Human Recombinant NCSTN protein, His Tag (V2LY-0526-LY5786)

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Basic Information

Expressed Host
HEK293 Cells
Protein Species
Human
Tag
His Tag
Protein Construction
This product is Human Recombinant NCSTN protein, His Tag consist of Amino Acid: 1-669 and predicts a molecular mass of 72.4 kDa.
Molecule Mass
72.4 kDa
Sequence
Amino Acid: 1-669
Species
Human

Formulations & Storage [For reference only, actual COA shall prevail!]

Purity
>93% as determined by SDS-PAGE
Endotoxin
Please contact us for more information.
Format
Lyophilized
Reconstitution
Allow the vial and reconstitution buffer to equilibrate to room temperature. Briefly centrifuge or tap down the vial to ensure that all lyophilized powder is collected at the bottom of the vial. For the reconstitution of this product, we recommend adding PBS or sterile water to achieve a final antibody concentration of 1 mg/mL. Allow the vial to reconstitute for 10-15 minutes at room temperature with gentle agitation. Avoid vigorous shaking that can cause foaming and antibody denaturation. Aliquot into volumes based on your experiment and store liquid protein at -20°C or -80°C for long time.
Buffer
Lyophilized from sterile PBS, Glycerol, Trehalose
Preservative
None
Storage
Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
More Infomation

Target

Full Name
Nicastrin
Function
Essential subunit of the gamma-secretase complex, an endoprotease complex that catalyzes the intramembrane cleavage of integral membrane proteins such as Notch receptors and APP (amyloid-beta precursor protein) (PubMed:10993067, PubMed:12679784, PubMed:25043039, PubMed:26280335, PubMed:30598546, PubMed:30630874).

The gamma-secretase complex plays a role in Notch and Wnt signaling cascades and regulation of downstream processes via its role in processing key regulatory proteins, and by regulating cytosolic CTNNB1 levels.
Biological Process
Adult behavior Source: Ensembl
Amyloid-beta formation Source: ARUK-UCL
Amyloid precursor protein biosynthetic process Source: Ensembl
Amyloid precursor protein catabolic process Source: ARUK-UCL
Amyloid precursor protein metabolic process Source: UniProtKB
Cellular response to calcium ion Source: Ensembl
Central nervous system myelination Source: Ensembl
Cerebellum development Source: Ensembl
Dopamine receptor signaling pathway Source: Ensembl
Epithelial cell proliferation Source: Ensembl
Glutamate receptor signaling pathway Source: Ensembl
Learning or memory Source: Ensembl
Membrane protein ectodomain proteolysis Source: HGNC-UCL
Membrane protein intracellular domain proteolysis Source: ComplexPortal
Myeloid cell homeostasis Source: Ensembl
Neuron apoptotic process Source: Ensembl
Notch receptor processing Source: ARUK-UCL
Notch signaling pathway Source: UniProtKB-KW
Positive regulation of amyloid precursor protein biosynthetic process Source: Ensembl
Positive regulation of catalytic activity Source: HGNC-UCL
Positive regulation of endopeptidase activity Source: ARUK-UCL
Protein processing Source: HGNC-UCL
Proteolysis Source: UniProtKB
Regulation of long-term synaptic potentiation Source: Ensembl
Short-term synaptic potentiation Source: Ensembl
T cell proliferation Source: Ensembl
Cellular Location
Other locations
Membrane
Cytoplasmic vesicle membrane
Melanosome
Note: Identified by mass spectrometry in melanosome fractions from stage I to stage IV.
Involvement in disease
Acne inversa, familial, 1 (ACNINV1):
A chronic relapsing inflammatory disease of the hair follicles characterized by recurrent draining sinuses, painful skin abscesses, and disfiguring scars. Manifestations typically appear after puberty.
Topology
Extracellular: 34-669
Helical: 670-690
Cytoplasmic: 691-709
PTM
N-glycosylated.

Ratnamala, U., Jain, N. K., Jhala, D. D., Prasad, P. V., Saiyed, N., Nair, S., & Radhakrishna, U. (2023). An updated mutation spectrum of the γ-secretase complex: Novel NCSTN gene mutation in an Indian family with hidradenitis suppurativa and acne conglobata. Indian Journal of Dermatology, 68(2), 141.

Zhai, X., Xia, Z., Du, G., Zhang, X., Xia, T., Ma, D., ... & Zhang, H. (2023). LRP1B suppresses HCC progression through the NCSTN/PI3K/AKT signaling axis and affects doxorubicin resistance. Genes & Diseases, 10(5), 2082-2096.

Mintoff, D., Pace, N. P., & Borg, I. (2023). NCSTN in-frame deletion in maltese patients with hidradenitis suppurativa. JAMA dermatology, 159(9), 939-944.

Shi, T. W., Cao, W., Zhao, Q. Z., Yu, H. X., Zhang, S. S., & Hao, Y. B. (2023). Effects of NCSTN mutation on hair follicle components in mice. Dermatology, 239(1), 60-71.

Mintoff, D., Pace, N. P., Bauer, P., & Borg, I. (2021). A novel c. 671_682del NCSTN variant in a family with hidradenitis suppurativa: a pilot study. Clinical and Experimental Dermatology, 46(7), 1306-1308.

Hessam, S., Gambichler, T., Skrygan, M., Scholl, L., Sand, M., Meyer, T., ... & Bechara, F. G. (2021). Increased expression profile of NCSTN, Notch and PI3K/AKT3 in hidradenitis suppurativa. Journal of the European Academy of Dermatology and Venereology, 35(1), 203-210.

He, Y., Li, C., Xu, H., Duan, Z., Liu, Y., Zeng, R., ... & Wang, B. (2020). AKT‐dependent hyperproliferation of keratinocytes in familial hidradenitis suppurativa with a NCSTN mutation: a potential role of defective miR‐100‐5p. British Journal of Dermatology, 182(2), 500-502.

Li, H., Lan, T., Xu, L., Liu, H., Wang, J., Li, J., ... & Wu, H. (2020). NCSTN promotes hepatocellular carcinoma cell growth and metastasis via β-catenin activation in a Notch1/AKT dependent manner. Journal of Experimental & Clinical Cancer Research, 39(1), 1-18.

Takeichi, T., Matsumoto, T., Nomura, T., Takeda, M., Niwa, H., Kono, M., ... & Akiyama, M. (2020). A novel NCSTN missense mutation in the signal peptide domain causes hidradenitis suppurativa, which has features characteristic of an autoinflammatory keratinization disease. British Journal of Dermatology, 182(2), 491-493.

Yang, J., Wang, L., Huang, Y., Liu, K., Lu, C., Si, N., ... & Zhang, X. (2020). Keratin 5-Cre-driven deletion of Ncstn in an acne inversa-like mouse model leads to a markedly increased IL-36a and Sprr2 expression. Frontiers of Medicine, 14, 305-317.

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For research use only. Not intended for any clinical use.

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