Abstract
Spine morphogenesis and plasticity are intimately linked to cognition, and there is strong evidence that aberrant regulation of spine plasticity is associated with physiological, behavioral, and pathological conditions. The neuronal guanine nucleotide exchange factor (GEF) kalirin is emerging as a key regulator of structural and functional plasticity at dendritic spines. Here, we review recent studies that have genetically and functionally linked kalirin signaling to a number of human disorders. Kalirin signaling may thus represent a disease mechanism and provide a novel therapeutic target.
Publication types
-
Research Support, N.I.H., Extramural
-
Review
MeSH terms
-
Alzheimer Disease / genetics
-
Alzheimer Disease / metabolism
-
Alzheimer Disease / physiopathology
-
Animals
-
Dendritic Spines / metabolism
-
Dendritic Spines / pathology
-
Guanine Nucleotide Exchange Factors / deficiency
-
Guanine Nucleotide Exchange Factors / genetics
-
Guanine Nucleotide Exchange Factors / physiology*
-
Humans
-
Protein Serine-Threonine Kinases / deficiency
-
Protein Serine-Threonine Kinases / genetics
-
Protein Serine-Threonine Kinases / physiology*
-
Schizophrenia / genetics
-
Schizophrenia / metabolism
-
Schizophrenia / physiopathology
-
Signal Transduction / genetics*
-
Structure-Activity Relationship
-
Synaptic Transmission / genetics
Substances
-
Guanine Nucleotide Exchange Factors
-
KALRN protein, human
-
Protein Serine-Threonine Kinases