Disease relevance of NOC3L

• RESULTS: The cumulative incidence of atopic dermatitis over the first 2 years of life (AD24) amounted to 20.1%, and there was a significant association with AD history of the mother (OR 2.5, 95%CI 1.46-4.26) and of the father (OR 3.53, 95%CI 1.90-6.54) [1].

High impact information on NOC3L

• Here we report the cloning of the full-length cDNA and characterization of an unknown gene isolated previously and named fad24 (factor for adipocyte differentiation 24) [2].
• Furthermore, overexpression of fad24 in NIH-3T3 cells promoted adipogenesis in the presence of a ligand for peroxisome proliferator-activated receptor gamma [2].
• Using multiple logistic regression analysis, the prediction of AD24 by AD of parents, of RW24 by asthma of parents, and of sensitization by cord blood IgE was of low accuracy [1].
• RNAi-mediated knockdown of fad24 or antisense fad158 inhibited adipogenesis of 3T3-L1 preadipocytes and decreased expressions of PPARgamma and C/EBPalpha [3].
• The database research of amino acid sequences revealed that fad24 has a basic leucine zipper motif and an NOC domain, and fad158 has four transmembrane domains and eight leucine-rich repeats [3].

Anatomical context of NOC3L

• Moreover, it was found that FAD24 localizes in the nucleus, especially within nuclear speckles and nucleolus, and FAD158 localizes to the endoplasmic reticulum (ER) [3].
• Furthermore, the constitutive overexpression of fad24 or fad158 in the mouse fibroblast cell line NIH-3T3 resulted in adipocyte conversion when stimulated with adipogenic inducers and PPARgamma ligand BRL49653 [3].

Associations of NOC3L with chemical compounds

• The expression of fad24 and fad158 transiently increased after the addition of adipogenic inducers [insulin, dexamethasone, 3-isobutyl-1-methylxanthine, fetal bovine serum (FBS)] [3].

References