Author

Indraneel Banerjee

Royal Manchester Children's HospitalORCID 0000-0003-4280-7470Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Genetic & Genomic Medicine· 3

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:human· 3 Approach:statistical model· 3 Research Focus:variant calling· 2 Assay:whole-exome sequencing· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1

Frequent Co-Authors

Jayne HoughtoniD· 3 shared Matthew Neil WakelingiD· 3 shared Sarah Elizabeth FlanaganiD· 3 shared Antonia DastamaniiD· 2 shared Birgit M. Rami-MerhariD· 2 shared Elisa De FrancoiD· 2 shared Jasmin J. HopkinsiD· 2 shared Jonna M. E. MännistöiD· 2 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

3 shared papersGenetic & Genomic Medicine

Jayne HoughtonORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Genetic & Genomic MedicineEBioMedicinePeer-reviewedMay 25, 2026

Low-level mosaic variants causing the pancreatic disease congenital hyperinsulinism can be detected from blood DNA

Jasmin J Bennett, Thomas W. Laver, Jonna M. E. Männistö…·Sarah Elizabeth Flanagan

This study detects low-level mosaic variants in blood DNA from individuals with congenital hyperinsulinism using tNGS and confirms them with ddPCR.

DOI 10.1016/j.ebiom.2026.106308

humanwhole-exome sequencing

𝕏 PostBluesky

Genetic & Genomic MedicineEuropean Journal of Human GeneticsPeer-reviewedApr 11, 2024

Chromosome 20p11.2 deletions cause congenital hyperinsulinism via the likely disruption of FOXA2

Thomas William Laver, Matthew Neil Wakeling, Richard C. Caswell…·Sarah Elizabeth Flanagan

The paper identifies chromosome 20p11.2 deletions as a cause of congenital hyperinsulinism by disrupting FOXA2 expression in pancreatic beta-cells.

7 citations

humanwhole-exome sequencing

𝕏 PostBluesky

Genetic & Genomic MedicineNature GeneticsPeer-reviewedNov 1, 2022

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…·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.

66 citationstop 1%

humanbulk RNA-seq

𝕏 PostBluesky