Related Experiment Video

Updated: Apr 3, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α
11:27

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

9.6K

Association between NF-κBI and NF-κBIA polymorphisms and coronary artery disease

Serdal Arslan1, Özge Korkmaz2, Nil Özbilüm3

  • 1Department of Medical Biology, Cumhuriyet University, 58140 Sivas, Turkey.

Biomedical Reports
|September 26, 2015
PubMed

Insights

The NF-κB1 -94 DD genotype is linked to an increased risk of developing coronary artery disease (CAD). This finding highlights a potential genetic marker for CAD susceptibility.

Area of Science:

  • Genetics
  • Cardiovascular Disease
  • Molecular Biology

Background:

  • Coronary artery disease (CAD) remains a primary global cause of mortality.
  • Nuclear factor-kappa B (NF-κB) is a crucial transcription factor regulating cellular processes.
  • Genetic variations in NF-κB pathway genes may influence CAD susceptibility.

Purpose of the Study:

  • To investigate the association between polymorphisms in the NF-κB1 -94 gene and the NF-κBIA 3'-untranslated region (3'-UTR) with coronary artery disease (CAD).
  • To determine if specific genotypes or haplotypes of these genes are risk factors for CAD development.

Main Methods:

  • Case-control study involving 226 CAD patients and 201 healthy controls.
  • Genotyping of NF-κB1 -94 W/D and NF-κBIA 3'-UTR A→G polymorphisms.
  • Statistical analysis including allele and genotype frequencies, linkage disequilibrium, and haplotype analysis.

Main Results:

  • No significant association was found for the NF-κBIA 3'-UTR A→G polymorphism.
  • A significantly higher frequency of the D allele and DD genotype of NF-κB1 -94 was observed in CAD patients compared to controls (P=0.028).
  • Close linkage between the two genes was detected, with AD and GD haplotypes significantly associated with CAD risk (P<0.001; P=0.015, respectively).

Conclusions:

  • The NF-κB1 -94 DD genotype is identified as a significant risk factor for the development of coronary artery disease.
  • The findings suggest a potential role for NF-κB1 genetic variations in CAD pathogenesis.
  • Further research is warranted to explore the functional mechanisms underlying this association.

Keywords:
coronary artery diseasegenetic polymorphismnuclear factor-κB1nuclear factor-κBIA

More Related Videos

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.9K
NF-&#954;B-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

11.3K

Related Concept Videos

NF-&#954;B-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
10.3K
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

2.5K
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
8.9K
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
1.6K
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
767
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
112