Description
NOTCH3 Antibody | 62-184 | Gentaur UK, US & Europe Distribution
Host: Rabbit
Reactivity: Mouse
Homology: Predicted species reactivity based on immunogen sequence: Human
Immunogen: This NOTCH3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 2291-2321 amino acids from the C-terminal region of human NOTCH3.
Research Area: Neuroscience, Signal Transduction
Tested Application: WB, IHC-P, IF
Application: For WB starting dilution is: 1:1000
For IF starting dilution is: 1:10~50
For IHC-P starting dilution is: 1:50~100
Specificiy: N/A
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 244 kDa
Validation: N/A
Isoform: N/A
Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
Clonality: Polyclonal
Clone: N/A
Isotype: Rabbit Ig
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: batch dependent
Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Alternate Name: Neurogenic locus notch homolog protein 3, Notch 3, Notch 3 extracellular truncation, Notch 3 intracellular domain, NOTCH3
User Note: Optimal dilutions for each application to be determined by the researcher.
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) .