HES1 (D6P2U) Rabbit mAb

• 产品编号：CST-11988S      品牌：CST       原厂货号：11988S
• 产品分类：抗体 > 一抗 > 蛋白特异性一抗
• 应用分类：

描述：

HES1 (D6P2U)Rabbit mAb可以识别内源性的总HES1 蛋白。此单克隆抗体由合重组蛋白免疫动物产生，该重组蛋白与人HES1蛋白氨基酸一致。HES1 (Hairy and Enhancer of Split 1)是含有碱性螺旋-环-螺旋（bHLH）转录因子HES家族七个成员之一，发挥抑制bHLH-依赖基因转录的作用（1）。HES1被认为在维持胚胎和成体干细胞/祖细胞多潜能性过程发挥抑制促进分化的基因转录的作用（1,2）。HES1尤其被认为是经典Notch信号通路的抑制因子（3）。HES1在介导Notch-依赖的T细胞系定向（4）过程中发挥作用，也被报道是Notch-诱导的T细胞急性淋巴细胞白血病（T-ALL）的关键介导因子（4，5）。HES1也被报道在多种癌细胞中介导了Notch-诱导的分化抑制。将APC-突变小鼠的小肠肿瘤细胞HES1进行条件性敲除后会降低肿瘤细胞的增殖，同时促进其向上皮细胞系的分化（6）。在人骨肉瘤细胞（OS）中发现HES1过表达会抑制Notch拮抗剂Dtx1的表达，导致OS细胞侵润能力增加（7）。HES1引起的其他基因转录抑制包括Neurogenin-2, Math1/Atoh1 和 the NOTCH ligands DLL1 以及 Jagged1 (6,8,9)。

1. Kageyama, R. et al. (2007) Development 134, 1243-51.
2. Hatakeyama, J. et al. (2004) Development 131, 5539-50.
3. Kobayashi, T. and Kageyama, R. (2010) Genes Cells 15, 689-98.
4. Wendorff, A.A. et al. (2010) Immunity 33, 671-84.
5. Espinosa, L. et al. (2010) Cancer Cell 18, 268-81.
6. Ueo, T. et al. (2012) Development 139, 1071-82.
7. Zhang, P. et al. (2010) Oncogene 29, 2916-26.
8. Kageyama, R. et al. (2008) Dev Growth Differ 50 Suppl 1, S97-103.
9. Kobayashi, T. et al. (2009) Genes Dev 23, 1870-5.

原厂资料：

Specificity / Sensitivity

HES1 (D6P2U) Rabbit mAb recognizes endogenous levels of total HES1 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with recombinant protein specific to human HES1 protein.

Background

HES1 (Hairy and Enhancer of Split 1) is one of seven members of the HES family of basic helix-loop-helix (bHLH) transcription factors which function primarily to repress transcription of bHLH-dependent genes (1). HES1 is understood to play an important conserved role in maintaining pluripotency of embryonic and adult stem/progenitor cells via the transcriptional repression of genes that promote differentiation (1,2). HES1 is particularly well known as a repressive mediator of the canonical Notch signaling pathway (3). HES1 plays a key role in mediating Notch-dependent T cell lineage commitment (4), and has been reported to be an essential mediator of Notch-induced T cell acute lymphoblastic leukemia (T-ALL) (4,5). HES1 is also reported to mediate Notch-induced repression of differentiation in a number of cancer cell types. A conditional deletion of HES1 from intestinal tumor cells in APC-mutant mice reduced tumor cell proliferation, while promoting differentiation toward epithelial lineages (6). Overexpression of HES1 in a human osteosarcoma (OS) cell line was shown to repress expression of the Notch antagonist Dtx1, leading to increased OS cell invasiveness (7). Other genes subject to transcriptional repression by HES1 include Neurogenin-2, Math1/Atoh1 and the NOTCH ligands DLL1 and Jagged1 (6,8,9).

1. Kageyama, R. et al. (2007) Development 134, 1243-51.
2. Hatakeyama, J. et al. (2004) Development 131, 5539-50.
3. Kobayashi, T. and Kageyama, R. (2010) Genes Cells 15, 689-98.
4. Wendorff, A.A. et al. (2010) Immunity 33, 671-84.
5. Espinosa, L. et al. (2010) Cancer Cell 18, 268-81.
6. Ueo, T. et al. (2012) Development 139, 1071-82.
7. Zhang, P. et al. (2010) Oncogene 29, 2916-26.
8. Kageyama, R. et al. (2008) Dev Growth Differ 50 Suppl 1, S97-103.
9. Kobayashi, T. et al. (2009) Genes Dev 23, 1870-5.

注意事项：

Storage: Supplied in 10 mM sodium HEPES (pH 7.5), 150
mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02%
sodium azide. Store at –20°C. Do not aliquot the antibody.