R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
ASCL1 (E6Y1B) Rabbit mAb #55467
Filter:
- WB
- IP
- IF
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 30 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
| Immunofluorescence (Immunocytochemistry) | 1:100 - 1:400 |
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.
Protocol
Specificity / Sensitivity
ASCL1 (E6Y1B) Rabbit mAb recognizes endogenous levels of total ASCL1 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the carboxy terminus 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.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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