TET1 (E2J2D) Rabbit mAb #71128
- WB
- C&R
Supporting Data
| REACTIVITY | M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 300 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- C&R-CUT & RUN
Species Cross-Reactivity Key:
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| CUT&RUN | 1:50 |
Storage
Protocol
Specificity / Sensitivity
TET1 (E2J2D) Rabbit mAb recognizes endogenous levels of total TET1 protein.
Species Reactivity:
Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of mouse TET1 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). TET1 is highly expressed in embryonic stem cells and is essential for maintaining stem cell pluripotency through demethylation of the Nanog promoter (8). Aberrant TET1 expression has also been implicated in a variety of cancers, including hepatocellular carcinoma, T-cell acute lymphoblastic leukemia (T-ALL), and triple-negative breast cancer (TNBC), among others (9-11).
- 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.
- Ito, S. et al. (2010) Nature 466, 1129-33.
- Shirai, K. et al. (2021) Cancer Sci 112, 2855-2869.
- Bamezai, S. et al. (2021) Leukemia 35, 389-403.
- Good, C.R. et al. (2018) Cancer Res 78, 4126-4137.
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