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- Table of Contents
Facts about Methyl-CpG-binding domain protein 4.
Mismatch-specific DNA N-glycosylase involved in DNA repair.
Has thymine glycosylase activity and is unique for G:T mismatches within methylated and unmethylated CpG websites.Can also remove uracil or 5-fluorouracil in G:U mismatches. Has no lyase activity.
Human | |
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Gene Name: | MBD4 |
Uniprot: | O95243 |
Entrez: | 8930 |
Belongs to: |
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No superfamily |
EC 3.2.2.-; G/T mismatch glycosylase; G/U mismatch glycosylase; MBD4; MED1G/5-fluorouracil mismatch glycosylase with biphasic kinetics; methyl-CpG binding domain protein 4; methyl-CpG-binding domain protein 43,N(4)-ethenocytosine glycosylase; Methyl-CpG-binding endonuclease 1; Methyl-CpG-binding protein MBD4; Mismatch-specific DNA N-glycosylase; putative methyl-CpG binding protein
Mass (kDA):
66.051 kDA
Human | |
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Location: | 3q21.3 |
Sequence: | 3; NC_000003.12 (129430944..129440179, complement) |
Nucleus.
Steven Boster is a name everyone has heard of, but do they really mean what he stands for or what his research entails? For a quick overview on Steven Boster and his MBD4 Marker, read on. We will also discuss the clinical applications and biological significance of this marker. We hope this review will help to inform you about Boster’s research.
Medulloblastoma (MB), the most common malignant head tumor in children, accounts for approximately 10% pediatric cancer mortality. About 30% of MB victims already have metastatic disease when they are diagnosed. The effectiveness of current treatments to this aggressive type pediatric brain tumor is low. It is crucial to develop novel treatments for MB. It is difficult to develop specific therapies because the underlying mechanisms that control MB metastasis remain poorly understood. A key pathway in the MB pathogenesis is the hepatocyte growth factor/cmet signaling pathway. Metastatic MB cells are known to overexpress cMET. This protein is associated with poor outcomes. Metastatic cells also express the receptor for platelet-derived Growth Factor.
Mbd4 can perform novel functions in DNA damage repair. It interacts with the DNA mismatch repair protein, MLh2. It has been shown to interact with the DNA mismatch repair protein MLh2. The mechanisms behind Mbd4 activation are still unclear. This review will examine some of the clinical applications of MBD4 markers.
Ovarian Cancer is one of the most fatal cancers in women. It is also a leading cause of death. Because of its nonspecific symptoms, it is difficult to detect the disease early. Survival rates for survivors are also very low. The discovery of epigenetic signatures plays an important role in ovarian cancergenesis and is being considered as diagnostic biomarkers. This is especially important to women with high levels MBD4.
Immunoblotting was used to determine the molecular mass (or molecular mass) of a protein. MBD4 expression was seen in Raji and human HepG2 hepatocellular carcinoma cell lines. MBD4 was also expressed high in the C2C12 mice myoblast line. Western blotting was used to detect MBD4 using a goat antihuman MBD4 antibody. MBD4 could be detected using Immunoblot Buffer Group 1 for detection. It has a molecular masses of 68 kDa.
MBD4 activity at nucleosomes corresponded approximately to 40% of its DNA substrate. MBD4 was active on mismatched constructs but showed high affinity for the labeled template DNA template. MBD4 binding was blocked by the mismatch at position 160. It may have prevented MBD4 activity, as it was so close at the end of a DNA fragment.
MBD4 plays a functional role in the mammary gland. It is also expressed in various tissues and the brain. It is a crucial part of the endocrine system in the human body. In addition to the MBD4 protein, MBD4 mRNA is an important marker of certain brain diseases. It is not known if it is involved in the formation of Alzheimer's.
Western blot analysis of MBD4 expression showed that MBD4 protein expression varies during differentiation. MBD4 protein expression was the highest after differentiation induction. MBD4 expression also decreased the mRNA expression of PPARg, aP2, and other genes. These results indicate that MBD4 plays a significant role in preadipocyte differentiation. It is therefore important to identify the MBD4 genetic code in order for us to study the development and progression of diabetes.
The binding affinity of MBD4 and CDKN1A/p21 is dependent on the density of methylated CpGs. MBD4 or DNMT1 could coopt MBD4 to repress CDKN1A/p21. By co-opting CDKN1A/p21 methylation, MBD4 and DNMT1 might repress the transcription of the tumor suppressor gene.
PMID: 9774669 by Hendrich B., et al. Identification and characterization of a family of mammalian methyl- CpG binding proteins.
PMID: 10441743 by Hendrich B., et al. Genomic structure and chromosomal mapping of the murine and human mbd1, mbd2, mbd3, and mbd4 genes.