ASCL1 (E5S4Q) XP® Rabbit mAb #10585
- WB
- IHC
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 30 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| IHC Leica Bond | 1:400 - 1:1600 |
| Immunohistochemistry (Paraffin) | 1:100 - 1:400 |
Storage
For a carrier free (BSA and azide free) version of this product see product #53049.
Protocol
Specificity / Sensitivity
ASCL1 (E5S4Q) XP® Rabbit mAb recognizes endogenous levels of total ASCL1 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro83 of human ASCL1 protein.
Background
Achaete-scute homolog 1 (ASCL1), also known as MASH-1, is a basic helix-loop-helix (BHLH) transcription factor which plays an essential role in the differentiation of neuroendocrine cells and neural tissues (1-3). ASCL1 directly binds the E-box motif (5'-CANNTG-3') on promoters, with dimerization with other BHLH proteins required for efficient DNA binding (4). Acting as a pioneer transcription factor, ASCL1 also accesses closed chromatin, allowing other factors to promote transcription of neuronal genes and activate neural pathways (5). Research studies have shown that knockdown of the ASCL1 gene leads to inhibition of growth and induction of apoptosis in SCLC cells in vitro (6). Additionally, ASCL1 is overexpressed in both classic SCLC as well as NSCLC with neuroendocrine features, suggesting its role in the pathogenesis of those malignancies (7). ASCL1 plays a crucial role in promoting SCLC carcinogenesis by upregulating the expression of DLL3, a nonfunctioning Notch ligand, leading to inhibition of the Notch signaling pathway (8).
- Ball, D.W. et al. (1993) Proc Natl Acad Sci U S A 90, 5648-52.
- Cau, E. et al. (1997) Development 124, 1611-21.
- Borges, M. et al. (1997) Nature 386, 852-5.
- Henke, R.M. et al. (2009) Dev Biol 328, 529-40.
- Wapinski, O.L. et al. (2013) Cell 155, 621-35.
- Jiang, T. et al. (2009) Cancer Res 69, 845-54.
- Augustyn, A. et al. (2014) Proc Natl Acad Sci U S A 111, 14788-93.
- Borromeo, M.D. et al. (2016) Cell Rep 16, 1259-72.
Limited Uses
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