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NR2E3 Matched Antibody Pair (817) (APMAB-817LY)

This antibody pair set can be used for detecting and quantifying protein level of human NR2E3.
See all NR2E3 antibodies

Specifications

ApplIcation
Sandwich ELISA
Specificity
Human
Capture Antibody
Mouse anti-NR2E3 monoclonal antibody, 100 ug
Detection Antibody
Anti-NR2E3 Rabbit polyclonal antibody, 50 ug
Dilutions
10 ng/ml-100 ng/ml
Format
Liquid
Storage
Aliquot and store at -20°Cor -80°C. Avoid freeze-thaw cycles.
Introduction
This protein is part of a large family of nuclear receptor transcription factors involved in signaling pathways. Nuclear receptors have been shown to regulate pathways involved in embryonic development, as well as in maintenance of proper cell function in adults. Members of this family are characterized by discrete domains that function in DNA and ligand binding. This gene encodes a retinal nuclear receptor that is a ligand-dependent transcription factor. Defects in this gene are a cause of enhanced S cone syndrome. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008]
Alternative Names
Nuclear Receptor Subfamily 2 Group E Member 3; Retina-Specific Nuclear Receptor; PNR; RNR; Nuclear Receptor Subfamily 2, Group E, Member 3; Photoreceptor-Specific Nuclear Receptor; ESCS; RP37; Rd7;
Entrez Gene ID
UniProt ID

Xiao, S., Yi, Z., Xiao, X., Li, S., Jia, X., Lian, P., ... & Zhang, Q. (2023). Clinical and genetic features of nr2e3-associated retinopathy: A report of eight families with a longitudinal study and literature review. Genes, 14(8), 1525.

Xie, S., Hu, Y., Jin, J., Fu, L., Zhang, C., Yang, Q., ... & Sheng, Z. (2023). Regulation of the stem‑like properties of estrogen receptor‑positive breast cancer cells through NR2E3/NR2C2 signaling. Experimental and Therapeutic Medicine, 26(4), 1-11.

Toms, M., Ward, N., & Moosajee, M. (2023). Nuclear Receptor Subfamily 2 Group E Member 3 (NR2E3): Role in Retinal Development and Disease. Genes, 14(7), 1325.

Iannaccone, A., Brabbit, E., Lopez-Miro, C., Love, Z., Griffiths, V., Kedrov, M., & Haider, N. B. (2021). Interspecies correlations between human and mouse NR2E3-associated recessive disease. Journal of clinical medicine, 10(3), 475.

Li, S., Datta, S., Brabbit, E., Love, Z., Woytowicz, V., Flattery, K., ... & Haider, N. B. (2021). Nr2e3 is a genetic modifier that rescues retinal degeneration and promotes homeostasis in multiple models of retinitis pigmentosa. Gene Therapy, 28(5), 223-241.

Diakatou, M., Dubois, G., Erkilic, N., Sanjurjo-Soriano, C., Meunier, I., & Kalatzis, V. (2021). Allele-specific knockout by CRISPR/Cas to treat autosomal dominant retinitis pigmentosa caused by the G56R mutation in NR2E3. International Journal of Molecular Sciences, 22(5), 2607.

Al-Khuzaei, S., Broadgate, S., Halford, S., Jolly, J. K., Shanks, M., Clouston, P., & Downes, S. M. (2020). Novel pathogenic sequence variants in NR2E3 and clinical findings in three patients. Genes, 11(11), 1288.

Bohrer, L. R., Wiley, L. A., Burnight, E. R., Cooke, J. A., Giacalone, J. C., Anfinson, K. R., ... & Tucker, B. A. (2019). Correction of NR2E3 associated enhanced S-cone syndrome patient-specific iPSCs using CRISPR-Cas9. Genes, 10(4), 278.

Xie, S., Han, S., Qu, Z., Liu, F., Li, J., Yu, S., ... & Liu, M. (2019). Knockout of Nr2e3 prevents rod photoreceptor differentiation and leads to selective L-/M-cone photoreceptor degeneration in zebrafish. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1865(6), 1273-1283.

Naessens, S., Ruysschaert, L., Lefever, S., Coppieters, F., & De Baere, E. (2019). Antisense oligonucleotide-based downregulation of the G56R pathogenic variant causing NR2E3-associated autosomal dominant retinitis pigmentosa. Genes, 10(5), 363.

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

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We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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