N5038
Anti-NOTCH3 antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-Notch homolog 3 (Drosophila)
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About This Item
UNSPSC Code:
12352203
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
mol wt
antigen ~230 kDa (cleaved), antigen ~280 kDa
species reactivity
human, mouse, rat
technique(s)
western blot: 1:500-1:1,000
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... NOTCH3(4854)
mouse ... Notch3(18131)
rat ... Notch3(56761)
General description
NOTCH homolog-3 (NOTCH3) is a transmembrane protein and a transcriptional activator. It is expressed in the arteries and the gene encoding it is located on chromosome 19.
Immunogen
synthetic peptide corresponding to residues 1661-1676 of human NOTCH3.
Biochem/physiol Actions
Mutations in the gene encoding NOTCH homolog 3 (NOTCH3) have been associated with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
Physical form
solution in phosphate buffered saline, containing 0.02% sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class
12 - Non Combustible Liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
Regulatory Information
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Homozygous NOTCH3 null mutation and impaired NOTCH3 signaling in recessive early-onset arteriopathy and cavitating leukoencephalopathy.
Pippucci T
EMBO Molecular Medicine, 7(6), 848-858 (2015)
Common NOTCH3 Variants and Cerebral Small-Vessel Disease.
Rutten-Jacobs LC
Stroke, 46(6), 1482-1487 (2015)
Jing Xie et al.
Cell transplantation, 26(6), 967-982 (2017-02-12)
Retinal regeneration and self-repair, whether in response to injury or degenerative disease, are severely impeded by glial scar formation by Müller cells (specialized retinal macroglia). We have previously demonstrated that the activation of Müller cells and gliosis in the degenerative