anti-Methyl-CpG Binding Domain Protein 1 (MBD1) 抗体

Human Methyl-CpG Binding Domain Protein 1 (MBD1) interaction partners

1. ZEB1 silenced SIRT3 expression via interaction with MBD1 to promote aerobic glycolysis in pancreatic cancer.

2. MBD1 may be a tumor suppressor gene in advanced colorectal cancer (CRC)and affect the development and metastasis of CRC by regulating 8 tumor suppressor genes through binding with SP1.

3. Our findings imply that reduced stability and enhanced dynamics of MBD1 or MBD6 is the origin of ATP7B dysfunction in Wilson disease patients with the G85V or G591D mutation.

4. MBD1 regulates localization and activity of Tet1 in a CXXC3 domain-dependent manner.

5. the binding of MBD1 to nucleosomes demonstrates sequence preferences depending on the position of the methyl groups on the nucleosome.

6. c-myc plays a key role in MBD1 mediated epigenetic silencing of KEAP1.

7. Molecular dynamic simulation reveals mechanism of the recognition of dimethylated CpG sites by MBD1 protein.

8. MBD1 targets short interspersed nuclear elements, but does not exclude RNA Polymerase III.

9. This study investigates the genetic association between methyl-CpG-binding domain (MBD) gene polymorphisms and schizophrenia.

10. We demonstrated the importance of Aire's interaction with the ATF7ip-MBD1 protein complex in maintaining central tolerance

11. an important function of MBD1 in DNA repair and mediation of chemoradioresistance of cancer cells

12. higher MBD1 expression correlated with lymph node metastasis and poor survival in pancreatic cancer; gain- and loss-of-function studies in vitro validated MBD1 as a potent oncogene promoting pancreatic cancer cell invasion and epithelial-mesenchymal transition

13. MBD1-containing chromatin associated factor 2, epithelial malignancy-related vimentin and exocytosis-related annexin A2 were changed upon exposure to airborne nanoparticle PM(0.056).

14. This review tries to match MeCP2 structural domains, or their lack, and specific chromatin features needed for proper recruitment of MeCP2 to its functions as either activator or repressor. We specifically focused on MeCP2's role in Rett syndrome

15. lack of binding to mCpG and interaction with NuRD/Mi2 components HDAC1 and MTA2

16. investigation of role of specific mutations in autism

17. 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.

18. MCAF interacts with the transcriptional repression domain of MBD1

19. Suv39h1 enhanced MBD1-mediated transcriptional repression via MBD, not the C-terminal transcriptional repression domain of MBD1. MBD1 links to histone deacetylases through Suv39h1, causing methylation and deacetylation of histones for gene inactivation

20. Additional evidence of variable expression in the Rett disorder phenotype is presented by a small mixed gender group of children with autistic disorder.

Mouse (Murine) Methyl-CpG Binding Domain Protein 1 (MBD1) interaction partners

1. MBD1 regulates localization and activity of Tet1 in a CXXC3 domain-dependent manner.

2. MBD1 has a role in neural stem cell maintenance and epigenetic regulation.

3. MBD1 targets short interspersed nuclear elements, but does not exclude RNA Polymerase III.

4. We demonstrated the importance of Aire's interaction with the ATF7ip-MBD1 protein complex in maintaining central tolerance

5. H19 lncRNA controls gene expression of the Imprinted Gene Network by recruiting MBD1.

6. regulatory loop formed by MBD1 and miR-195 is an important component of the epigenetic network that controls aNSC fate

7. MBD1, miR-184, and Numbl form a regulatory network that helps control the balance between proliferation and differentiation of adult neural stem/progenitor cells.

8. Results indicate that MBD1 can interpret the CpG dinucleotide as a repressive signal in vivo regardless of its methylation status.

9. These data show, for the first time, the involvement of methyl-CpG binding domain proteins in the regulation of the MAGE-A genes.

10. Mbd1(-/-) mice exhibit several core deficits associated with autism, including reduced social interaction, learning deficits, anxiety, defective sensory motor gating, depression and abnormal brain serotonin activity.

11. Mbd1 and DNA methylation-mediated epigenetic mechanism regulated the expression of stem cell mitogen Fgf-2 in adult neural stem/progenitor cells.