of the hippocampus and cortex, and in the adult retina.
Mbd3-deficient embryonic stem cells could be maintained in the absence of leukaemia inhibitory factor (LIF) and could initiate differentiation in embryoid bodies or chimeric embryos, but failed to commit to developmental lineages.
These results demonstrate the importance of Mbd3/NuRD for the development of pluripotent cells in vivo.
A 1072 base pair fragment of the MBD3 promoter is sufficient to drive expression in cell lines and primary cultured neurons.
Chromatin immunoprecipitation shows that MBD3 is bound to the H19 DMD; MBD3-depleted preimplantation embryos have reduced cell numbers, suggesting a role for MBD3 in cell division.
Methyl-CpG binding domain 3b (Mbd3b) protein is a novel binding partner of Evi1, i.e., a member of the Mi-2/NuRD histone deacetylase complex.
Component of Nucleosome Remodelling and Histone Deacetylation (NuRD) co-repressor complex
Does not bind DNA by itself. Recruits histone deacetylases and DNA methyltransferases. Acts as transcriptional repressor and plays a role in gene silencing.
methyl-CpG binding domain protein 3
, methyl-CpG binding protein MBD3 long form
, methyl-CpG-binding domain protein 3
, methyl-CpG-binding protein MBD3