货号 | 36449S |
同种亚型 | Rabbit IgG |
反应种属 | Mouse |
应用 | WB,IP,IF,F |
目标/特异性 | TET2 (D6C7K) Rabbit mAb recognizes endogenous levels of total TET2 protein. |
使用方法 | Western Blotting (1:1000) Immunoprecipitation (1:50) Immunofluorescence (Immunocytochemistry) (1:800) Flow Cytometry (1:100) |
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. |
Western blot analysis of extracts from mES, F9, and NIH/3T3 cell lines using TET2 (D6C7K) Rabbit mAb (Mouse Specific) (upper) and α-Actinin (D6F6) XP® Rabbit mAb #6487 (lower). As expected, mES and F9 cells are positive for TET2 expression, while NIH/3T3 cells are negative for TET2 expression. | |
Immunoprecipitation of TET2 from mES cell extracts. Lane 1 is 10% input, lane 2 is Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is TET2 (D6C7K) Rabbit mAb (Mouse Specific). Western blot analysis was performed using TET2 (D6C7K) Rabbit mAb (Mouse Specific). | |
Confocal immunofluorescent analysis of F9 cells (left, positive) and NIH/3T3 cells (right, negative) using TET2 (D6C7K) Rabbit mAb (Mouse Specific) (green). Actin filaments were labeled with DyLight™ 554 Phalloidin #13054 (red). | |
Flow cytometric analysis of C2C12 cells (blue) and mES cells (green) using TET2 mouse (D6C7K) Rabbit mAb (Mouse Specific) (solid line) compared to concentration-matched Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (dashed line). Anti-rabbit IgG (H+L), F(ab)2 Fragment (Alex Fluor® 488 Conjugate) #4412 was used as a secondary antibody. |