Understanding Human Variation in Infectious Disease Susceptibility through Clinical and Cellular GWAS
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Vyšlo v časopise:
Understanding Human Variation in Infectious Disease Susceptibility through Clinical and Cellular GWAS. PLoS Pathog 9(8): e32767. doi:10.1371/journal.ppat.1003424
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Pearls
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1003424
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Zdroje
1. RaychaudhuriS (2011) Mapping rare and common causal alleles for complex human diseases. Cell 147: 57–69.
2. AllisonAC (1954) Protection afforded by sickle-cell trait against subtertian malareal infection. Br Med J 1: 290–294.
3. DeanM, CarringtonM, WinklerC, HuttleyGA, SmithMW, et al. (1996) Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene. Hemophilia Growth and Development Study, Multicenter AIDS Cohort Study, Multicenter Hemophilia Cohort Study, San Francisco City Cohort, ALIVE Study. Science 273: 1856–1862.
4. JostinsL, RipkeS, WeersmaRK, DuerrRH, McGovernDP, et al. (2012) Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 491: 119–124.
5. HugotJP, ChamaillardM, ZoualiH, LesageS, CezardJP, et al. (2001) Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature 411: 599–603.
6. OguraY, BonenDK, InoharaN, NicolaeDL, ChenFF, et al. (2001) A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature 411: 603–606.
7. InoharaN, OguraY, FontalbaA, GutierrezO, PonsF, et al. (2003) Host recognition of bacterial muramyl dipeptide mediated through NOD2. Implications for Crohn's disease. J Biol Chem 278: 5509–5512.
8. SabbahA, ChangTH, HarnackR, FrohlichV, TominagaK, et al. (2009) Activation of innate immune antiviral responses by Nod2. Nat Immunol 10: 1073–1080.
9. MaedaS, HsuLC, LiuH, BankstonLA, IimuraM, et al. (2005) Nod2 mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing. Science 307: 734–738.
10. HampeJ, FrankeA, RosenstielP, TillA, TeuberM, et al. (2007) A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat Genet 39: 207–211.
11. TravassosLH, CarneiroLA, RamjeetM, HusseyS, KimYG, et al. (2010) Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry. Nat Immunol 11: 55–62.
12. CooneyR, BakerJ, BrainO, DanisB, PichulikT, et al. (2010) NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation. Nat Med 16: 90–97.
13. Hindorff LA, MacArthur J, Morales J, Junkins HA, Hall PN, et al. A catalog of published genome-wide association studies. Available: http://www.genome.gov/gwastudies/. Accessed 3 July 2013.
14. LiMJ, WangP, LiuX, LimEL, WangZ, et al. (2012) GWASdb: a database for human genetic variants identified by genome-wide association studies. Nucleic Acids Res 40: D1047–1054 Available: http://jjwanglab.org:8080/gwasdb/. Accessed 3 July 2013.
15. ZhangF, LiuH, ChenS, LowH, SunL, et al. (2011) Identification of two new loci at IL23R and RAB32 that influence susceptibility to leprosy. Nat Genet 43: 1247–1251.
16. ZhangFR, HuangW, ChenSM, SunLD, LiuH, et al. (2009) Genomewide association study of leprosy. N Engl J Med 361: 2609–2618.
17. GeD, FellayJ, ThompsonAJ, SimonJS, ShiannaKV, et al. (2009) Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance. Nature 461: 399–401.
18. ShiKQ, LiuWY, LinXF, FanYC, ChenYP, et al. (2012) Interleukin-28B polymorphisms on the SVR in the treatment of naive chronic hepatitis C with pegylated interferon-alpha plus ribavirin: a meta-analysis. Gene 507: 27–35.
19. UrbanT, CharltonMR, GoldsteinDB (2012) Introduction to the genetics and biology of interleukin-28B. Hepatology 56: 361–366.
20. HillAV (2012) Evolution, revolution and heresy in the genetics of infectious disease susceptibility. Philos Trans R Soc Lond B Biol Sci 367: 840–849.
21. KleinC, LohmannK, ZieglerA (2012) The promise and limitations of genome-wide association studies. JAMA 308: 1867–1868.
22. TebitDM, ArtsEJ (2011) Tracking a century of global expansion and evolution of HIV to drive understanding and to combat disease. Lancet Infect Dis 11: 45–56.
23. StrangerBE, NicaAC, ForrestMS, DimasA, BirdCP, et al. (2007) Population genomics of human gene expression. Nat Genet 39: 1217–1224.
24. ZellerT, WildP, SzymczakS, RotivalM, SchillertA, et al. (2010) Genetics and beyond–the transcriptome of human monocytes and disease susceptibility. PLoS ONE 5: e10693 doi:10.1371/journal.pone.0010693
25. Degner JF, Bell JT, Pritchard JK. eQTL Browser. Available: http://eqtl.uchicago.edu/cgi-bin/gbrowse/eqtl/. Accessed 3 July 2013.
26. CermakT, DoyleEL, ChristianM, WangL, ZhangY, et al. (2011) Efficient design and assembly of custom TALEN and other TAL effector-based constructs for DNA targeting. Nucleic Acids Res 39: e82.
27. CossartP, BoquetP, NormarkS, RappuoliR (1996) Cellular microbiology emerging. Science 271: 315–316.
28. KoDC, ShuklaKP, FongC, WasnickM, BrittnacherMJ, et al. (2009) A genome-wide in vitro bacterial-infection screen reveals human variation in the host response associated with inflammatory disease. Am J Hum Genet 85: 214–227.
29. BergsbakenT, FinkSL, CooksonBT (2009) Pyroptosis: host cell death and inflammation. Nat Rev Microbiol 7: 99–109.
30. KoDC, GamazonER, ShuklaKP, PfuetznerRA, WhittingtonD, et al. (2012) Functional genetic screen of human diversity reveals that a methionine salvage enzyme regulates inflammatory cell death. Proc Natl Acad Sci U S A 109: E2343–E2352.
31. LoeuilletC, DeutschS, CiuffiA, RobyrD, TafféP, et al. (2008) In vitro whole-genome analysis identifies a susceptibility locus for HIV-1. PLoS Biol 6: e32 doi:10.1371/journal.pbio.0060032
32. HuangRS, DuanS, BleibelWK, KistnerEO, ZhangW, et al. (2007) A genome-wide approach to identify genetic variants that contribute to etoposide-induced cytotoxicity. Proc Natl Acad Sci U S A 104: 9758–9763.
33. WenY, GorsicLK, WheelerHE, ZiliakDM, HuangRS, et al. (2011) Chemotherapeutic-induced apoptosis: a phenotype for pharmacogenomics studies. Pharmacogenet Genomics 21: 476–488.
34. WheelerHE, GamazonER, WingC, NjiajuUO, NjokuC, et al. (2013) Integration of cell line and clinical trial genome-wide analyses supports a polygenic architecture of Paclitaxel-induced sensory peripheral neuropathy. Clin Cancer Res 19: 491–499.
35. FumagalliM, SironiM, PozzoliU, Ferrer-AdmetllaA, PattiniL, et al. (2011) Signatures of environmental genetic adaptation pinpoint pathogens as the main selective pressure through human evolution. PLoS Genet 7: e1002355 doi:10.1371/journal.pgen.1002355
Štítky
Hygiena a epidemiológia Infekčné lekárstvo LaboratóriumČlánok vyšiel v časopise
PLOS Pathogens
2013 Číslo 8
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