Author

Chandran Ka

InsermORCID 0009-0007-9183-325XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Genetics· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 2 Approach:statistical model· 2 Research Focus:differential expression· 1 Assay:DNA methylation· 1

Frequent Co-Authors

Gérald Le GaciD· 2 shared Ahmad ElbahnsiiD· 1 shared Arnaud BoullingiD· 1 shared Claude FéreciD· 1 shared Claude HoudayeriD· 1 shared D.N. CooperiD· 1 shared Emmanuelle MassoniD· 1 shared Isabelle Berlivet· 1 shared

Activity by Year

2019-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

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2 shared papersMolecular Biology

Gérald Le GacORCID

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2 papers

Recent·Most cited

Insights into the role of glycerophospholipids on the iron export function of SLC40A1 and the molecular mechanisms of ferroportin disease.

Rim Debbiche, Ahmad Elbahnsi, Kévin Uguen, Chandran Ka, Isabelle Callebaut, Gérald Le Gac

The paper investigates how glycerophospholipids influence SLC40A1 conformational changes and identifies key residues linked to ferroportin disease.

The FASEB Journal · Jul 3, 2024Peer-reviewedMolecular Biology

First estimation of the scale of canonical 5’ splice site GT>GC mutations generating wild-type transcripts and their medical genetic implications

Jin‐Huan Lin, Xin‐Ying Tang, Arnaud Boulling, Wen‐Bin Zou, Emmanuelle Masson, Yann Fichou, Loann Raud, Marlène Le Tertre, Shun‐Jiang Deng, Isabelle Berlivet, Chandran Ka, Matthew E. Mort, Matthew Hayden, Raphaël Leman, Claude Houdayer, , Jian‐Min Chen

The paper estimates that 15-18% of canonical GT 5' splice sites can generate wild-type transcripts when mutated to GC, with implications for disease and splicing mechanisms.

Human Mutation · May 27, 2019Peer-reviewedGenetics