rs6679677 is a genetic variant on gene PHTF1 associated with Arthritis and Giant cell arteritis.
This variant is located on chromosome 1. The variations at position 113761186 are the genetic letters A/A, C/C, A/C, C/T
Since humans have each twice (one from each parent), these letter-variations occur on both chromosomes. People can have the same or different letters on both chromosomes. Every person's individual variation combination is referred to as genotype. For variant rs6679677 there are 4 currently known genotypes : A/A, C/C, A/C or C/T
rs6679677 is located on gene PHTF1 in chromsome 1. Use the genome browser to explore the location of rs6679677 and its genetic neighbourhood.
rs6679677 affects the following conditions and traits:
rs6679677 affects the following conditions:
We do not have any data that links rs6679677 to any drugs.
rs6679677 is commonly tested together with other variants on the same gene.
This interactive browser visualizes what no human can see with the naked eye - our DNA. From a down to a specific position on a . The position you are looking at here is the exact location of variant rs on gene PHTF1. Explore more variants and their effects on the body by browsing left and right along the DNA strand.
Mutations are random changes in the DNA and genetic variations are differences in the DNA among people. Variants are tiny changes in just one piece of the DNA while haplotypes are groups of these changes that usually come together.
Dr. Wallerstorfer
The different genotypes of variant rs6679677 can affect the expression or likelyhood of developing certain traits or conditions. Current research shows that 6 conditions and 0 traits are associated with rs6679677. The following table shows the relationship between genotypes and conditions and traits.
Genetic variants can influence how our body reacts to certain drugs. The presence of specific genetic variants can increase or decrease the efficiency and effectiveness of a drug, impacting how well it works inside our system. Additionally, certain genetic variants can heighten or lessen the toxicity of a drug, thereby affecting the risk of unwanted side effects. They can also alter how a drug is metabolized, which influences the appropriate dosage one should receive.
Dr. Wallerstorfer
Clinical Testing
Scientific Studies
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Unisex Symbol for both Genders
Scientific studies classifications aim to uncover how genetic variants function and their roles in diseases, traits, and evolution. Variants are categorized based on their functional impact, such as loss-of-function (reduces gene activity), gain-of-function (increases gene activity), neutral (no significant impact), or evolutionary conservation. This classification uses experimental data, population studies, and computational analyses to understand variant effects. Unlike clinical testing, which focuses on immediate health impacts, scientific studies explore broader genetic mechanisms and long-term implications.
Genotype
A
A
Level of evidence
Increased likelihood
Unisex
2 Sources
Participants: 1337982
The genotype with the letters A/A is considered a risk factor for developing the disease. Carriers of this genetic result are at increased risk of developing the disease.
Genotype
A
C
Level of evidence
Increased likelihood
Unisex
2 Sources
Participants: 1337982
The genotype with the letters A/C is considered a risk factor for developing the disease. Carriers of this genetic result are at increased risk of developing the disease.
Genotype
A
A
Level of evidence
Increased likelihood
Unisex
2 Sources
Participants: 1337982
The genotype with the letters A/A is considered a risk factor for developing the disease. Carriers of this genetic result are at increased risk of developing the disease.
Genotype
A
C
Level of evidence
Increased likelihood
Unisex
2 Sources
Participants: 1337982
The genotype with the letters A/C is considered a risk factor for developing the disease. Carriers of this genetic result are at increased risk of developing the disease.
The genetic variant rs6679677 impacts how certain medications work in the body. This difference may cause some of us to require different dosage amounts to achieve the desired effects, while others might experience more apparent side-effects. As a result, healthcare providers may need to adjust prescriptions for those individuals with rs6679677. Ultimately, understanding our genetic makeup helps improve the overall effectiveness and usability of medications. Tailoring treatments based on genetics ensures a safer, more personalized healthcare experience.
rs6679677 is commonly tested together with other variants on the same gene.
Conditions and traits are often affected by more than one variant. It is important to understand these other factors to get a better understanding of how genetics affect certain conditions and traits. The following grid shows other variants that affect the same conditions and traits as rs6679677.
Knowing your genome can actually tell you a lot about your ancestors.
The prevalence of the different genotypes is based on the native inhabitants of a region. In the map below you see how common each genotype is in the native inhabitants of those regions. Since genetic material is passed down form generation to generation, your DNA shows traces of the geographical origins of your ancestors.
This data is based on “The 1000 Genomes Project” which established one of the most detailed overviews of human genetic variations across the globe. The regions are broadly categorized into five continental groups: Africa, America, Europe, South Asia and East Asia. All continental groups together display the global prevalence. Click through the regions, to learn more about the local prevalence of the possible genotypes.
At present, there is no distribution data available for SNP 6679677. 6679677.
All of the resources below examine variant rs
Bettina Mieth, Alexandre Rozier, Juan Antonio Rodriguez, Marina M C Höhne, Nico Görnitz, Klaus-Robert Müller
Xiangyu Ge, Mojca Frank-Bertoncelj, Kerstin Klein, Amanda McGovern, Tadeja Kuret, Miranda Houtman, Blaž Burja, Raphael Micheroli, Chenfu Shi, Miriam Marks, Andrew Filer, Christopher D. Buckley, Gisela Orozco, Oliver Distler, Andrew P. Morris, Paul Martin, Stephen Eyre, Caroline Ospelt
Daniel Ho, Denis M. Nyaga, William Schierding, Richard Saffery, Jo K. Perry, John A. Taylor, Mark H. Vickers, Andreas W. Kempa-Liehr, Justin M. O’Sullivan