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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 (show JUN Proteins), 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 (show TGFB1 Proteins)/Smad (show SMAD1 Proteins) 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 (show DPEP1 Proteins)) 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 (show DPEP2 Proteins) and MBD3 is implicated in gastric carcinogenesis.
MBD3 is enriched at active promoters, whereas MBD2 (show DPEP2 Proteins) is bound at methylated promoters and enriched at exon sequences of active genes.
These factors lead to a binding affinity hierarchy of p66alpha (show GATAD2A Proteins) for the different MBD2 (show DPEP2 Proteins) homologues (MBD2 (show DPEP2 Proteins) approximately MBD3 > MBD3L1 (show MBD3L1 Proteins) approximately MBD3L2 (show MBD3L2 Proteins)).
It has been shown that chromatin localization of Mbd2 (show MBD2 Proteins) and Mbd3 is highly overlapping, and both proteins are interdependent for chromatin association.
Smek/Mbd3 interaction regulates neuronal gene expression and neuronal differentiation during cortical development.
This work revealed the critical function of miR (show MLXIP Proteins)-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 (show DEFB103A Proteins) 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 (show APEX1 Proteins) and POLB (show POLB Proteins) as well as the 5-methyl-CpG-binding domain protein MBD3 in individual morula embryos.
cyclin-dependent kinase 2-associated protein 1 (CDK2AP1 (show CDK2AP1 Proteins)), an essential gene for early embryonic development, plays a role in pluripotency of ESC by engaging MBD3 to the promoter region of Wnt (show WNT2 Proteins) signaling genes
Study finds that Mbd3 and Brg1 (show SMARCA4 Proteins) antagonistically regulate a common set of genes by regulating promoter nucleosome occupancy; furthermore, both Mbd3 and Brg1 (show SMARCA4 Proteins) play key roles in the biology of 5-hydroxymethylcytosine.
the transactivation domain of c-Jun (show JUN Proteins) recruits Mbd3/NuRD to AP-1 (show JUN Proteins) target genes to mediate gene repression, and this repression is relieved by JNK (show MAPK8 Proteins)-mediated c-Jun (show JUN Proteins) N-terminal phosphorylation
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