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Article Info.
2009.09.30; 42(9) pp. 568~573

Regulation of ANKRD9 expression by lipid metabolic perturbations  


Xiaofei Wang1,2,*, Robert F. Newkirk1, Wilfrid Carre2,3, Purnima Ghose1, Barry Igobudia1, James G. Townsel4 & Larry A. Cogburn2  


1Department of Biological Sciences, Tennessee State University, 3500 John A Merritt Blvd, Nashville, TN 37221, 2Department of Animal and Food Sciences, University of Delaware, Newark, DE 19716, USA, 3Department of Genetics and Genomics, Roslin Institute, Roslin EH25 9PS, Scotland, UK, 4Department of Physiology, Meharry Medical College, Nashville, TN 37208, USA  


Fatty acid oxidation (FAO) defects cause abnormal lipid accumulation in various tissues, which provides an opportunity to uncover novel genes that are involved in lipid metabolism. During a gene expression study in the riboflavin deficient induced FAO disorder in the chicken, we discovered the dramatic increase in mRNA levels of an uncharacterized gene, ANKRD9. No functions have been ascribed to ANKRD9 and its orthologs, although their sequences are well conserved among vertebrates. To provide insight into the function of ANKRD9, the expression of ANKRD9 mRNA in lipidperturbed paradigms was examined. The hepatic mRNA level of ANKRD9 was repressed by thyroid hormone (T3) and fasting, elevated by re-feeding upon fasting. However, ANKRD9 mRNA level is reduced in response to apoptosis. Transient transfection assay with green fluorescent protein tagged- ANKRD9 showed that this protein is localized within the cytoplasm. These findings point to the possibility that ANKRD9 is involved in intracellular lipid accumulation. [BMB reports 2009; 42(9): 568-573]  


ANKRD9, Ankyrin repeat, Chicken, Fatty acid oxidation, Liver, Riboflavin deficient