4.7 Article

Lack of Truncated IFITM3 Transcripts in Cells Homozygous for the rs12252-C Variant That is Associated With Severe Influenza Infection

期刊

JOURNAL OF INFECTIOUS DISEASES
卷 217, 期 2, 页码 257-262

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jix512

关键词

IFITM3; influenza A virus; rs12252

资金

  1. Medical Research Council, UK
  2. National Natural Science Foundation of China [81271842, 81228020, 81320108017]
  3. Beijing Natural Science Foundation [7132098]
  4. National S and T Major Project for Infectious Diseases Control [2012ZX10001006-001-008, 2013ZX10001004-001-002]
  5. Beijing Municipal Administration of Hospitals [XMLX201411]
  6. Beijing Key Laboratory [BZ0373]
  7. Capital Health Development [TG-2015-19]
  8. Medical Research Council [1612663, G1001046, MR/L018942/1, G0600520] Funding Source: researchfish
  9. MRC [G0600520, MR/L018942/1, G1001046] Funding Source: UKRI

向作者/读者索取更多资源

Interferon-induced transmembrane 3 (IFITM3) is known to restrict the entry of a range of enveloped viruses. The single nucleotide polymorphism rs12252-C within IFITM3 has been shown to be associated with severe influenza A virus infection. It has been suggested that rs12252-C results in expression of a truncated IFITM3 protein lacking the first 21 amino acids. By performing high-throughput RNA sequencing on primary dendritic cells and peripheral blood mononuclear cells isolated from pandemic H1N1 influenza and human immunodeficiency virus-1 (HIV-1) infected patients we show that full-length IFITM3 mRNA is dominantly expressed (> 99%) across all rs12252 genotypes. Full-length IFITM3 protein can be detected in all genotypes.

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