Overview

rs9332701 is a genetic variant associated with Budd-chiari syndrome and Factor v deficiency.

This variant is located on chromosome 1. The variations at position 169515529 are the genetic letters A/A, G/G, A/G

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 rs9332701 there are 3 currently known genotypes : A/A, G/G or A/G

Short Overview

Variant Location

rs9332701 is located on gene in chromsome 1. Use the genome browser to explore the location of rs9332701 and its genetic neighbourhood.

Pharmacogenetics

We do not have any data that links rs9332701 to any drugs.

Diagnostics

rs9332701 is commonly tested together with other variants on the same gene.

Genome Browser

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. Explore more variants and their effects on the body by browsing left and right along the DNA strand.

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Did you know genetic variants affect drugs?

Mutations are changes in genes 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.

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Dr. Wallerstorfer

Conditions & Traits of rs9332701

The different genotypes of variant rs9332701 can affect the likelyhood of developing certain traits or conditions. Current research shows that 4 conditions and 0 traits are associated with rs9332701. The following table shows the relationship between genotypes and conditions and traits.

Did you know genetic variants affect drugs?

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.

doctor_quote

Dr. Wallerstorfer

Variant Table Legend

Clinical Testing

Scientific Studies

Biological Male Symbol

Biological Female Symbol

Unisex Symbol for both Genders

Classification of Variants

Variants can be classified either based on clinical tests or scientific studies. In the classification based on clinical tests, the variants are divided into five categories from Disease Causing (harmful) to No Effect (not harmful). This classification is based on family histories, laboratory tests and computer predictions and is intended to help doctors make medical decisions. The aim is to recognize the immediate health impact of variants on the human body. Classification based on scientific studies, however, is about understanding the long-term effects. It aims to identify the influence of genetic variants in conditions, traits, and evolution. Variants are classified into different categories based on their functional impact: Loss-of-Function (reduced gene activity), Gain-of-Function (increased gene activity), Neutral (no significant impact) and Evolutionary Conservation. This classification uses experimental data, population studies, and computational analyses.

Genotype

A

A

Level of evidence

No Effect

Unisex

1 Sources

Participants: 0

The genotype with the letters A/A is thought to have no effect on your disease risk. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

G

G

Level of evidence

Likely no effect

Unisex

1 Sources

Participants: 0

The genotype with the letters G/G is thought to have no effect on your disease risk. This means that the scientific evidence is still somewhat unclear about its effect. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

A

G

Level of evidence

Likely no effect

Unisex

1 Sources

Participants: 0

The genotype with the letters A/G is thought to have no effect on your disease risk. This means that the scientific evidence is still somewhat unclear about its effect. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

A

A

Level of evidence

No Effect

Unisex

1 Sources

Participants: 0

The genotype with the letters A/A is thought to have no effect on your disease risk. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

G

G

Level of evidence

No Effect

Unisex

1 Sources

Participants: 0

The genotype with the letters G/G is thought to have no effect on your disease risk. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

A

G

Level of evidence

No Effect

Unisex

1 Sources

Participants: 0

The genotype with the letters A/G is thought to have no effect on your disease risk. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

A

A

Level of evidence

No Effect

Unisex

1 Sources

Participants: 0

The genotype with the letters A/A is thought to have no effect on your disease risk. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

G

G

Level of evidence

No Effect

Unisex

1 Sources

Participants: 0

The genotype with the letters G/G is thought to have no effect on your disease risk. Carriers of this genetic result are usually not at risk of developing the disease.

Genotype

A

G

Level of evidence

No Effect

Unisex

1 Sources

Participants: 0

The genotype with the letters A/G is thought to have no effect on your disease risk. Carriers of this genetic result are usually not at risk of developing the disease.

Diagnostics

rs9332701 is commonly tested together with other variants on the same gene.

Related variants

Diseases and traits are often influenced by multiple genetic variants. To better understand how genetics affects certain diseases and traits, it is important to consider these additional factors. The following table shows other variants that are also associated with the same diseases and traits as rs9332701.

Genotype Distribution

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 9332701. 9332701.

The Genotype Distribution in the selected area is:
Legend:
Included regions
Excluded regions
no-data

Studies and Sources

All of the resources below examine variant rs9332701

Connecting genetic risk to disease end points through the human blood plasma proteome. (2/27/17)

Karsten Suhre, Matthias Arnold, Aditya Mukund Bhagwat, Richard J Cotton, Rudolf Engelke, Johannes Raffler, Hina Sarwath, Gaurav Thareja, Annika Wahl, Robert Kirk DeLisle, Larry Gold, Marija Pezer, Gordan Lauc, Mohammed A El-Din Selim, Dennis O Mook-Kanamori, Eman K Al-Dous, Yasmin A Mohamoud, Joel Malek, Konstantin Strauch, Harald Grallert, Annette Peters, Gabi Kastenmüller, Christian Gieger, Johannes Graumann

PubMed: 28240269
Genomic atlas of the human plasma proteome. (June 2018)

Benjamin B Sun, Joseph C Maranville, James E Peters, David Stacey, James R Staley, James Blackshaw, Stephen Burgess, Tao Jiang, Ellie Paige, Praveen Surendran, Clare Oliver-Williams, Mihir A Kamat, Bram P Prins, Sheri K Wilcox, Erik S Zimmerman, An Chi, Narinder Bansal, Sarah L Spain, Angela M Wood, Nicholas W Morrell, John R Bradley, Nebojsa Janjic, David J Roberts, Willem H Ouwehand, John A Todd, Nicole Soranzo, Karsten Suhre, Dirk S Paul, Caroline S Fox, Robert M Plenge, John Danesh, Heiko Runz, Adam S Butterworth

PubMed: 29875488
Mapping the proteo-genomic convergence of human diseases. (11/12/21)

Maik Pietzner, Eleanor Wheeler, Julia Carrasco-Zanini, Adrian Cortes, Mine Koprulu, Maria A Wörheide, Erin Oerton, James Cook, Isobel D Stewart, Nicola D Kerrison, Jian'an Luan, Johannes Raffler, Matthias Arnold, Wiebke Arlt, Stephen O'Rahilly, Gabi Kastenmüller, Eric R Gamazon, Aroon D Hingorani, Robert A Scott, Nicholas J Wareham, Claudia Langenberg

PubMed: 34648354
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