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Your search keyword '"Foote, S.J."' showing total 3 results
Start Over Author "Foote, S.J." Publisher nature publishing group
3 results on '"Foote, S.J."'

1. Several alleles of the multidrug-resistance gene are closely linked to chloroquine resistance in Plasmodium falciparum

Author

Foote, S.J., Kyle, D.E., Martin, R.K., Oduola, A.M.J., Forsyth, K., Kemp, D.J., and Cowman, A.F.

Subjects
Drug resistance -- Research, Antimalarials -- Research, Malaria -- Drug therapy, Chloroquine -- Research, Plasmodium falciparum -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Chloroquine is the drug most frequently used to treat malaria, but in many areas of the world, the parasite Plasmodium falciparum, which causes malaria, has become resistant to chloroquine. It has been shown that chloroquine-resistant parasites can rid themselves of chloroquine, using a protein which functions as a transporter molecule. A similar protein has been identified in the resistance of cancer cells to many different types of drugs; this protein is encoded by the gene mdr. A homologue to mdr has been found in Plasmodium falciparum, and there are multiple copies of the gene in chloroquine-resistant isolates. The genes from different isolates have been sequenced, and mutations, or changes, have been found compared with genes from isolates that are sensitive to chloroquine. However, resistance to chloroquine does not occur as frequently as it would if the resistance was simply due to the inheritance of the one mutated gene. The inheritance of the mutated mdr gene is necessary, but not sufficient, for drug resistance. Therefore, it is thought that more than one gene is needed for the resistance of Plasmodium falciparum to chloroquine to occur. Further study is need to identify the other genes and how they interact with the transporter protein gene. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

2. Genome-wide association study identifies new multiple sclerosis susceptibility loci on chromosomes 12 and 20

Author

Bahlo, M., Booth, D.R., Broadley, S.A., Brown, M.A., Foote, S.J., Griffiths, L.R., Kilpatrick, T.J., Lechner-Scott, J., Moscato, P., Perreau, V.M., Rubio, J.P., Scott, R.J., Stankovich, J., Stewart, G.J., Taylor, B.V., Wiley, J., Clarke, G., Cox, M.B., Csurhes, P.A., Danoy, P., Drysdale, K., Field, J., Greer, J.M., Guru, P., Hadler, J., McMorran, B.J., Jensen, C.J., Johnson, L.J., McCallum, R., Merriman, M., Merriman, T., Pryce, K., Tajouri, L., Wilkins, E.J., Browning, B.L., Browning, S.R., Perera, D., Broadley, S., Butzkueven, H., Carroll, W.M., Chapman, C., Kermode, A.G., Marriott, M., Mason, D., Heard, R.N., Pender, M.P., Slee, M., Tubridy, N., Willoughby, E., Bahlo, M., Booth, D.R., Broadley, S.A., Brown, M.A., Foote, S.J., Griffiths, L.R., Kilpatrick, T.J., Lechner-Scott, J., Moscato, P., Perreau, V.M., Rubio, J.P., Scott, R.J., Stankovich, J., Stewart, G.J., Taylor, B.V., Wiley, J., Clarke, G., Cox, M.B., Csurhes, P.A., Danoy, P., Drysdale, K., Field, J., Greer, J.M., Guru, P., Hadler, J., McMorran, B.J., Jensen, C.J., Johnson, L.J., McCallum, R., Merriman, M., Merriman, T., Pryce, K., Tajouri, L., Wilkins, E.J., Browning, B.L., Browning, S.R., Perera, D., Broadley, S., Butzkueven, H., Carroll, W.M., Chapman, C., Kermode, A.G., Marriott, M., Mason, D., Heard, R.N., Pender, M.P., Slee, M., Tubridy, N., and Willoughby, E.

Abstract

To identify multiple sclerosis (MS) susceptibility loci, we conducted a genome-wide association study (GWAS) in 1,618 cases and used shared data for 3,413 controls. We performed replication in an independent set of 2,256 cases and 2,310 controls, for a total of 3,874 cases and 5,723 controls. We identified risk-associated SNPs on chromosome 12q13–14 (rs703842, P = 5.4 times 10-11; rs10876994, P = 2.7 times 10-10; rs12368653, P = 1.0 times 10-7) and upstream of CD40 on chromosome 20q13 (rs6074022, P = 1.3 times 10-7; rs1569723, P = 2.9 times 10-7). Both loci are also associated with other autoimmune diseases1, 2, 3, 4, 5. We also replicated several known MS associations (HLA-DR15, P = 7.0 times 10-184; CD58, P = 9.6 times 10-8; EVI5-RPL5, P = 2.5 times 10-6; IL2RA, P = 7.4 times 10-6; CLEC16A, P = 1.1 times 10-4; IL7R, P = 1.3 times 10-3; TYK2, P = 3.5 times 10-3) and observed a statistical interaction between SNPs in EVI5-RPL5 and HLA-DR15 (P = 0.001).

Published
2009

3. Replication of KIAA0350, IL2RA, RPL5 and CD58 as multiple sclerosis susceptibility genes in Australian.

Author

Rubio, J.P., Stankovich, J., Field, J., Tubridy, N., Marriott, M., Chapman, C., Bahlo, M., Perera, D., Johnson, L.J., Tait, B.D., Varney, M.D., Speed, T.P., Taylor, B.V., Foote, S.J., Butzkueven, H., Kilpatrick, T.J., Rubio, J.P., Stankovich, J., Field, J., Tubridy, N., Marriott, M., Chapman, C., Bahlo, M., Perera, D., Johnson, L.J., Tait, B.D., Varney, M.D., Speed, T.P., Taylor, B.V., Foote, S.J., Butzkueven, H., and Kilpatrick, T.J.

Abstract

A recent genome-wide association study (GWAS) conducted by the International Multiple Sclerosis Genetics Consortium (IMSGC) identified a number of putative MS susceptibility genes. Here we have performed a replication study in 1134 Australian MS cases and 1265 controls for 17 risk-associated single nucleotide polymorphisms (SNPs) reported by the IMSGC. Of 16 SNPs that passed quality control filters, four, each corresponding to a different non-human leukocyte antigen (HLA) gene, were associated with disease susceptibility: KIAA0350 (rs6498169) P=0.001, IL2RA (rs2104286) P=0.033, RPL5 (rs6604026) P=0.041 and CD58 (rs12044852) P=0.042. There was no association (P=0.58) between rs6897932 in the IL7R gene and the risk of MS. No interactions were detected between the replicated IMSGC SNPs and HLA-DRB1*15, gender, disease course, disease progression or age-at-onset. We used a novel Bayesian approach to estimate the extent to which our data increased or decreased evidence for association with the six most-associated IMSGC loci. These analyses indicated that even modest P-values, such as those reported here, can contribute markedly to the posterior probability of ‘true’ association in replication studies. In conclusion, these data provide support for the involvement of four non-HLA genes in the pathogenesis of MS, and combined with previous data, increase to genome-wide significance (P=3 × 10−8) evidence of an association between KIAA0350 and risk of disease.

Published
2008

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