Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

MLLT1/ENL Antibody #12141

No. Size Price
12141S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
12141 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 80 Rabbit

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

MLLT1/ENL Antibody recognizes endogenous levels of total MLLT1/ENL protein.

MLLT1/ENL Antibody能够检测内源性MLLT1/ENL总蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala343 of human MLLT1/ENL protein. Antibodies are purified by protein A and peptide affinity chromatography.

该多克隆抗体是采用合成的与人源 MLLT1/ENL L蛋白 Ala343残基周围序列相对应的肽段免疫动物而生产的。。并经过Protein A和多肽亲和层析纯化而成。

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using MLLT1/ENL Antibody.Western blot方法检测不同细胞系的提取物,使用的抗体为 MLLT1/ENL Antibody。


The super elongation complex (SEC) plays a critical role in regulating RNA polymerase II (RNAPII) transcription elongation (1). The SEC is composed of AFF4, AFF1/AF4, MLLT3/AF9, and MLLT1/ENL proteins. The pathogenesis of mixed lineage leukemia is often associated with translocations of the SEC subunits joined to the histone H3 Lys4 methyltransferase mixed lineage leukemia (MLL) gene (1-4). The SEC has been found to contain RNAPII elongation factors eleven-nineteen lysine-rich leukemia (ELL), ELL2, and ELL3, along with the associated factors EAF1 and EAF2, which can increase the catalytic rate of RNAPII transcription in vitro, (1,2,5-7). The SEC positive transcription elongation factor b (P-TEFb) phosphorylates the C-terminal domain within the largest subunit of RNAP II at Ser2 of the heptapeptide repeat. The SEC negative transcription elongation factors, DRB-induced stimulating factor (DSIF) and negative elongation factor (NELF), signal the transition from transcription initiation and pausing to productive transcription elongation (2,8-10). The chromosomal translocation of MLL with the members of the SEC leads to SEC recruitment to MLL regulated genes, such as the highly developmentally regulated Hox genes, implicating the misregulation and overexpression of these genes as underlying contributors to leukemogenesis (1,2,9,11). MLL translocated to 1/eleven-nineteen-leukemia (MLLT1/ENL) is also found as part of the histone H3 Lys79 methyltransferase disruptor of telomeric silencing-like (Dot1L) complex that has been suggested to play a role in transcription elongation. This complex regulates the expression of genes, such as the Wnt-signaling pathway target genes that control cell proliferation and differentiation during development (12,13).

super elongation complex (SEC)在调控RNA polymerase II (RNAPII)转录延伸中具有至关重要的作用(1)。SEC由AFF4, AFF1/AF4, MLLT3/AF9以及 MLLT1/ENL蛋白组成。混合系白血病的发病机制经常与SEC亚基移位到组蛋白H3 Lys4位点的甲基转移酶混合系白血病基因上(1-4)。研究发现,SEC含有RNAPII延伸因子eleven-nineteen lysine-rich leukemia (ELL), ELL2, 和 ELL3。这些延伸因子与关联因子EAF1和EAF2一起能够提高RNAPII体外转录的催化速度(1,2,5-7)。SEC positive transcription elongation factor b (P-TEFb)能够磷酸化RNAPII最大亚基的C-末端结构域七肽重复序列的Ser2位点。 SEC负转录延伸因子,DRB-induced stimulating factor (DSIF) 以及negative elongation factor (NELF) 能够传递从转录起始和中止到生产型转录延伸的转变信号(2,8-10)。MLL的染色体移位和SEC的成员一起可以倒是SEC募集到MLL调控的级以上,比如发育中被高度调控的Hox基因,这些基因的错误调控和过表达会潜在促进白血病生成(1,2,9,11)。研究发现,被移位到1/eleven-nineteen-leukemia (MLLT1/ENL) 上的MLL同样是telomeric silencing-like (Dot1L) 复合物上的组蛋白H3 Lys79位点甲基转移酶干扰物的一部分。Dot1L复合物曾被认为在转录延长中起作用。该复合物能够调控基因的表达,比如在发育过程中控制细胞增殖和分化的Wnt-信号通路的靶基因(12,13)。

  1. Mohan, M. et al. (2010) Nat Rev Cancer 10, 721-8.
  2. Lin, C. et al. (2010) Mol Cell 37, 429-37.
  3. Drexler, H.G. et al. (2004) Leukemia 18, 227-32.
  4. Smith, E. et al. (2011) Genes Dev 25, 661-72.
  5. Shilatifard, A. et al. (1996) Science 271, 1873-6.
  6. Shilatifard, A. et al. (1997) Proc Natl Acad Sci U S A 94, 3639-43.
  7. Miller, T. et al. (2000) J Biol Chem 275, 32052-6.
  8. Lin, C. et al. (2011) Genes Dev 25, 1486-98.
  9. Yokoyama, A. et al. (2010) Cancer Cell 17, 198-212.
  10. Cho, S. et al. (2010) Cell Cycle 9, 1697-705.
  11. Shah, N. and Sukumar, S. (2010) Nat Rev Cancer 10, 361-71.
  12. Mohan, M. et al. (2010) Genes Dev 24, 574-89.
  13. Nguyen, A.T. and Zhang, Y. (2011) Genes Dev 25, 1345-58.

Application References

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