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Regulates APAF1 expression and plays an important role in the regulation of stress-induced apoptosis. Additionally we are shipping UACA Antibodies (62) and and many more products for this protein.
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The down-regulation of APIP (show APIP ELISA Kits) and UACA expression suggests that the threshold to activate the apoptosome apparatus may be decreased in non-small cell lung cancer cells.
UACA is a novel candidate for eye muscle autoantigens in thyroid-associated ophthalmopathy
Nucling plays an important role in mammary gland involution by regulating NF-kappaB (show NFKB1 ELISA Kits) and STAT3 (show STAT3 ELISA Kits) signaling pathways
Findings indicate that UACA functions as a Rab39A effector in the retinoic acid-induced differentiation of Neuro2A cells.
Data from knockout mice suggest that nucling plays important role in induction of apoptosis in liver/hepatocytes damaged by cytotoxic stressors; nucling acts through modulation of NFkappaB signaling.
Nucling expression is induced by canonical NF-kappaB (show NFKB1 ELISA Kits) signalling pathway, whereas Nucling is undergoing proteasome degradation, as well as being cleaved by caspase (show CASP3 ELISA Kits) system under stress conditions
Nucling deficiency could be a powerful tool to reveal the NF-kappaB (show NFKB1 ELISA Kits)-related molecular networks leading to hepatitis and hepatocellular carcinoma development.
Nucling was shown to interfere with NF-kappaB (show NFKB1 ELISA Kits) activation via the nuclear translocation process of NF-kappaB (show NFKB1 ELISA Kits)/p65 (show NFkBP65 ELISA Kits), thus inhibiting the expression of galectin-3 (show LGALS3 ELISA Kits).
Nucling recruits and transports the apoptosome complex during stress-induced apoptosis
These results indicate an important role for Nucling in MPTP (show PTPN2 ELISA Kits)-induced neuronal degeneration and suggest that the suppression of Nucling would be of therapeutic benefit for the treatment of neurodegeneration in PD.
a novel function of Nucling as a suppressor of nuclear factor-kappaB, mediated by its cytoplasmic retention through physical interaction
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. Modulates isoactin dynamics to regulate the morphological alterations required for cell growth and motility. Interaction with ARF6 may modulate cell shape and motility after injury (By similarity).
nuclear membrane binding protein
, uveal autoantigen with coiled coil domains and ankyrin repeats
, nuclear membrane binding protein NUCLING
, nuclear membrane-binding protein
, beta-actin-binding protein
, uveal autoantigen with coiled-coil domains and ankyrin repeats protein