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10.2217/epi-2021-0476

http://scihub22266oqcxt.onion/10.2217/epi-2021-0476
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35021853!8763212!35021853
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suck abstract from ncbi


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pmid35021853      Epigenomics 2022 ; 14 (3): 153-162
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  • The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks #MMPMID35021853
  • Shirvaliloo M
  • Epigenomics 2022[Feb]; 14 (3): 153-162 PMID35021853show ga
  • Smoking could predispose individuals to a more severe COVID-19 by upregulating a particular gene known as mdig, which is mediated through a number of well-known histone modifications. Smoking might regulate the transcription-activating H3K4me3 mark, along with the transcription-repressing H3K9me3 and H3K27me3 marks, in a way to favor SARS-CoV-2 entry by enhancing the expression of ACE2, NRP1 and NRP2, AT1R, CTSD and CTSL, PGE2 receptors 2-4, SLC6A20 and IL-6, all of which interact either directly or indirectly with important receptors, facilitating viral entry in COVID-19.
  • |*Epigenesis, Genetic[MESH]
  • |*Protein Processing, Post-Translational[MESH]
  • |Angiotensin-Converting Enzyme 2/genetics/metabolism[MESH]
  • |COVID-19/diagnosis/*genetics/metabolism/virology[MESH]
  • |Cathepsin D/genetics/metabolism[MESH]
  • |Cathepsin L/genetics/metabolism[MESH]
  • |Dioxygenases/*genetics/metabolism[MESH]
  • |Histone Demethylases/*genetics/metabolism[MESH]
  • |Histones/*genetics/metabolism[MESH]
  • |Humans[MESH]
  • |Interleukin-6/genetics/metabolism[MESH]
  • |Membrane Transport Proteins/genetics/metabolism[MESH]
  • |Methylation[MESH]
  • |Neuropilin-1/genetics/metabolism[MESH]
  • |Neuropilin-2/genetics/metabolism[MESH]
  • |Nuclear Proteins/*genetics/metabolism[MESH]
  • |Protein Isoforms/genetics/metabolism[MESH]
  • |Receptor, Angiotensin, Type 1/genetics/metabolism[MESH]
  • |Receptors, Prostaglandin E/genetics/metabolism[MESH]
  • |Risk Factors[MESH]
  • |SARS-CoV-2/genetics/growth & development/metabolism[MESH]
  • |Smoking/*genetics/metabolism/pathology[MESH]


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