M6569
Anti-MBD1 antibody produced in rabbit
~1 mg/mL, affinity isolated antibody, buffered aqueous solution
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关于此项目
Conjugate:
unconjugated
Clone:
polyclonal
Application:
ARR, IF, WB
Citations:
5
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen ~80 kDa
species reactivity
human
concentration
~1 mg/mL
technique(s)
indirect immunofluorescence: 1-2 μg/mL using HeK 293T cells transfected with MBD1 (isoform 3), fixed with paraformaldehyde-triton, microarray: suitable, western blot: 0.25-0.5 μg/mL using extracts of HEK 293T cells transfected with MBD1 (isoform 3)
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... MBD1(4152)
General description
MBD1 gene is mapped to human chromosome 18q21.1.
Methyl-CpG binding domain protein 1 (MBD1) exists as five isoforms.
Immunogen
synthetic peptide corresponding to amino acids 591-605 of human MBD1, conjugated to KLH via an N-terminal added lysine residue. This sequence is found in MBD1 isoforms.
Application
Anti-MBD1 antibody produced in rabbit may be used for immunofluorescence and immunoblotting.
Biochem/physiol Actions
Anti MBD1 recognizes recombinant human MBD1 (~80 kDa).
MBD1 can act as a transcriptional repressor. It mediates transcriptional repression by recruiting heterochromatin-binding protein (HP1), the histone methyl transferase Suv39h1 and histone deacetylase using the methyl binding domain (MBD). The transcriptional repression domain (TRD) of MBD1 mediates its interaction with MBD1-containing chromatin-associated factor (MCAF-1).
Methyl-CpG binding domain protein 1 (MBD1) aids pancreatic cancer cells in drug resistance and contributes to disease progression. It gets recruited to those sites where DNA damage has occurred and the protein has also shown to be involved in suppression of gene transcription. MBD1 acts as a link between methylation of DNA and repression of transcription.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, and 15 mM sodium azide.
Preparation Note
For continuous use, store at 2-8 °C for up to one month. For extended storage, freeze in working aliquots. Repeated freezing and thawing is not recommended. Storage in frost-free freezers is also not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilu-tions should be discarded if not used within 12 hours.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Proteomic analysis of differential proteins in pancreatic carcinomas: Effects of MBD1 knock-down by stable RNA interference.
Liu C
BMC Cancer, 8, 121-121 (2008)
Mechanism of transcriptional regulation by methyl-CpG binding protein MBD1.
Fujita N
Molecular and Cellular Biology, 20(14), 5107-5118 (2000)
Holly N Cukier et al.
Neurogenetics, 11(3), 291-303 (2009-11-19)
Misregulation of the methyl-CpG-binding protein 2 (MECP2) gene has been found to cause a myriad of neurological disorders including autism, mental retardation, seizures, learning disabilities, and Rett syndrome. We hypothesized that mutations in other members of the methyl-CpG-binding domain (MBD)
Takaya Ichimura et al.
The Journal of biological chemistry, 280(14), 13928-13935 (2005-02-05)
DNA methylation cooperates with methylation at lysine 9 of histone H3 (H3-K9), a modified histone molecule that is targeted by heterochromatin protein 1, to form a transcriptionally silent chromatin. Methyl CpG-binding protein MBD1 recognizes methylated CpG dinucleotide and recruits H3-K9
Silencing of MBD1 reverses pancreatic cancer therapy resistance through inhibition of DNA damage repair.
Xu J
International Journal of Oncology, 42(6), 2046-2052 (2013)
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