Pharmacogenomics of GPCR Drug Targets

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Pharmacogenomics of GPCR Drug Targets. / Hauser, Alexander Sebastian; Chavali, Sreenivas; Masuho, Ikuo; Jahn, Leonie; Martemyanov, Kirill; Gloriam, David E.; Babu, Madan.

In: Cell, Vol. 172, 01.2018, p. 41–54.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Hauser, AS, Chavali, S, Masuho, I, Jahn, L, Martemyanov, K, Gloriam, DE & Babu, M 2018, 'Pharmacogenomics of GPCR Drug Targets', Cell, vol. 172, pp. 41–54. https://doi.org/10.1016/j.cell.2017.11.033

APA

Hauser, A. S., Chavali, S., Masuho, I., Jahn, L., Martemyanov, K., Gloriam, D. E., & Babu, M. (2018). Pharmacogenomics of GPCR Drug Targets. Cell, 172, 41–54. https://doi.org/10.1016/j.cell.2017.11.033

Vancouver

Hauser AS, Chavali S, Masuho I, Jahn L, Martemyanov K, Gloriam DE et al. Pharmacogenomics of GPCR Drug Targets. Cell. 2018 Jan;172:41–54. https://doi.org/10.1016/j.cell.2017.11.033

Author

Hauser, Alexander Sebastian ; Chavali, Sreenivas ; Masuho, Ikuo ; Jahn, Leonie ; Martemyanov, Kirill ; Gloriam, David E. ; Babu, Madan. / Pharmacogenomics of GPCR Drug Targets. In: Cell. 2018 ; Vol. 172. pp. 41–54.

Bibtex

@article{a705b9e8e14341bca9ef43becd6c9adf,
title = "Pharmacogenomics of GPCR Drug Targets",
abstract = "Natural genetic variation in the human genome is a cause of individual differences in responses to medications and is an underappreciated burden on public health. Although 108 G-protein-coupled receptors (GPCRs) are the targets of 475 (∼34%) Food and Drug Administration (FDA)-approved drugs and account for a global sales volume of over 180 billion US dollars annually, the prevalence of genetic variation among GPCRs targeted by drugs is unknown. By analyzing data from 68,496 individuals, we find that GPCRs targeted by drugs show genetic variation within functional regions such as drug- and effector-binding sites in the human population. We experimentally show that certain variants of μ-opioid and Cholecystokinin-A receptors could lead to altered or adverse drug response. By analyzing UK National Health Service drug prescription and sales data, we suggest that characterizing GPCR variants could increase prescription precision, improving patients{\textquoteright} quality of life, and relieve the economic and societal burden due to variable drug responsiveness.",
author = "Hauser, {Alexander Sebastian} and Sreenivas Chavali and Ikuo Masuho and Leonie Jahn and Kirill Martemyanov and Gloriam, {David E.} and Madan Babu",
year = "2018",
month = jan,
doi = "10.1016/j.cell.2017.11.033",
language = "English",
volume = "172",
pages = "41–54",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",

}

RIS

TY - JOUR

T1 - Pharmacogenomics of GPCR Drug Targets

AU - Hauser, Alexander Sebastian

AU - Chavali, Sreenivas

AU - Masuho, Ikuo

AU - Jahn, Leonie

AU - Martemyanov, Kirill

AU - Gloriam, David E.

AU - Babu, Madan

PY - 2018/1

Y1 - 2018/1

N2 - Natural genetic variation in the human genome is a cause of individual differences in responses to medications and is an underappreciated burden on public health. Although 108 G-protein-coupled receptors (GPCRs) are the targets of 475 (∼34%) Food and Drug Administration (FDA)-approved drugs and account for a global sales volume of over 180 billion US dollars annually, the prevalence of genetic variation among GPCRs targeted by drugs is unknown. By analyzing data from 68,496 individuals, we find that GPCRs targeted by drugs show genetic variation within functional regions such as drug- and effector-binding sites in the human population. We experimentally show that certain variants of μ-opioid and Cholecystokinin-A receptors could lead to altered or adverse drug response. By analyzing UK National Health Service drug prescription and sales data, we suggest that characterizing GPCR variants could increase prescription precision, improving patients’ quality of life, and relieve the economic and societal burden due to variable drug responsiveness.

AB - Natural genetic variation in the human genome is a cause of individual differences in responses to medications and is an underappreciated burden on public health. Although 108 G-protein-coupled receptors (GPCRs) are the targets of 475 (∼34%) Food and Drug Administration (FDA)-approved drugs and account for a global sales volume of over 180 billion US dollars annually, the prevalence of genetic variation among GPCRs targeted by drugs is unknown. By analyzing data from 68,496 individuals, we find that GPCRs targeted by drugs show genetic variation within functional regions such as drug- and effector-binding sites in the human population. We experimentally show that certain variants of μ-opioid and Cholecystokinin-A receptors could lead to altered or adverse drug response. By analyzing UK National Health Service drug prescription and sales data, we suggest that characterizing GPCR variants could increase prescription precision, improving patients’ quality of life, and relieve the economic and societal burden due to variable drug responsiveness.

U2 - 10.1016/j.cell.2017.11.033

DO - 10.1016/j.cell.2017.11.033

M3 - Journal article

C2 - 29249361

VL - 172

SP - 41

EP - 54

JO - Cell

JF - Cell

SN - 0092-8674

ER -

ID: 186780451