Pseudokinase-converting mutation in protein kinase C alpha drives chordoid glioma by pathway rewiring

C Charlotte Bellamy (Institut du Cerveau, Paris Brain Institute (ICM, CNRS, Inria, Inserm), équipe labellisée Ligue Nationale contre le Cancer, Hôpital de la Pitié Salpêtrière, Sorbonne Université) H Hannah Tovell T Tiffany H. Kao A Alexandr Kornev (LSP Consulting LLC) Q Quentin Letourneur (Assistance Publique - Hôpitaux de Paris, Sorbonne Université, Site de Recherche Intégrée sur le Cancer Curamus) J Janan Arslan (Institut du Cerveau, Paris Brain Institute (ICM, CNRS, Inria, Inserm), équipe labellisée Ligue Nationale contre le Cancer, Hôpital de la Pitié Salpêtrière, Sorbonne Université) S Selina Schwaighofer (Institute of Molecular Biology and Center for Molecular Biosciences (CMBI), University of Innsbruck) T Timothy R. Baffi (Department of Pharmacology, University of California, San Diego) F Florent Dingli (CurieCoreTech Mass Spectrometry Proteomics, Institut Curie, Paris Sciences Lettres (PSL) Research University) D Damarys Loew J Julie Lerond (Institut du Cerveau, Paris Brain Institute (ICM, CNRS, Inria, Inserm), équipe labellisée Ligue Nationale contre le Cancer, Hôpital de la Pitié Salpêtrière, Sorbonne Université) S Stephane Liva (Inserm, U900, Institute Curie) B Brigitte Izac (CNRS, INSERM, Institut Cochin, Université Paris Cité) M Muriel Andrieu (Université Paris Cité, CNRS UMR 8104, Inserm U1016) H Homa Adle-Biassette (Assistance Publique - Hôpitaux de Paris, Hôpital Lariboisière, Department of Pathology) J Jean-Vianney Barnier (CNRS, Institut des Neurosciences Paris-Saclay, Université Paris-Saclay) E Eduard Stefan (Institute of Molecular Biology and Center for Molecular Biosciences (CMBI), University of Innsbruck) S Susan S. Taylor M Marc Sanson A Alexandra C. Newton F Franck Bielle

Abstract

Chordoid glioma (ChG) is a rare, low-grade brain tumor characterized by a novel recurrent point mutation, D463H, in the kinase domain of protein kinase C alpha (PKCα). The mutation is invariably an Asp to His substitution, suggesting a unique function beyond catalytic inactivation associated with other cancer-associated PKCα mutations. Here, we show that this mutation converts PKCα into a pseudokinase, abolishing catalytic activity, and, additionally, confers novel scaffolding functions. Activity assays in vitro and in cellulo revealed that PKCα D463H is catalytically inactive and functions as a dominant-negative to suppress endogenous PKC activity. Molecular dynamics simulations predicted that mutation to His, but not Asn, not only destabilizes the active site, but stabilizes the substrate-binding helices in the kinase C-lobe to potentially promote aberrant interactions. Supporting this, phosphoproteomic, proximity labeling, and coimmunoprecipitation mass spectrometry data from cells overexpressing PKCα D463H identified both altered phosphorylation of substrates and binding to multiple proteins involved in cell–cell junctions compared to WT enzyme. Last, single nuclei RNAseq established that ChG derives from specialized tanycytes. Our data reveal that this disease-defining, fully penetrant mutation converts PKCα into a pseudokinase with novel scaffold functions that uniquely rewire the cellular interactome to impair cell junction function.

Article Details

Volume / Issue Vol. 123, Issue 29
Published July 21, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (21)

C

Charlotte Bellamy

Institut du Cerveau, Paris Brain Institute (ICM, CNRS, Inria, Inserm), équipe labellisée Ligue Nationale contre le Cancer, Hôpital de la Pitié Salpêtrière, Sorbonne Université

H

Hannah Tovell

T

Tiffany H. Kao

A

Alexandr Kornev

LSP Consulting LLC

Q

Quentin Letourneur

Assistance Publique - Hôpitaux de Paris, Sorbonne Université, Site de Recherche Intégrée sur le Cancer Curamus

J

Janan Arslan

Institut du Cerveau, Paris Brain Institute (ICM, CNRS, Inria, Inserm), équipe labellisée Ligue Nationale contre le Cancer, Hôpital de la Pitié Salpêtrière, Sorbonne Université

S

Selina Schwaighofer

Institute of Molecular Biology and Center for Molecular Biosciences (CMBI), University of Innsbruck

T

Timothy R. Baffi

Department of Pharmacology, University of California, San Diego

F

Florent Dingli

CurieCoreTech Mass Spectrometry Proteomics, Institut Curie, Paris Sciences Lettres (PSL) Research University

D

Damarys Loew

J

Julie Lerond

Institut du Cerveau, Paris Brain Institute (ICM, CNRS, Inria, Inserm), équipe labellisée Ligue Nationale contre le Cancer, Hôpital de la Pitié Salpêtrière, Sorbonne Université

S

Stephane Liva

Inserm, U900, Institute Curie

B

Brigitte Izac

CNRS, INSERM, Institut Cochin, Université Paris Cité

M

Muriel Andrieu

Université Paris Cité, CNRS UMR 8104, Inserm U1016

H

Homa Adle-Biassette

Assistance Publique - Hôpitaux de Paris, Hôpital Lariboisière, Department of Pathology

J

Jean-Vianney Barnier

CNRS, Institut des Neurosciences Paris-Saclay, Université Paris-Saclay

E

Eduard Stefan

Institute of Molecular Biology and Center for Molecular Biosciences (CMBI), University of Innsbruck

S

Susan S. Taylor

M

Marc Sanson

A

Alexandra C. Newton

F

Franck Bielle