Common nonsynonymous polymorphisms in the NOD2 gene are associated with resistance or susceptibility to tuberculosis disease in African Americans
Journal of Infectious Diseases, ISSN: 0022-1899, Vol: 197, Issue: 12, Page: 1713-1716
2008
- 91Citations
- 56Captures
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations91
- Citation Indexes91
- 91
- CrossRef55
- Captures56
- Readers56
- 56
Article Description
Pattern-recognition receptors (PRRs) play a key role in innate immunity against intracellular bacteria. NOD2 is one of the PRRs that contribute to the immune response to Mycobacterium tuberculosis infection. We sequenced coding regions of the NOD2 gene in 377 African Americans with tuberculosis (TB) disease and 187 ethnically matched control subjects. Three common nonsynonymous single-nucleotide polymorphisms - Pro268Ser, Arg702Trp, and Ala725Gly - demonstrated significant associations with TB disease. This finding may contribute to the future development of immunotherapy and immunoprophylaxis for TB disease. © 2008 by the Infectious Diseases Society of America. All rights reserved.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=46349104997&origin=inward; http://dx.doi.org/10.1086/588384; http://www.ncbi.nlm.nih.gov/pubmed/18419343; https://academic.oup.com/jid/article-lookup/doi/10.1086/588384; https://dx.doi.org/10.1086/588384; https://academic.oup.com/jid/article/197/12/1713/866782
Oxford University Press (OUP)
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