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NOTCH3 Antibody (C-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q9UM47 |
|---|---|
| Clone Names | 2091807 |
| Gene ID | 4854 |
|---|---|
| Other Names | Neurogenic locus notch homolog protein 3, Notch 3, Notch 3 extracellular truncation, Notch 3 intracellular domain, NOTCH3 |
| Target/Specificity | The synthetic peptide sequence used to generate the antibody AP6220a was selected from the C-term region of human NOTCH3 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay. |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | NOTCH3 |
|---|---|
| Function | Functions as a receptor for membrane-bound ligands Jagged1, Jagged2 and Delta1 to regulate cell-fate determination (PubMed:15350543). Upon ligand activation through the released notch intracellular domain (NICD) it forms a transcriptional activator complex with RBPJ/RBPSUH and activates genes of the enhancer of split locus. Affects the implementation of differentiation, proliferation and apoptotic programs (By similarity). |
| Cellular Location | Cell membrane; Single-pass type I membrane protein |
| Tissue Location | Ubiquitously expressed in fetal and adult tissues. |
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Provided below are standard protocols that you may find useful for product applications.
Background
NOTCH3 is the third discovered human homologue of the Drosophilia melanogaster type I membrane protein notch. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signalling pathway that plays a key role in neural development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remains to be determined. Mutations in NOTCH3 have been identified as the underlying cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
References
Suwanwela, N., et al., J Med Assoc Thai 86(2):178-182 (2003).Ahearn, E.P., et al., Am. J. Med. Genet. 114(6):652-658 (2002).Bellavia, D., et al., Proc. Natl. Acad. Sci. U.S.A. 99(6):3788-3793 (2002).Ito, D., et al., J. Neurol. Neurosurg. Psychiatr. 72(3):382-384 (2002).Joutel, A., et al., Lancet 350(9090):1511-1515 (1997).
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