TET2 (D6B9Y) Rabbit mAb #18950
- WB
- IP
- ChIP
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 280 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- ChIP-Chromatin Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
For optimal ChIP results, use 20 μl of antibody and 10 μg of chromatin (approximately 4 x 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunoprecipitation | 1:100 |
Chromatin IP | 1:25 |
Storage
Protocol
Specificity / Sensitivity
TET2 (D6B9Y) Rabbit mAb recognizes endogenous levels of total TET2 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the carboxy terminus of human TET2 protein.
Background
Methylation of DNA at cytosine residues is a heritable, epigenetic modification that is critical for proper regulation of gene expression, genomic imprinting, and mammalian development (1,2). 5-methylcytosine is a repressive epigenetic mark established de novo by two enzymes, DNMT3a and DNMT3b, and is maintained by DNMT1 (3, 4). 5-methylcytosine was originally thought to be passively depleted during DNA replication. However, subsequent studies have shown that Ten-Eleven Translocation (TET) proteins TET1, TET2, and TET3 can catalyze the oxidation of methylated cytosine to 5-hydroxymethylcytosine (5-hmC) (5). Additionally, TET proteins can further oxidize 5-hmC to form 5-formylcytosine (5-fC) and 5-carboxylcytosine (5-caC), both of which are excised by thymine-DNA glycosylase (TDG), effectively linking cytosine oxidation to the base excision repair pathway and supporting active cytosine demethylation (6,7). TET2 is the most frequently mutated gene in myeloid dysplastic syndrome (MDS), a dysplasia of myeloid, megakaryocytic, and/or erythroid cell lineages, of which 30% progress to acute myeloid leukemia (AML) (8, 9). It is also mutated in diffuse large B-cell lymphoma (10). TET2 protein expression is often reduced in solid tumors such as prostate cancer, melanoma, and oral squamous cell carcinoma (11-13).
- Hermann, A. et al. (2004) Cell Mol Life Sci 61, 2571-87.
- Turek-Plewa, J. and Jagodziński, P.P. (2005) Cell Mol Biol Lett 10, 631-47.
- Okano, M. et al. (1999) Cell 99, 247-57.
- Li, E. et al. (1992) Cell 69, 915-26.
- Tahiliani, M. et al. (2009) Science 324, 930-5.
- He, Y.F. et al. (2011) Science 333, 1303-7.
- Ito, S. et al. (2011) Science 333, 1300-3.
- Langemeijer, S.M. et al. (2009) Nat Genet 41, 838-42.
- Yamazaki, J. et al. (2012) Epigenetics 7, 201-7.
- Asmar, F. et al. (2013) Haematologica 98, 1912-20.
- Nickerson, M.L. et al. (2013) Hum Mutat 34, 1231-41.
- Lian, C.G. et al. (2012) Cell 150, 1135-46.
- Jäwert, F. et al. (2013) Anticancer Res 33, 4325-8.
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