R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
NeuroD1 (D35G2) Rabbit mAb #4373
Filter:
- WB
- IP
- ChIP
Inquiry Info. # 4373
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Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 49 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- ChIP-Chromatin Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
For optimal ChIP results, use 10 μl of antibody and 10 μg of chromatin (approximately 4 x 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Chromatin IP | 1:50 |
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
NeuroD1 (D35G2) Rabbit mAb detects endogenous levels of total NeuroD1 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide surrounding Gln15 of human NeuroD1 protein.
Background
NeuroD1 is a member of the basic helix-loop-helix (bHLH) family of transcription factors. These proteins function by forming heterodimers with E-proteins and binding to the canonical E-box sequence CANNTG (1,2). Neuronal activity results in CaMKII-mediated phosphorylation of NeuroD1 at Ser336, which is necessary for formation and growth of dendrites (3,4). NeuroD1 is also phosphorylated at Ser274 though the results are context dependent as phosphorylation by Erk stimulates NeuroD1 activity in pancreatic β-cells while phosphorylation by GSK-3β inhibits NeuroD1 in neurons (3). NeuroD1 is crucially important in both the pancreas and developing nervous system, and plays a large role in the development of the inner ear and mammalian retina (3). Mice lacking NeuroD1 become severely diabetic and die shortly after birth due to defects in β-cell differentiation (2,3,5,6). The lack of NeuroD1 in the brain results in severe defects in development (5). Human mutations have been linked to a number of types of diabetes, including type I diabetes mellitus and maturity-onset diabetes of the young (1,3).
- Schonhoff, S.E. et al. (2004) Endocrinology 145, 2639-2644.
- Sharma, A. et al. (1999) Mol. Cell Biol. 19, 704-713.
- Chae, J.H. et al. (2004) Mol. Cells 18, 271-288.
- Gaudillière, B. et al. (2004) Neuron 41, 229-241.
- Miyata, T. et al. (1999) Genes Dev. 13, 1647-1652.
- Naya, F.J. et al. (1997) Genes Dev. 11, 2323-2334.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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