Identifying genetic susceptibility factors for tuberculosis in Africans: a combined approach using a candidate gene study and a genome-wide screen

2000 ◽  
Vol 98 (3) ◽  
pp. 245 ◽  
Author(s):  
Richard BELLAMY
2017 ◽  
Vol 30 (20) ◽  
pp. 2433-2439 ◽  
Author(s):  
Tsegaselassie Workalemahu ◽  
Daniel A. Enquobahrie ◽  
Mahlet G. Tadesse ◽  
Karin Hevner ◽  
Bizu Gelaye ◽  
...  

2015 ◽  
Vol 113 (04) ◽  
pp. 772-781 ◽  
Author(s):  
Jason H. Karnes ◽  
Robert M. Cronin ◽  
Jerome Rollin ◽  
Alexander Teumer ◽  
Claire Pouplard ◽  
...  

SummaryHeparin-induced thrombocytopenia (HIT) is an unpredictable, potentially catastrophic adverse effect of heparin treatment resulting from an immune response to platelet factor 4 (PF4)/heparin complexes. No genome-wide evaluations have been performed to identify potential genetic influences on HIT. Here, we performed a genome-wide association study (GWAS) and candidate gene study using HIT cases and controls identified using electronic medical records (EMRs) coupled to a DNA biobank and attempted to replicate GWAS associations in an independent cohort. We subsequently investigated influences of GWAS-associated single nucleotide polymorphisms (SNPs) on PF4/heparin antibodies in non-heparin treated individuals. In a recessive model, we observed significant SNP associations (odds ratio [OR] 18.52; 95% confidence interval [CI] 6.33-54.23; p=3.18×10-9) with HIT near the T-Cell Death-Associated Gene 8 (TDAG8). These SNPs are in linkage disequilibrium with a missense TDAG8 SNP. TDAG8 SNPs trended toward an association with HIT in replication analysis (OR 5.71; 0.47-69.22; p=0.17), and the missense SNP was associated with PF4/heparin antibody levels and positive PF4/heparin antibodies in non-heparin treated patients (OR 3.09; 1.14-8.13; p=0.02). In the candidate gene study, SNPs at HLA-DRA were nominally associated with HIT (OR 0.25; 0.15-0.44; p=2.06×10-6). Further study of TDAG8 and HLA-DRA SNPs is warranted to assess their influence on the risk of developing HIT.


2001 ◽  
Vol 120 (5) ◽  
pp. A468-A468 ◽  
Author(s):  
G GALLAGHER ◽  
P CHONG ◽  
J ESKDALE ◽  
A COOK ◽  
S CAIMS ◽  
...  

2021 ◽  
Vol 22 (2) ◽  
pp. 870
Author(s):  
Liang Ma ◽  
Yali Sun ◽  
Xinsen Ruan ◽  
Pei-Cheng Huang ◽  
Shi Wang ◽  
...  

Gibberella stalk rot (GSR) by Fusarium graminearum causes significant losses of maize production worldwide. Jasmonates (JAs) have been broadly known in regulating defense against pathogens through the homeostasis of active JAs and COI-JAZ-MYC function module. However, the functions of different molecular species of JAs and COI-JAZ-MYC module in maize interactions with Fusarium graminearum and regulation of diverse metabolites remain unknown. In this study, we found that exogenous application of MeJA strongly enhanced resistance to GSR. RNA-seq analysis showed that MeJA activated multiple genes in JA pathways, which prompted us to perform a genome-wide screening of key JA signaling components in maize. Yeast Two-Hybrid, Split-Luciferase, and Pull-down assays revealed that the JA functional and structural mimic coronatine (COR) functions as an essential ligand to trigger the interaction between ZmCOIa and ZmJAZ15. By deploying CRISPR-cas9 knockout and Mutator insertional mutants, we demonstrated that coi1a mutant is more resistant, whereas jaz15 mutant is more susceptible to GSR. Moreover, JA-deficient opr7-5opr8-2 mutant displayed enhanced resistance to GSR compared to wild type. Together, these results provide strong evidence that ZmJAZ15 plays a pivotal role, whereas ZmCOIa and endogenous JA itself might function as susceptibility factors, in maize immunity to GSR.


1994 ◽  
Vol 4 (3) ◽  
pp. 373
Author(s):  
R.R. Crowe ◽  
Z.W. Wang ◽  
D.W. Black ◽  
N.C. Andreasen ◽  
J. Gelernter ◽  
...  

Author(s):  
Paula L Hedley ◽  
Ole Haundrup ◽  
Paal S Andersen ◽  
Frederik H Aidt ◽  
Morten Jensen ◽  
...  

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