Product Pathways - Development
HES1 (D6P2U) Rabbit mAb #11988
|11988S||100 µl (10 western blots)||---||In Stock||---|
|11988||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Monkey||Endogenous||30||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IHC-P=Immunohistochemistry (Paraffin)
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.
Western blot analysis of extracts from various cell lines using HES1 (D6P2U) Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human lung carcinoma using HES1 (D6P2U) Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human breast carcinoma using HES1 (D6P2U) Rabbit mAb.
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).
- Kageyama, R. et al. (2007) Development 134, 1243-51.
- Hatakeyama, J. et al. (2004) Development 131, 5539-50.
- Kobayashi, T. and Kageyama, R. (2010) Genes Cells 15, 689-98.
- Wendorff, A.A. et al. (2010) Immunity 33, 671-84.
- Espinosa, L. et al. (2010) Cancer Cell 18, 268-81.
- Ueo, T. et al. (2012) Development 139, 1071-82.
- Zhang, P. et al. (2010) Oncogene 29, 2916-26.
- Kageyama, R. et al. (2008) Dev Growth Differ 50 Suppl 1, S97-103.
- Kobayashi, T. et al. (2009) Genes Dev 23, 1870-5.
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