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Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
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Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
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Gregor Mendel's work (1822 - 1884) was primarily focused on pea plants. Through his initial experiments, he determined that every gene in a diploid cell has two variants called alleles inherited from each parent. He suggested that amongst these two alleles, one allele is dominant in character and the other recessive. The combination of alleles determines the phenotype of a gene in an organism.
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The human genome is over 99.9% identical between individuals, yet genetic differences exist at millions of bases. The human genome contains approximately 3 million variant positions per individual, many of which are heterozygous, contributing to genetic diversity and individual traits. Genetic variations include single-nucleotide polymorphisms (SNPs), insertions, deletions, and copy number variations (CNVs).SNPs, the most common variation, involve single-base changes in DNA. These can be...
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Human Genetics

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Related Experiment Video

Updated: Jul 14, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

Published on: November 1, 2015

Current status of lupus genetics.

Andrea L Sestak1, Swapan K Nath, Amr H Sawalha

  • 1Oklahoma Medical Research Foundation, Arthritis and Immunology Research Program, 825 NE 13th St, Oklahoma City, Oklahoma 73104, USA. andrea-sestak@omrf.ouhsc.edu

Arthritis Research & Therapy
|May 19, 2007
PubMed
Summary

Over 100 genetic risk factors for systemic lupus erythematosus have been identified in the last 40 years. This review covers known, disputed, and future discoveries in lupus genetics.

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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
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Published on: November 1, 2015

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Area of Science:

  • Immunogenetics
  • Rheumatology

Background:

  • Systemic lupus erythematosus (SLE) is a complex autoimmune disease with a significant genetic component.
  • Over 100 genetic risk factors for SLE have been identified over the past four decades.

Purpose of the Study:

  • To review the current state of knowledge regarding genetic risk factors for SLE.
  • To highlight areas of consensus and controversy in lupus genetics.
  • To identify future research directions in the field of SLE pathogenesis.

Main Methods:

  • Review of published literature on SLE genetics.
  • Analysis of findings from case studies, family linkage studies, and case-control genetic association studies.
  • Synthesis of data from global patient cohorts.

Main Results:

  • Numerous genes associated with SLE pathogenesis have been identified, including HLA-DR, FCGR3A, PTPN22, CTLA4, and MBL.
  • While many associations have been reported, replication across diverse populations remains a challenge.
  • Significant progress has been made in understanding the genetic architecture of SLE.

Conclusions:

  • A substantial number of genes contributing to SLE susceptibility and pathogenesis are likely identified.
  • Further research is needed to validate all reported associations and elucidate the functional roles of these genes.
  • Continued investigation into lupus genetics promises to yield deeper insights into disease mechanisms and potential therapeutic targets.