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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Methyl-CpG binding domain protein 3

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). However, unlike the other family members, MBD3 is not capable of binding to methylated DNA. The predicted MBD3 protein shares 71% and 94% identity with MBD2 (isoform 1) and mouse Mbd3. MBD3 is a subunit of the NuRD, a multisubunit complex containing nucleosome remodeling and histone deacetylase activities. MBD3 mediates the association of metastasis-associated protein 2 (MTA2) with the core histone deacetylase complex. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: demethylase, Histone, MECP2, hBD-4, CAN
Papers on MBD3
Methyl-CpG-binding domain protein 3-like 2 (MBD3L2) promotes Tet2 enzymatic activity for mediating 5mC oxidation.
Yu et al., Shanghai, China. In J Cell Sci, Feb 2016
Here we found that MBD3 and its analogue MBD3L2 can specifically modulate the enzymatic activity of Tet2 protein, but not Tet1 and Tet3 proteins, in converting 5mC into 5hmC.
Abnormal DNA methylation in the lumbar spinal cord following chronic constriction injury in rats.
Yang et al., Fuzhou, China. In Neurosci Lett, Feb 2016
Our results showed that DNMT3a, DNMT3b and methyl-CpG binding protein 2 (MeCP2) expression increased, MBD2 expression decreased, and DNMT1, MBD1 and MBD3 expression hardly changed in the lumbar spinal cord in CCI rats on day 14 after surgery.
Cigarette smoke induces proteasomal-mediated degradation of DNA methyltransferases and methyl CpG-/CpG domain-binding proteins in embryonic orofacial cells.
Pisano et al., Louisville, United States. In Reprod Toxicol, Dec 2015
Primary cultures of 1-BA cells, exposed to 80μg/mL cigarette smoke extract (CSE) for 24h, exhibited a >13% decline in global DNA methylation and triggered proteasomal-mediated degradation of Dnmts (DNMT-1 and -3a), methyl CpG binding protein 2 (MeCP2) and methyl-CpG binding domain protein 3 (MBD-3).
Expression of epigenetic modifiers is not significantly altered by exposure to secondhand smoke.
Besaratinia et al., Los Angeles, United States. In Lung Cancer, Nov 2015
RESULTS AND CONCLUSION: Quantification of the expression of genes encoding DNA methyltransferases (Dnmt1, Dnmt3a, Dnmt3b and Dnmt3l), methyl binding domain proteins (Mecp2, Mbd2 and Mbd3) and histone deacetylases (Hdac1 and Hdac2) by quantitative reverse-transcription polymerase chain reaction analysis showed modest but not statistically significant differences in the relative transcription of these key epigenetic regulators between SHS-exposed mice and age-matched controls.
Positive and negative regulators of the metallothionein gene (review).
Takahashi, Sagamihara, Japan. In Mol Med Report, Jul 2015
The present review focuses on PU.1 and several other negative regulators of this gene, including PZ120, DNA methyltransferase 3a with Mbd3 and Brg1 complex, CCAAT enhancer binding protein α and Ku protein, and describes the suppression of the MT genes through these transcription factors.
Towards elucidating the stability, dynamics and architecture of the nucleosome remodeling and deacetylase complex by using quantitative interaction proteomics.
Vermeulen et al., Nijmegen, Netherlands. In Febs J, May 2015
Altogether, these findings extend our understanding of MBD3-NuRD structure and stability.
Reprogramming barriers and enhancers: strategies to enhance the efficiency and kinetics of induced pluripotency.
Ebrahimi, Yazd, Iran. In Cell Regen (lond), 2014
Different strategies have been applied for enhancing reprogramming efficiency, including depletion/inhibition of barriers (p53, p21, p57, p16(Ink4a)/p19(Arf), Mbd3, etc.), overexpression of enhancing genes (e.g., FOXH1, C/EBP alpha, UTF1, and GLIS1), and administration of certain cytokines and small molecules.
MBD3/NuRD facilitates induction of pluripotency in a context-dependent manner.
Silva et al., Cambridge, United Kingdom. In Cell Stem Cell, 2014
By knocking out MBD3, an essential scaffold subunit of the NuRD complex, at different time points in reprogramming, we found that efficient formation of reprogramming intermediates and induced pluripotent stem cells from neural stem cells requires NuRD activity.
MBD2 and MBD3: elusive functions and mechanisms.
Stunnenberg et al., Nijmegen, Netherlands. In Front Genet, 2013
This review focuses on two members of the methyl binding proteins, namely MBD2 and MBD3 that reside in very similar complexes, yet appear to have very different biological roles.
Deterministic direct reprogramming of somatic cells to pluripotency.
Hanna et al., Israel. In Nature, 2013
Here we show that depleting Mbd3, a core member of the Mbd3/NuRD (nucleosome remodelling and deacetylation) repressor complex, together with OSKM transduction and reprogramming in naive pluripotency promoting conditions, result in deterministic and synchronized iPS cell reprogramming (near 100% efficiency within seven days from mouse and human cells).
Removing reprogramming roadblocks: Mbd3 depletion allows deterministic iPSC generation.
Hochedlinger et al., Boston, United States. In Cell Stem Cell, 2013
Transcription factor-induced pluripotency is extremely inefficient and assumed to be stochastic.
Methylation-dependent and -independent genomic targeting principles of the MBD protein family.
Schübeler et al., Basel, Switzerland. In Cell, 2013
Interestingly, MBD3 also occupies these sites, but like MBD2, binding is independent of the presence of hydroxymethylation.
Pulmonary surfactant protein A protects lung epithelium from cytotoxicity of human β-defensin 3.
Kuroki et al., Sapporo, Japan. In J Biol Chem, 2012
SP-A protects lung epithelium from tissue injury caused by BD3
Mbd3/NURD complex regulates expression of 5-hydroxymethylcytosine marked genes in embryonic stem cells.
Fazzio et al., Worcester, United States. In Cell, 2012
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.
[DNA methylation in Drosophila, a review of recent studies].
Zhang et al., Xi'an, China. In Yi Chuan, 2011
dDNMT2 shows significant homology to the mammalian methyltransferases DNMT2 family, and dMBD2/3 encodes a protein with distinct homology to mammalian methyl-binding proteins MBD2 and MBD3.
Psychological stress regulates antimicrobial peptide expression by both glucocorticoid and β-adrenergic mechanisms.
Elias et al., Barcelona, Spain. In Eur J Dermatol, 2011
In these studies, PS again provoked a decline in both mouse cathelicidin (CAMP) and mouse β-defensin 3 (mBD3) expression, in a GC-dependent fashion.
c-Jun N-terminal phosphorylation antagonises recruitment of the Mbd3/NuRD repressor complex.
Behrens et al., London, United Kingdom. In Nature, 2011
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
Chronic colitis induces expression of β-defensins in murine intestinal epithelial cells.
Hammarström et al., Umeå, Sweden. In Clin Exp Immunol, 2011
Mouse beta-defensin 3 was strongly up-regulated in colonic epithelium of 15 (but not 5) week-old IL-2(-/-) mice and in dextran-sulfate-induced chronic (but not acute) colitis, but not in IL-2(+/-) 15-week-old mice.
Antifungal activity of recombinant mouse beta-defensin 3.
Li et al., Chengdu, China. In Lett Appl Microbiol, 2010
Epithelial and mucosal tissues expressed bd3 and recombinant bd3 exhibits antifungal activity.
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