Author

Callan L Buechsenschuetz

The Francis Crick InstituteORCID 0000-0002-2613-0933Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Developmental Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Approach:statistical model· 1

Frequent Co-Authors

Ambrosius P. SnijdersiD· 1 shared Angelina S Norris· 1 shared Claudio BussiiD· 1 shared Darryl HaywardiD· 1 shared Dorota Gibbins· 1 shared Elizabeth FisheriD· 1 shared Emmanuel DeauiD· 1 shared Eva Lana‐ElolaiD· 1 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 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

1 shared paperDevelopmental Biology

Ambrosius P. SnijdersORCID

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Developmental BiologybioRxivPreprintSep 18, 2023

Congenital heart defects in Down syndrome are caused by increased dosage of DYRK1A

Eva Lana‐Elola, Rifdat Aoidi, Miriam Llorian…·Victor L. J. Tybulewicz

The paper shows increased DYRK1A dosage causes mitochondrial dysfunction and congenital heart defects in Down syndrome, which can be mitigated by a DYRK1A inhibitor.

DOI 10.1101/2023.09.18.558244

humanmouse

𝕏 PostBluesky

NeuroscienceeLifePeer-reviewedNov 1, 2021

A novel, ataxic mouse model of Ataxia Telangiectasia caused by a clinically relevant nonsense mutation

H. Daniel Perez, May F. Abdallah, Jose I Chavira…·Paul J. Mathews

This paper describes a novel mouse model of Ataxia Telangiectasia with a nonsense mutation in Atm, showing ataxia, cerebellar defects, and potential therapeutic response to SMRT compounds.

28 citations

mouseexperimental assay

𝕏 PostBluesky