| 货号 | 18950S |
| 同种亚型 | Rabbit IgG |
| 反应种属 | Human |
| 应用 | WB,IP,CHIP |
| 目标/特异性 | TET2 (D6B9Y) Rabbit mAb recognizes endogenous levels of total TET2 protein. |
| 使用方法 | Western Blotting (1:1000) Immunoprecipitation (1:100) Chromatin IP (1:25) |
| 供应商 | CST |
| 灵敏度 | Endogenous |
| 背景 | 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). |
| 存放说明 | -20C |
| 计算分子量 | 280 |
| 参考文献 | 1 . Hermann, A. et al. (2004) Cell Mol Life Sci 61, 2571-87. 2 . Turek-Plewa, J. and Jagodziński, P.P. (2005) Cell Mol Biol Lett 10, 631-47. 3 . Okano, M. et al. (1999) Cell 99, 247-57. 4 . Li, E. et al. (1992) Cell 69, 915-26. 5 . Tahiliani, M. et al. (2009) Science 324, 930-5. 6 . He, Y.F. et al. (2011) Science 333, 1303-7. 7 . Ito, S. et al. (2011) Science 333, 1300-3. 8 . Langemeijer, S.M. et al. (2009) Nat Genet 41, 838-42. 9 . Yamazaki, J. et al. (2012) Epigenetics 7, 201-7. 10 . Asmar, F. et al. (2013) Haematologica 98, 1912-20. 11 . Nickerson, M.L. et al. (2013) Hum Mutat 34, 1231-41. 12 . Lian, C.G. et al. (2012) Cell 150, 1135-46. 13 . Jäwert, F. et al. (2013) Anticancer Res 33, 4325-8. |
Chromatin immunoprecipitations were performed with cross-linked chromatin from 293T cells and either TET2 (D6B9Y) Rabbit mAb or Normal Rabbit IgG #2729 using SimpleChIP® Plus Enzymatic Chromatin IP Kit (Magnetic Beads) #9005. The enriched DNA was quantified by real-time PCR using SimpleChIP®Human ZNF335 Promoter Primers #25946, human TAF12 exon1 primers, and SimpleChIP® Human α Satellite Repeat Primers #4486. The amount of immunoprecipitated DNA in each sample is represented as signal relative to the total amount of input chromatin, which is equivalent to one. | |
Western blot analysis of extracts from DLD-1 or 293T cells, either wild type (+/+) or TET2 knockout (-/-), using TET2 (D6B9Y) Rabbit mAb (upper) and α-Actinin (D6F6) XP® Rabbit mAb #6487 (lower). As expected, DLD-1 and 293T (+/+) cells are positive for TET2 expression, while TET2 knockout (-/-) cells are negative. |
