Claudia Huebner
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Claudia Huebner has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
- Brian L. Browning
Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, Washington, United States of America
3 shared publications Ivonne Petermann
Nutrigenomics New Zealand
3 shared publicationsLynnette R. Ferguson
Discipline of Nutrition, FM&HS, The University of Auckland, Auckland, New Zealand
3 shared publications- Murray Lindsay Barclay
Department of Medicine, University of Otago, Christchurch, New Zealand
3 shared publications - Richard Blair Gearry
Department of Medicine University of Otago Christchurch Christchurch New Zealand
3 shared publications - Andrew Neil Shelling
Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, The University of Auckland, Auckland 1142, New Zealand
2 shared publications
Latest Publications
- 1 February 2010
- Published by Oxford University Press (OUP) in Inflammatory Bowel Diseases
- Vol. 16 (2) , 282-295
Characterization of single-nucleotide polymorphisms relevant to inflammatory bowel disease in commonly used gastrointestinal cell lines
Background. The era of genome-wide association studies (GWAS) has led to the identification of many inflammatory bowel disease (IBD)–associated single-nucleoti
- 1 February 2010
- Published by Oxford University Press (OUP) in Inflammatory Bowel Diseases
- Vol. 16 (2) , 282-295
Characterization of single-nucleotide polymorphisms relevant to inflammatory bowel disease in commonly used gastrointestinal cell lines
Background. The era of genome-wide association studies (GWAS) has led to the identification of many inflammatory bowel disease (IBD)–associated single-nucleoti
- 1 December 2009
- Published by Oxford University Press (OUP) in Inflammatory Bowel Diseases
- Vol. 15 (12) , 1784-1793
Genetic analysis of MDR1 and inflammatory bowel disease reveals protective effect of heterozygous variants for ulcerative colitis
Background. Single nucleotide polymorphisms (SNPs) in the multidrug transporter MDR1 have been associated with inflammatory bowel disease (IBD) in different st
- 1 December 2009
- Published by Oxford University Press (OUP) in Inflammatory Bowel Diseases
- Vol. 15 (12) , 1784-1793
Genetic analysis of MDR1 and inflammatory bowel disease reveals protective effect of heterozygous variants for ulcerative colitis
Background. Single nucleotide polymorphisms (SNPs) in the multidrug transporter MDR1 have been associated with inflammatory bowel disease (IBD) in different st
- 9 March 2009
- Published by Elsevier in Human Immunology
- Vol. 70 (6) , 440-446
Interactions among genes influencing bacterial recognition increase IBD risk in a population-based New Zealand cohort
- 9 March 2009
- Published by Elsevier in Human Immunology
- Vol. 70 (6) , 440-446
Interactions among genes influencing bacterial recognition increase IBD risk in a population-based New Zealand cohort
- Open Access
- 1 January 2009
- Published by Springer Nature in BMC Research Notes
- Vol. 2 (1) , 52
Nucleotide-binding oligomerization domain containing 1 (NOD1) haplotypes and single nucleotide polymorphisms modify susceptibility to inflammatory bowel diseases in a New Zealand caucasian population: a case-control study
The nucleotide-binding oligomerization domain containing 1 (NOD1) gene encodes a pattern recognition receptor that senses pathogens, leading to downstream responses characteristic of innate immunity. We investigated the role of NOD1 single nucleotide polymorphisms (SNPs) on IBD risk in a New Zealand Caucasian population, and studied Nod1 expression in response to bacterial invasion in the Caco2 cell line. DNA samples from 388 Crohn's disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis patients and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common SNPs in NOD1, using the MassARRAY® iPLEX Gold assay. Transcriptional activation of the protein produced by NOD1 (Nod1) was studied after infection of Caco2 cells with Escherichia coli LF82. Carrying the rs2075818 G allele decreased the risk of CD (OR = 0.66, 95% CI = 0.50–0.88, p < 0.002) but not UC. There was an increased frequency of the three SNP (rs2075818, rs2075822, rs2907748) haplotype, CTG (p = 0.004) and a decreased frequency of the GTG haplotype (p = 0.02).in CD. The rs2075822 CT or TT genotypes were at an increased frequency (genotype p value = 0.02), while the rs2907748 AA or AG genotypes showed decreased frequencies in UC (p = 0.04), but not in CD. Functional assays showed that Nod1 is produced 6 hours after bacterial invasion of the Caco2 cell line. The NOD1 gene is important in signalling invasion of colonic cells by pathogenic bacteria, indicative of its' key role in innate immunity. Carrying specific SNPs in this gene significantly modifies the risk of CD and/or UC in a New Zealand Caucasian population.
- 1 January 2009
- Published by Springer Nature in BMC Research Notes
- Vol. 2 (1) , 52
Open AccessNucleotide-binding oligomerization domain containing 1 (NOD1) haplotypes and single nucleotide polymorphisms modify susceptibility to inflammatory bowel diseases in a New Zealand caucasian population: a case-control study
The nucleotide-binding oligomerization domain containing 1 (NOD1) gene encodes a pattern recognition receptor that senses pathogens, leading to downstream responses characteristic of innate immunity. We investigated the role of NOD1 single nucleotide polymorphisms (SNPs) on IBD risk in a New Zealand Caucasian population, and studied Nod1 expression in response to bacterial invasion in the Caco2 cell line. DNA samples from 388 Crohn's disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis patients and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common SNPs in NOD1, using the MassARRAY® iPLEX Gold assay. Transcriptional activation of the protein produced by NOD1 (Nod1) was studied after infection of Caco2 cells with Escherichia coli LF82. Carrying the rs2075818 G allele decreased the risk of CD (OR = 0.66, 95% CI = 0.50–0.88, p < 0.002) but not UC. There was an increased frequency of the three SNP (rs2075818, rs2075822, rs2907748) haplotype, CTG (p = 0.004) and a decreased frequency of the GTG haplotype (p = 0.02).in CD. The rs2075822 CT or TT genotypes were at an increased frequency (genotype p value = 0.02), while the rs2907748 AA or AG genotypes showed decreased frequencies in UC (p = 0.04), but not in CD. Functional assays showed that Nod1 is produced 6 hours after bacterial invasion of the Caco2 cell line. The NOD1 gene is important in signalling invasion of colonic cells by pathogenic bacteria, indicative of its' key role in innate immunity. Carrying specific SNPs in this gene significantly modifies the risk of CD and/or UC in a New Zealand Caucasian population.