期刊
NEURON
卷 29, 期 1, 页码 229-242出版社
CELL PRESS
DOI: 10.1016/S0896-6273(01)00193-3
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资金
- NIDA NIH HHS [DA-00266] Funding Source: Medline
- NIDDK NIH HHS [DK-32948] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R56DK032948, R37DK032948, R01DK032948] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [P50DA000266] Funding Source: NIH RePORTER
Spine function requires precise control of the actin cytoskeleton. Kalirin-7, a GDP/GTP exchange factor for Rad, interacts with PDZ proteins such as PSD-95, colocalizing with PSD-95 at synapses of cultured hippocampal neurons. PSD-95 and Kalirin-7 interact in vivo and in heterologous expression systems. In primary cortical neurons, transfected Kalirin-7 is targeted to spines and increases the number and size of spine-like structures. A Kalirin-7 mutant unable to interact with PDZ proteins remains in the cell soma, inducing local formation of aberrant filopodial neurites. Kalirin-7 with an inactivated GEF domain reduces the number of spines below control levels. These results provide evidence that PDZ proteins target Kalirin-7 to the PSD, where it regulates dendritic morphogenesis through Rad signaling to the actin cytoskeleton.
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