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Zamara Mariam

As seen in: MDPI, Science Magazine, BioRxiv
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Articles

In vivo functional profiling and structural characterization of the human GLP1R A316T variant

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By Seungmin Shin, Na Wu, Liliane El Eid, Yusman Manchanda, Gregory Austin, Kieran Deane-Alder, Roxana-Maria Rujan, Zamara Mariam, Affiong I. Oqua, Matthew Belousoff, Kyle W Sloop, Guy A. Rutter, àlex Montoya, Dominic J. Withers, Steven J. Millers
| Science Magazine Verified
Abstract Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective therapies for type 2 diabetes (T2D) and obesity, yet patient responses are variable, with GLP1R gene variation potentially linked to therapeutic outcomes. A GLP1R natural missense variant, A316T, protects against T2D and cardiovascular disease. Here, we generated and characterized a human GLP1R A316T mouse model.
Open in Who Shared Issue with article?

In vivo functional profiling and structural characterisation of the human Glp1r A316T variant

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By Liliane El Eid, Kieran Deane-Alder, Roxana-Maria Rujan, Zamara Mariam
| BioRxiv
Abstract Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective therapies for type 2 diabetes (T2D) and obesity, yet patient responses are variable. Variation in the human Glp1r gene might be directly linked to therapeutic responses. A naturally occurring missense variant, A316T, protects against T2D and cardiovascular disease. Here, we have generated and characterised a human Glp1r A316T mouse model.
Open in Who Shared Issue with article?

In vivo functional profiling and structural characterisation of the human Glp1r A316T variant

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By Liliane El Eid, Kieran Deane-Alder, Roxana-Maria Rujan, Zamara Mariam
| BioRxiv
Abstract Glucagon-like peptide-1 receptor (GLP-1R) agonists (GLP-1RAs) are a highly effective therapy class for type 2 diabetes (T2D) and obesity, yet there are variable patient responses. Variation in the human Glp1r gene leading to altered receptor structure, signal transduction, and function might be directly linked to variable therapeutic responses in patients.
Open in Who Shared Issue with article?
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