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10.1016/j.cmet.2015.04.010

http://scihub22266oqcxt.onion/10.1016/j.cmet.2015.04.010
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suck abstract from ncbi


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pmid25980348
      Cell+Metab 2015 ; 21 (6 ): 855-67
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  • snoRNA U17 regulates cellular cholesterol trafficking #MMPMID25980348
  • Jinn S ; Brandis KA ; Ren A ; Chacko A ; Dudley-Rucker N ; Gale SE ; Sidhu R ; Fujiwara H ; Jiang H ; Olsen BN ; Schaffer JE ; Ory DS
  • Cell Metab 2015[Jun]; 21 (6 ): 855-67 PMID25980348 show ga
  • Cholesterol is required for the growth and viability of mammalian cells and is an obligate precursor for steroid hormone synthesis. Using a loss-of-function screen for mutants with defects in intracellular cholesterol trafficking, a Chinese hamster ovary cell mutant with haploinsufficiency of the U17 snoRNA was isolated. U17 is an H/ACA orphan snoRNA, for which a function other than ribosomal processing has not previously been identified. Through expression profiling, we identified hypoxia-upregulated mitochondrial movement regulator (HUMMR) mRNA as a target that is negatively regulated by U17 snoRNA. Upregulation of HUMMR in U17 snoRNA-deficient cells promoted the formation of ER-mitochondrial contacts, decreasing esterification of cholesterol and facilitating cholesterol trafficking to mitochondria. U17 snoRNA and HUMMR regulate mitochondrial synthesis of steroids in vivo and are developmentally regulated in steroidogenic tissues, suggesting that the U17 snoRNA-HUMMR pathway may serve a previously unrecognized, physiological role in gonadal tissue maturation.
  • |*Up-Regulation [MESH]
  • |Animals [MESH]
  • |Biological Transport, Active/physiology [MESH]
  • |CHO Cells [MESH]
  • |Cholesterol/genetics/*metabolism [MESH]
  • |Cricetinae [MESH]
  • |Cricetulus [MESH]
  • |Eye Proteins/*biosynthesis/genetics [MESH]
  • |Mice [MESH]
  • |Mitochondria/genetics/*metabolism [MESH]
  • |Mitochondrial Proteins/*biosynthesis/genetics [MESH]
  • |NIH 3T3 Cells [MESH]


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