|Application ||WB, IF, FC|
|Other Accession||55075, 108049|
|Isotype||Mouse / IgG1, kappa|
|Other Names||Uveal autoantigen with coiled-coil domains and ankyrin repeats, UACA, KIAA1561|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||UACA / Nucling (Nuclear Membrane Marker) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Regulates APAF1 expression and plays an important role in the regulation of stress-induced apoptosis. Promotes apoptosis by regulating three pathways, apoptosome up-regulation, LGALS3/galectin-3 down-regulation and NF-kappa-B inactivation. Regulates the redistribution of APAF1 into the nucleus after proapoptotic stress. Down-regulates the expression of LGALS3 by inhibiting NFKB1 (By similarity).|
|Cellular Location||Nucleus. Cytoplasm. Cytoplasm, cytoskeleton. Note=Expressed diffusely in cytoplasm|
|Tissue Location||Highly expressed in skeletal muscle, heart, kidney and pancreas. Expressed in choroid, retina and epidermal melanocytes. Expressed in eye muscles and thyroid follicular cells.|
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UACA (Uveal Autoantigen with Coiled-coil domains and Ankyrin repeats) is a 1,416 amino acid nuclear membrane protein. It was originally identified as an autoantigen in patients with panuveitis, a characteristic of Vogt-Koyanagi-Harada disease, and in patients with Graves' disease. UACA was also later identified as Nucling, an mRNA differentially expressed in F9 embryonal carcinoma cells during cardiac muscle differentiation. UACA appears to function as a pro-apoptotic protein that recruits the apaf-1-pro-caspase-9 complex for the induction of apoptosis to mediate the cell-death pathway.
Yamada, K., et al. 2001. Identification of a novel autoantigen UACA in patients with panuveitis. Biochem. Biophys. Res. Commun. 280: 1169-1176. | Ohkura, T., et al. 2004. Detection of the novel autoantibody (anti-UACA antibody) in patients with Graves disease. Biochem. Biophys. Res. Commun. 321: 432-440
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