Shu-Min Chou
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Shu-Min Chou has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
Ain Nur Ali
Genome Institute of Singapore (GIS), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore
1 shared publication- Bruno Reversade
Laboratory of Human Genetics and Therapeutics, King Abdullah University of Science and Technology, Thuwal 23955, Kingdom of Saudi Arabia
1 shared publication - Carine Bonnard
Skin Research Institute of Singapore (SRIS), A*STAR, Singapore, Singapore
1 shared publication Fang Yuan
Program in Neuroscience & Behavioral Disorders, Duke-NUS Medical School, Singapore, Singapore
1 shared publicationGunaseelan Narayanan
Program in Neuroscience & Behavioral Disorders, Duke-NUS Medical School, Singapore, Singapore
1 shared publication- Haofei Wang
McAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, USA
1 shared publication
Latest Publications
- Open Access
- 19 March 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
IVNS1ABP mutation drives cellular senescence in newly identified progeroid neuropathy
We identified a new progeroid syndrome with severe neuropathy and intellectual deficits but its underlying cellular and molecular mechanism is unknown. Exome sequencing revealed a homozygous mutation in the IVNS1ABP gene, which encodes IVNS1ABP, an influenza virus non-structural protein-1 binding protein. To investigate disease mechanisms, we generated isogenic induced pluripotent stem cells (iPSCs) from patient fibroblasts and differentiated them into neural progenitor cells (NPCs). Mutant IVNS1ABP fibroblasts, iPSCs, and NPCs exhibited defective cytokinesis, increased DNA damage, and premature cellular senescence. Consistent with these findings, cerebral organoids showed early differentiation of NPCs into neurons. Molecular profiling as well as biochemical and cellular analysis revealed altered binding of mutant IVNS1ABP to actin / actin-associated proteins and dysregulated actin dynamics during cytokinesis. Taken together, we propose that mutant IVNS1ABP dysregulates actin polymerization and organization which is at least partly responsible for the cellular senescence phenotypes in this progeroid neuropathy.
- 19 March 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
Open AccessIVNS1ABP mutation drives cellular senescence in newly identified progeroid neuropathy
We identified a new progeroid syndrome with severe neuropathy and intellectual deficits but its underlying cellular and molecular mechanism is unknown. Exome sequencing revealed a homozygous mutation in the IVNS1ABP gene, which encodes IVNS1ABP, an influenza virus non-structural protein-1 binding protein. To investigate disease mechanisms, we generated isogenic induced pluripotent stem cells (iPSCs) from patient fibroblasts and differentiated them into neural progenitor cells (NPCs). Mutant IVNS1ABP fibroblasts, iPSCs, and NPCs exhibited defective cytokinesis, increased DNA damage, and premature cellular senescence. Consistent with these findings, cerebral organoids showed early differentiation of NPCs into neurons. Molecular profiling as well as biochemical and cellular analysis revealed altered binding of mutant IVNS1ABP to actin / actin-associated proteins and dysregulated actin dynamics during cytokinesis. Taken together, we propose that mutant IVNS1ABP dysregulates actin polymerization and organization which is at least partly responsible for the cellular senescence phenotypes in this progeroid neuropathy.