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Mouse Anti-NCSTN Recombinant Antibody (CBWJN-1238) (CBMAB-N1518-WJ)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
CBWJN-1238
Antibody Isotype
IgG1
Application
ICC

Basic Information

Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

Format
Lyophilized
Buffer
PBS, Trehalose
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Nicastrin
Introduction
This gene encodes a type I transmembrane glycoprotein that is an integral component of the multimeric gamma-secretase complex. The encoded protein cleaves integral membrane proteins, including Notch receptors and beta-amyloid precursor protein, and may be a stabilizing cofactor required for gamma-secretase complex assembly. The cleavage of beta-amyloid precursor protein yields amyloid beta peptide, the main component of the neuritic plaque and the hallmark lesion in the brains of patients with Alzheimer's disease; however, the nature of the encoded protein's role in Alzheimer's disease is not known for certain. Mutations in this gene are associated with familial acne inversa. A pseudogene of this gene is present on chromosome 21. Alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined. [provided by RefSeq, Feb 2014]
Entrez Gene ID
23385
UniProt ID
Q92542
Alternative Names
Nicastrin; Anterior Pharynx-Defective 2; ATAG1874; KIAA0253;
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.
More Infomation

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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