<div is a human gene whose product dLC1 (Deleted in Liver Cancer 1) is a GTPase-activating protein (GAP) that specifically inactivates Rho family GTPases, primarily RhoA, Rac1, and Cdc42. Through GAP activity, DLC1 regulates actin cytoskeleton dynamics, cell adhesion, migration, and proliferation. This page covers the gene's normal function, disease associations, expression patterns, and key research findings relevant to neurodegeneration. [1]
DLC1 (Deleted in Liver Cancer 1) is a GTPase-activating protein (GAP) that specifically inactivates Rho family GTPases, primarily RhoA, Rac1, and Cdc42. Through GAP activity, DLC1 regulates actin cytoskeleton dynamics, cell adhesion, migration, and proliferation.
In neurons, DLC1 plays critical roles in axonal guidance, dendritic spine morphology, and synaptic plasticity. It is enriched in growth cones and regulates actin polymerization necessary for neurite outgrowth.
DLC1 is a tumor suppressor frequently deleted in cancers, and its loss contributes to increased cell motility and invasion.
Parkinson's Disease:
Huntington's Disease:
Other:
Expressed in multiple brain regions including cortex, hippocampus, cerebellum, and substantia nigra. Highest in neurons with particular enrichment in dendritic spines.
No DLC1-targeted therapeutics. Rho kinase (ROCK) inhibitors under investigation for neuroprotection.