GeneSet Information

Tier III GS75690 • P values for microsatellite markers located intragenically or in the immediate vicinity of represented genes associated with Crohn's disease

DESCRIPTION:

P values were generated using three different procedures as described in the methods' section. Briefly, data were analysed by means of contingency tables, initially comparing allele distributions represented by the AIF (after analyses with pooled DNA), then after summation of alleles < 5% in order to focus on the major alleles and, finally, after comparison of each single allele between the control and patient cohorts.

LABEL:

MicroSat Mark Cr.Dis.

SCORE TYPE:

P-Value

DATE ADDED:

2010-06-28

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

Wagenleiter SE, Jagiello P, Akkad DA, Arning L, Griga T, Klein W, Epplen JT

TITLE:

On the genetic involvement of apoptosis-related genes in Crohn's disease as revealed by an extended association screen using 245 markers: no evidence for new predisposing factors.

JOURNAL:

Journal of negative results in biomedicine Nov 2005, Vol 4, pp. 8

ABSTRACT:

Crohn's disease (CD) presents as an inflammatory barrier disease with characteristic destructive processes in the intestinal wall. Although the pathomechanisms of CD are still not exactly understood, there is evidence that, in addition to e.g. bacterial colonisation, genetic predisposition contributes to the development of CD. In order to search for predisposing genetic factors we scrutinised 245 microsatellite markers in a population-based linkage mapping study. These microsatellites cover gene loci the encoded protein of which take part in the regulation of apoptosis and (innate) immune processes. Respective loci contribute to the activation/suppression of apoptosis, are involved in signal transduction and cell cycle regulators or they belong to the tumor necrosis factor superfamily, caspase related genes or the BCL2 family. Furthermore, several cytokines as well as chemokines were included. The approach is based on three steps: analyzing pooled DNAs of patients and controls, verification of significantly differing microsatellite markers by genotyping individual DNA samples and, finally, additional reinvestigation of the respective gene in the region covered by the associated microsatellite by analysing single-nucleotide polymorphisms (SNPs). Using this step-wise process we were unable to demonstrate evidence for genetic predisposition of the chosen apoptosis- and immunity-related genes with respect to susceptibility for CD. PUBMED: 16318629
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Annotation Information

No sequence read archive data associated with this GeneSet.


Social Control, Formal (D012926)
Tumor Necrosis Factor-alpha (D014409)
Alleles (D000483)
Family (D005190)
Humans (D006801)
DNA (D004247)
Cytokines (D016207)
Chromosome Mapping (D002874)
Patients (D010361)
Nuclear Proteins (D009687)
Genetic Markers (D005819)
B-Cell Maturation Antigen (D053301)
Tables (D020501)
Microsatellite Repeats (D018895)
Neoplasms (D009369)
Genetic Predisposition to Disease (D020022)
Trans-Activators (D015534)
Genotype (D005838)
Cells (D002477)
Methods (D008722)
Causality (D015984)
Crohn Disease (D003424)
Chemokines (D018925)
Signal Transduction (D015398)
Polymorphism, Single Nucleotide (D020641)
Association (D001244)
Cell Cycle (D002453)
Necrosis (D009336)
Apoptosis (D017209)
necrosis (MP:0001651)
cell (GO:0005623)
transduction (GO:0009293)
signal transduction (GO:0007165)
cell cycle (GO:0007049)

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Supported by NIH R01 AA18776 jointly funded by NIAAA and NIDA, and JAX Center for Precision Genetics NIH U54 OD 020351