Author

Samar Sabir Hassan

ORCID 0000-0002-9741-3383Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Organism:human· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Andrew Tym HattersleyiD· 2 shared Elisa De FrancoiD· 2 shared Matthew B. JohnsoniD· 2 shared Matthew Neil WakelingiD· 2 shared Nick D. L. OwensiD· 2 shared Sarah Elizabeth FlanaganiD· 2 shared Sian EllardiD· 2 shared Abdelhadi M. HabebiD· 1 shared

Activity by Year

2022-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersGenetic & Genomic Medicine

Andrew Tym HattersleyORCID

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2 papers

Recent·Most cited

Primate-specific ZNF808 is essential for pancreatic development in humans

Elisa De Franco, Nick D. L. Owens, Hossam Montaser, Matthew Neil Wakeling, Jonna Saarimäki‐Vire, Athina Triantou, Hazem Ibrahim, Diego Balboa, Richard C. Caswell, Rachel E. Jennings, Jouni Kvist, Matthew B. Johnson, Sachin Muralidharan, Sian Ellard, Caroline Fiona Wright, , Michaël Imbeault

The paper identifies homozygous loss of function variants in ZNF808 as a cause of pancreatic agenesis in humans, showing its role in repressing transposable elements during pancreatic development.

Nature Genetics · Nov 16, 2023Peer-reviewedGenetic & Genomic Medicine

A novel disease mechanism leading to the expression of a disallowed gene in the pancreatic beta-cell identified by non-coding, regulatory mutations controlling HK1

Matthew Neil Wakeling, Nick D. L. Owens, Jessica R. Hopkinson, Matthew B. Johnson, Jayne Houghton, Antonia Dastamani, Christine S. Flaxman, Rebecca C. Wyatt, Thomas I. Hewat, Jasmin J. Hopkins, Thomas William Laver, Rachel van Heugten, Michael N. Weedon, Elisa De Franco, Kashyap Amratlal Patel, , Sarah Elizabeth Flanagan

The paper identifies non-coding mutations in a regulatory element of HK1 that lead to inappropriate expression in pancreatic beta-cells and cause congenital hyperinsulinism.

Nature Genetics · Nov 1, 2022Peer-reviewedGenetic & Genomic Medicine