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Regulation of ANKRD9 expression by lipid metabolic perturbations

  • Wang, Xiaofei (Department of Biological Sciences, Tennessee State University) ;
  • Newkirk, Robert F. (Department of Biological Sciences, Tennessee State University) ;
  • Carre, Wilfrid (Department of Animal and Food Sciences, University of Delaware) ;
  • Ghose, Purnima (Department of Biological Sciences, Tennessee State University) ;
  • Igobudia, Barry (Department of Biological Sciences, Tennessee State University) ;
  • Townsel, James G. (Department of Physiology, Meharry Medical College) ;
  • Cogburn, Larry A. (Department of Animal and Food Sciences, University of Delaware)
  • Published : 2009.09.30

Abstract

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 ($T_3$) 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.

Keywords

References

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