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Knockout and knock-in mouse models to study purinergic signaling

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

Standard

Knockout and knock-in mouse models to study purinergic signaling. / Rumney, Robin Mark Howard; Gorecki, Darek.

Purinergic Signalling: Methods and Protocols. ed. / Pablo Pelegrín. Springer, 2020. p. 17-43 (Methods in Molecular Biology; Vol. 2041).

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

Harvard

Rumney, RMH & Gorecki, D 2020, Knockout and knock-in mouse models to study purinergic signaling. in P Pelegrín (ed.), Purinergic Signalling: Methods and Protocols. Methods in Molecular Biology, vol. 2041, Springer, pp. 17-43. https://doi.org/10.1007/978-1-4939-9717-6_2

APA

Rumney, R. M. H., & Gorecki, D. (2020). Knockout and knock-in mouse models to study purinergic signaling. In P. Pelegrín (Ed.), Purinergic Signalling: Methods and Protocols (pp. 17-43). (Methods in Molecular Biology; Vol. 2041). Springer. https://doi.org/10.1007/978-1-4939-9717-6_2

Vancouver

Rumney RMH, Gorecki D. Knockout and knock-in mouse models to study purinergic signaling. In Pelegrín P, editor, Purinergic Signalling: Methods and Protocols. Springer. 2020. p. 17-43. (Methods in Molecular Biology). https://doi.org/10.1007/978-1-4939-9717-6_2

Author

Rumney, Robin Mark Howard ; Gorecki, Darek. / Knockout and knock-in mouse models to study purinergic signaling. Purinergic Signalling: Methods and Protocols. editor / Pablo Pelegrín. Springer, 2020. pp. 17-43 (Methods in Molecular Biology).

Bibtex

@inbook{22cf54acf52d41eab13cabf5c08e3c2b,
title = "Knockout and knock-in mouse models to study purinergic signaling",
abstract = "Purinergic signaling involves extracellular purines and pyrimidines acting upon specific cell surface purinoceptors classified into the P1, P2X, and P2Y families for nucleosides and nucleotides. This widespread signaling mechanism is active in all major tissues and influences a range of functions in health and disease. Orthologs to all but one of the human purinoceptors have been found in mouse, making this laboratory animal a useful model to study their function. Indeed, analyses of purinoceptors via knock-in or knockout approaches to produce gain or loss of function phenotypes have revealed several important therapeutic targets. None of the homozygous purinoceptor knockouts proved to be developmentally lethal, which suggest that either these receptors are not involved in key developmental processes or that the large number of receptors in each family allowed for functional compensation. Different models for the same purinoceptor often show compatible phenotypes but there have been examples of significant discrepancies. These revealed unexpected differences in the structure of human and mouse genes and emphasized the importance of the genetic background of different mouse strains. In this chapter, we provide an overview of the current knowledge and new trends in the modifications of purinoceptor genes in vivo. We discuss the resulting phenotypes, their applications and relative merits and limitations of mouse models available to study purinoceptor subtypes.",
keywords = "knock-in, knockout, genetically modified animals, purinergic signaling, purinoceptor",
author = "Rumney, {Robin Mark Howard} and Darek Gorecki",
year = "2020",
month = "1",
doi = "10.1007/978-1-4939-9717-6_2",
language = "English",
isbn = "978-1-4939-9716-9",
series = "Methods in Molecular Biology",
publisher = "Springer",
pages = "17--43",
editor = "Pablo Pelegr{\'i}n",
booktitle = "Purinergic Signalling: Methods and Protocols",

}

RIS

TY - CHAP

T1 - Knockout and knock-in mouse models to study purinergic signaling

AU - Rumney, Robin Mark Howard

AU - Gorecki, Darek

PY - 2020/1

Y1 - 2020/1

N2 - Purinergic signaling involves extracellular purines and pyrimidines acting upon specific cell surface purinoceptors classified into the P1, P2X, and P2Y families for nucleosides and nucleotides. This widespread signaling mechanism is active in all major tissues and influences a range of functions in health and disease. Orthologs to all but one of the human purinoceptors have been found in mouse, making this laboratory animal a useful model to study their function. Indeed, analyses of purinoceptors via knock-in or knockout approaches to produce gain or loss of function phenotypes have revealed several important therapeutic targets. None of the homozygous purinoceptor knockouts proved to be developmentally lethal, which suggest that either these receptors are not involved in key developmental processes or that the large number of receptors in each family allowed for functional compensation. Different models for the same purinoceptor often show compatible phenotypes but there have been examples of significant discrepancies. These revealed unexpected differences in the structure of human and mouse genes and emphasized the importance of the genetic background of different mouse strains. In this chapter, we provide an overview of the current knowledge and new trends in the modifications of purinoceptor genes in vivo. We discuss the resulting phenotypes, their applications and relative merits and limitations of mouse models available to study purinoceptor subtypes.

AB - Purinergic signaling involves extracellular purines and pyrimidines acting upon specific cell surface purinoceptors classified into the P1, P2X, and P2Y families for nucleosides and nucleotides. This widespread signaling mechanism is active in all major tissues and influences a range of functions in health and disease. Orthologs to all but one of the human purinoceptors have been found in mouse, making this laboratory animal a useful model to study their function. Indeed, analyses of purinoceptors via knock-in or knockout approaches to produce gain or loss of function phenotypes have revealed several important therapeutic targets. None of the homozygous purinoceptor knockouts proved to be developmentally lethal, which suggest that either these receptors are not involved in key developmental processes or that the large number of receptors in each family allowed for functional compensation. Different models for the same purinoceptor often show compatible phenotypes but there have been examples of significant discrepancies. These revealed unexpected differences in the structure of human and mouse genes and emphasized the importance of the genetic background of different mouse strains. In this chapter, we provide an overview of the current knowledge and new trends in the modifications of purinoceptor genes in vivo. We discuss the resulting phenotypes, their applications and relative merits and limitations of mouse models available to study purinoceptor subtypes.

KW - knock-in

KW - knockout

KW - genetically modified animals

KW - purinergic signaling

KW - purinoceptor

U2 - 10.1007/978-1-4939-9717-6_2

DO - 10.1007/978-1-4939-9717-6_2

M3 - Chapter (peer-reviewed)

SN - 978-1-4939-9716-9

T3 - Methods in Molecular Biology

SP - 17

EP - 43

BT - Purinergic Signalling: Methods and Protocols

A2 - Pelegrín, Pablo

PB - Springer

ER -

ID: 16025733