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Validated All-in-One™ qPCR Primer for MBD2(NM_003927.4) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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.
Gene References into function
- Methyl-CpG binding domain protein 2 represses transcription from hypermethylated pi-class glutathione S-transferase gene promoters in hepatocellular carcinoma cells
- MBD2 protein activates CpG sites within the promoter region of reporter genes
- interaction with two highly related p66 proteins
- interacts with latency-associated nuclear antigen of Kaposi's Sarcoma-associated herpesvirus (KSHV)to tether KSHV to cell chromosomes
- MBDin relieves MBD2 repression potential and reactivates transcription from methylated promoters
- Results show that methyl-CpG binding domain protein 1 (MBD1) is expressed in tumor cells, but methyl-CpG binding domain protein 2 (MBD2) and methyl CpG binding protein 2 (MeCP2) are not.
- MBD2a and RNA helicase A cooperatively enhanced CREB-dependent gene expression.
- MBD2 has a role in the methylation-mediated inhibition of ribosomal RNA gene expression
- Antisenses oligoDNA suppresses tumor growth in nude mice, a potential anticaner therapy approach.
- MBD2 gene expression may be significant factor in tumorigenesis.
- role of MBD3L1 as a methylation-dependent transcriptional repressor that may interchange with MBD3 as an MBD2-interacting component of the NuRD complex
- MBD3L2 interacts with MBD3 and components of the NuRD complex and can oppose MBD2-MeCP1-mediated methylation silencing
- MBD2 is associated with the methylated region of a CpG island containing the bidirectional promoter of the Breast cancer predisposition gene 1, BRCA1, and the Near BRCA1 2 (NBR2) gene.
- Genetic variations in rhis methylation related genes may potentially serve as a biomarker in risk estimates for breast cancer.
- MBD2 assembles into mutually exclusive distinct Mi-2/NuRD-like complex, called MBD2/NuRD.
- A previously unrecognized intracellular factor required for the efficient generation of protective memory CD8 T cells.
- Sex-specific time windows for concomitant upregulation of MBD2 are associated with prenatal remethylation of the human male and female germ line.
- Results suggest that modulation of MBD2 during gut development establishes a region-specific gene expression pattern that is essential for establishing correct segmental character.
- MBD2 and MBD4 transcript overexpression and inverse correlations with DNA methylation indices indicate that both enzymes may really have a direct and active role on the genome-wide DNA hypomethylation observed in CD4+ T cells from SLE patients.
- These data show, for the first time, the involvement of methyl-CpG binding domain proteins in the regulation of the MAGE-A genes.
- We found clinically relevant levels of Hcy (0-500 microM) induced elevation of SAH, declination of SAM and SAM/SAH ratio and reduced expression of SAHH and MBD2, but increased activity of DNMT3a and DNMT3b affecting DNA methylation
- MBD2 may play an important role in modulating NSCLC patient survival and thus be useful for identifying NSCLC patients who would benefit most from aggressive therapy.
- These findings implicate MBD2 in transcriptional repression of the methylated p14(ARF) tumor suppressor gene and suggest that repression by MBD2 selectively affects a subset of methylated promoters.
