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UBIAD1 encodes a protein thought to be involved in cholesterol and phospholipid metabolism. Additionally we are shipping UBIAD1 Antibodies (19) and UBIAD1 Kits (3) and many more products for this protein.
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Study identified a gene with important antioxidant features by analyzing a null allele of zebrafish ubiad1, called barolo (bar). bar mutants sh (show NOS3 Proteins)ow specific cardiovascular failure due to oxidative stress and reactive oxygen species-mediated cellular damage.
these findings disclose a novel sensing mechanism that allows for stringent metabolic control of intracellular trafficking of UBIAD1, which directly modulates reductase degradation and becomes disrupted in Schnyder corneal dystrophy (SCD (show SCD Proteins)).
UBIAD1 or menaquinone-4 could decrease vascular cell differentiation and calcification, probably via its potent role of inversely modulating cellular cholesterol.
Data show that sterols stimulate binding of prenyltransferase (show FDPS Proteins) UBIAD1 to HMG CoA reductase (show HMGCR Proteins), which is subject to sterol-accelerated, endoplasmic reticulum (ER)-associated degradation augmented by the nonsterol isoprenoid geranylgeraniol.
results suggest that YY1 (show YY1 Proteins) up-regulates UBIAD1 expression and UBIAD1 conversion activity through the UBIAD1 promoter
Golgi localization of UBIAD1 influences its tumor suppressant activity.
Loss of TERE1 may contribute to the altered lipid metabolic phenotype associated with progression in renal clear cell carcinoma via an uncoupling of reactive oxygen species/nitric oxide and SXR (show NR1I2 Proteins) signaling from apoptosis by elevation of cholesterol.
A TERE1-TBL2 (show TBL2 Proteins) complex likely functions in oxidative/nitrosative stress, lipid metabolism, and SXR (show NR1I2 Proteins) signaling pathways in its role as a tumor suppressor.
Physical association of UBIAD1 with enzymes involved in cholesterol synthesis and storage, providing direct links between UBIAD1 and cholesterol metabolism that are likely relevant to Schnyder corneal dystrophy disease pathology.
UBIAD1-mediated vitamin K2 synthesis is required for vascular endothelial cell survival and development.
Findings identify UBIAD1 as a nonmitochondrial CoQ10-forming enzyme with specific cardiovascular protective function via the modulation of eNOS (show NOS3 Proteins) activity.
UBIAD1 is responsible for vitamin K2 synthesis but may not be responsible for CoQ9 synthesis in mice.
This gene encodes a protein thought to be involved in cholesterol and phospholipid metabolism. Mutations in this gene are associated with Schnyder crystalline corneal dystrophy.
UbiA prenyltransferase domain containing 1
, transitional epithelia response protein
, ubiA prenyltransferase domain-containing protein 1
, protein barolo
, protein reddish
, unm t31131
, UbiA prenyltransferase domain-containing protein 1
, transitional epithelial response protein 1