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Target intelligence / Profile preview
Male-specific lethal 1 complex subunit 1 (MSL1)
- Target
- MSL1
- Molecular classification
- Chromatin-associated scaffolding protein, Epigenetic regulator, Histone modification complex subunit
01
Overview
Male-specific lethal 1 complex subunit 1 (MSL1) is a crucial non-catalytic scaffolding component of the MSL complex, which mediates histone H4 acetylation at lysine 16 (H4K16ac), a modification essential for preventing chromatin compaction and enabling transcriptional upregulation of genes, especially those on the X chromosome in dosage-compensation pathways. MSL1 anchors other core complex members (MSL2, MSL3, KAT8/MOF) and facilitates their interaction, enhancing histone acetyltransferase activity within the complex, which maintains genome integrity and chromosomal stability. In Drosophila, MSL1 is essential for binding the complex to high-affinity sites on the male X chromosome, while in humans it participates in broader chromatin regulation. There is no direct evidence implicating MSL1 as a therapeutic target, nor are there drugs, biomarkers, or notable direct risks associated with perturbation of its function. It is studied largely for its role in epigenetic regulation and as a model for dosage compensation mechanisms.
- Other names
- Male-specific lethal 1 homologMSL1MSL1L1MSL-1MSL1-like 1hMSL1DKFZp686P24239Male-specific lethal 1-like 1Male-specific lethal-1 homolog 1
02
Mechanism of action
No drugs target MSL1; mechanism of action is via complex formation and scaffolding for histone acetylation.
03
Biological functions
Assembly and scaffolding of the MSL chromatin-modifying complexPromotion of histone H4 acetylation at lysine 16 (H4K16ac), preventing chromatin compaction and regulating gene expressionPositive regulation of X chromosome gene transcription (dosage compensation in some species)Genome stability and integrity maintenanceAdaptor activity for protein-protein interactions
04
Disease associations
Potential involvement in chromosome instabilityAssociation (not causation) with congenital myasthenic syndrome type 12Epigenetic dysregulation (theoretical, not established as a driver)
05
Safety considerations
No known safety concerns related to direct targeting; as a central chromatin regulator, hypothetical perturbation might broadly affect gene expression and chromatin structure.
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