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This study investigates the catalytic role of Histone Deacetylase 4 (HDAC4) in metabolic processes and cardiac function.

March 23, 2026Open Access

Shedding light on the catalytic activity of Histone Deacetylase 4 in the context of cardiac and metabolic phenotypes using a genetic approach

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Genetic manipulation of HDAC4 reveals its potential role in metabolic alterations in mice, suggesting further investigation is needed.

This study investigates the catalytic role of Histone Deacetylase 4 (HDAC4) in metabolic processes and cardiac function.
Generated HDAC4H968Y mouse model with specific genetic substitution.
Conducted in vitro experiments to assess enzyme activity of modified HDAC4.
Utilized cell-based assays to evaluate histone acetylation and localization.
Employed acetyl proteomics to identify potential HDAC4 target proteins.
The HDAC4H968Y mutation resulted in enhanced class I and class IIb HDAC activity but reduced class IIa activity.
No significant changes in global histone acetylation or transcriptional activity were observed.
Identified potential novel HDAC4 deacetylation targets.
Observed metabolic alterations in insulin and glucose tolerance in mutant mice.

Friederike Charlotte Schreiter (2026) studied this question.

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March 23, 2026Open Access

View Full Paper

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Authors

Genetic manipulation of HDAC4 reveals its potential role in metabolic alterations in mice, suggesting further investigation is needed.

This study investigates the catalytic role of Histone Deacetylase 4 (HDAC4) in metabolic processes and cardiac function.
Generated HDAC4H968Y mouse model with specific genetic substitution.
Conducted in vitro experiments to assess enzyme activity of modified HDAC4.
Utilized cell-based assays to evaluate histone acetylation and localization.
Employed acetyl proteomics to identify potential HDAC4 target proteins.
The HDAC4H968Y mutation resulted in enhanced class I and class IIb HDAC activity but reduced class IIa activity.
No significant changes in global histone acetylation or transcriptional activity were observed.
Identified potential novel HDAC4 deacetylation targets.
Observed metabolic alterations in insulin and glucose tolerance in mutant mice.

Friederike Charlotte Schreiter (2026) studied this question.

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