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10.1016/j.tem.2016.02.002

http://scihub22266oqcxt.onion/10.1016/j.tem.2016.02.002
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C4811340!4811340 !26947522
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suck abstract from ncbi


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pmid26947522
      Trends+Endocrinol+Metab 2016 ; 27 (4 ): 204-215
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  • Apolipoprotein L1 and Kidney Disease in African Americans #MMPMID26947522
  • Friedman DJ ; Pollak MR
  • Trends Endocrinol Metab 2016[Apr]; 27 (4 ): 204-215 PMID26947522 show ga
  • Genetic variants in the Apolipoprotein L1 (APOL1) gene cause high rates of kidney disease in African Americans. These variants, found only in individuals with recent African ancestry, confer enhanced innate immunity against African trypanosomes. Although they are among the most powerful disease-causing common variants discovered to date, we are just beginning to understand how they promote kidney injury. Since APOL1 is present in only a few primate species, much of our current knowledge has come from natural experiments in humans and in vitro studies while awaiting the development of transgenic animal models. Understanding more about the function of ApoL1 and how the high-risk variants behave differently from other ApoL1 molecules is a high priority in kidney disease research.
  • |Africa [MESH]
  • |Animals [MESH]
  • |Apolipoprotein L1 [MESH]
  • |Apolipoproteins/blood/*genetics [MESH]
  • |Black or African American/*genetics [MESH]
  • |Disease Resistance [MESH]
  • |Gene Frequency [MESH]
  • |Genetic Predisposition to Disease [MESH]
  • |Genetic Variation [MESH]
  • |Genotype [MESH]
  • |Humans [MESH]
  • |Kidney Diseases/*genetics [MESH]
  • |Lipoproteins, HDL/blood/*genetics [MESH]
  • |Mutation [MESH]


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