Overview

rs1544935 is a genetic variant associated with Urolithiasis and Myocardial infarction.

This variant is located on chromosome 6. The variations at position 39156672 are the genetic letters G/G, T/T, G/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 rs1544935 there are 3 currently known genotypes : G/G, T/T or G/T

Short Overview

Variant Location

rs1544935 is located on gene in chromsome 6. Use the genome browser to explore the location of rs1544935 and its genetic neighbourhood.

Conditions & Traits

rs1544935 affects the following conditions and traits:

Pathogenicity

rs1544935 affects the following conditions:

Pharmacogenetics

We do not have any data that links rs1544935 to any drugs.

Diagnostics

rs1544935 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.

Loading Genome Browser...

Did you know genetic variants affect drugs?

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.

doctor_quote

Dr. Wallerstorfer

Conditions & Traits of rs1544935

The different genotypes of variant rs1544935 can affect the expression or likelyhood of developing certain traits or conditions. Current research shows that 2 conditions and 0 traits are associated with rs1544935. 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

Variant Classification based on Scientific Studies

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

G

G

Level of evidence

No Effect

Unisex

1 Sources

Participants: 178726

No available data

Genotype

G

T

Level of evidence

No Effect

Unisex

1 Sources

Participants: 178726

No available data

Genotype

G

G

Level of evidence

No Effect

Unisex

1 Sources

Participants: 178726

No available data

Genotype

G

T

Level of evidence

No Effect

Unisex

1 Sources

Participants: 178726

No available data

Pharmacogenetics

The genetic variant rs1544935 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 rs1544935. 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.

Drugs related to rs1544935

All drugs that are linked to rs1544935 are listed here.

Diagnostics

rs1544935 is commonly tested together with other variants on the same gene.

Related variants

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 rs1544935.

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 1544935. 1544935.

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 rs

Novel Risk Loci Identified in a Genome-Wide Association Study of Urolithiasis in a Japanese Population (May 2019)

Chizu Tanikawa, Yoichiro Kamatani, Chikashi Terao, Masayuki Usami, Atsushi Takahashi, Yukihide Momozawa, Kichiya Suzuki, Soichi Ogishima, Atsushi Shimizu, Mamoru Satoh, Keitaro Matsuo, Haruo Mikami, Mariko Naito, Kenji Wakai, Taiki Yamaji, Norie Sawada, Motoki Iwasaki, Shoichiro Tsugane, Kenjiro Kohri, Alan S.L. Yu, Takahiro Yasui, Yoshinori Murakami, Michiaki Kubo, Koichi Matsuda

PMC: 6493984
A comprehensive 1,000 Genomes-based genome-wide association meta-analysis of coronary artery disease. (October 2015)

Majid Nikpay, Anuj Goel, Hong-Hee Won, Leanne M Hall, Christina Willenborg, Stavroula Kanoni, Danish Saleheen, Theodosios Kyriakou, Christopher P Nelson, Jemma C Hopewell, Thomas R Webb, Lingyao Zeng, Abbas Dehghan, Maris Alver, Sebastian M Armasu, Kirsi Auro, Andrew Bjonnes, Daniel I Chasman, Shufeng Chen, Ian Ford, Nora Franceschini, Christian Gieger, Christopher Grace, Stefan Gustafsson, Jie Huang, Shih-Jen Hwang, Yun Kyoung Kim, Marcus E Kleber, King Wai Lau, Xiangfeng Lu, Yingchang Lu, Leo-Pekka Lyytikäinen, Evelin Mihailov, Alanna C Morrison, Natalia Pervjakova, Liming Qu, Lynda M Rose, Elias Salfati, Richa Saxena, Markus Scholz, Albert V Smith, Emmi Tikkanen, Andre Uitterlinden, Xueli Yang, Weihua Zhang, Wei Zhao, Mariza de Andrade, Paul S de Vries, Natalie R van Zuydam, Sonia S Anand, Lars Bertram, Frank Beutner, George Dedoussis, Philippe Frossard, Dominique Gauguier, Alison H Goodall, Omri Gottesman, Marc Haber, Bok-Ghee Han, Jianfeng Huang, Shapour Jalilzadeh, Thorsten Kessler, Inke R König, Lars Lannfelt, Wolfgang Lieb, Lars Lind, Cecilia M Lindgren, Marja-Liisa Lokki, Patrik K Magnusson, Nadeem H Mallick, Narinder Mehra, Thomas Meitinger, Fazal-Ur-Rehman Memon, Andrew P Morris, Markku S Nieminen, Nancy L Pedersen, Annette Peters, Loukianos S Rallidis, Asif Rasheed, Maria Samuel, Svati H Shah, Juha Sinisalo, Kathleen E Stirrups, Stella Trompet, Laiyuan Wang, Khan S Zaman, Diego Ardissino, Eric Boerwinkle, Ingrid B Borecki, Erwin P Bottinger, Julie E Buring, John C Chambers, Rory Collins, L Adrienne Cupples, John Danesh, Ilja Demuth, Roberto Elosua, Stephen E Epstein, Tõnu Esko, Mary F Feitosa, Oscar H Franco, Maria Grazia Franzosi, Christopher B Granger, Dongfeng Gu, Vilmundur Gudnason, Alistair S Hall, Anders Hamsten, Tamara B Harris, Stanley L Hazen, Christian Hengstenberg, Albert Hofman, Erik Ingelsson, Carlos Iribarren, J Wouter Jukema, Pekka J Karhunen, Bong-Jo Kim, Jaspal S Kooner, Iftikhar J Kullo, Terho Lehtimäki, Ruth J F Loos, Olle Melander, Andres Metspalu, Winfried März, Colin N Palmer, Markus Perola, Thomas Quertermous, Daniel J Rader, Paul M Ridker, Samuli Ripatti, Robert Roberts, Veikko Salomaa, Dharambir K Sanghera, Stephen M Schwartz, Udo Seedorf, Alexandre F Stewart, David J Stott, Joachim Thiery, Pierre A Zalloua, Christopher J O'Donnell, Muredach P Reilly, Themistocles L Assimes, John R Thompson, Jeanette Erdmann, Robert Clarke, Hugh Watkins, Sekar Kathiresan, Ruth McPherson, Panos Deloukas, Heribert Schunkert, Nilesh J Samani, Martin Farrall

PubMed: 26343387
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