Supplemental Data The Rac1-GEF Tiam1 Couples the NMDA Receptor to the Activity-Dependent Development of Dendritic Arbors and Spines
نویسندگان
چکیده
Antibodies Tiam1 antibodies were purchased (Santa Cruz) or generated by immunizing rabbits with GST-Tiam1 PDZ (aa 840–1025). Specificity of the Tiam1 antibodies was tested with peptide competition experiments (data not shown) and confirmed with RNAi (Figures 4A and 7B). Antibodies against pPak were generated previously (Shamah et al., 2001). Antibodies against the following proteins were purchased: FLAG (Sigma); NR1 (Pharmingen and Affinity BioReagents); Rac1 (Upstate Biotechnology); myc (Santa Cruz); PSD-95 (Affinity BioReagents); NR2B and synapsin (Chemicon); and Pak1, pAkt (Ser473), Akt, pERK1/2 (Thr202/Tyr204), ERK1/2, and p4E-BP1 (Thr37/46) (Cell Signaling).
منابع مشابه
The Rac1-GEF Tiam1 Couples the NMDA Receptor to the Activity-Dependent Development of Dendritic Arbors and Spines
NMDA-type glutamate receptors play a critical role in the activity-dependent development and structural remodeling of dendritic arbors and spines. However, the molecular mechanisms that link NMDA receptor activation to changes in dendritic morphology remain unclear. We report that the Rac1-GEF Tiam1 is present in dendrites and spines and is required for their development. Tiam1 interacts with t...
متن کاملDynamic control of excitatory synapse development by a Rac1 GEF/GAP regulatory complex.
The small GTPase Rac1 orchestrates actin-dependent remodeling essential for numerous cellular processes including synapse development. While precise spatiotemporal regulation of Rac1 is necessary for its function, little is known about the mechanisms that enable Rac1 activators (GEFs) and inhibitors (GAPs) to act in concert to regulate Rac1 signaling. Here, we identify a regulatory complex comp...
متن کاملKalirin-7 Controls Activity-Dependent Structural and Functional Plasticity of Dendritic Spines
Activity-dependent rapid structural and functional modifications of central excitatory synapses contribute to synapse maturation, experience-dependent plasticity, and learning and memory and are associated with neurodevelopmental and psychiatric disorders. However, the signal transduction mechanisms that link glutamate receptor activation to intracellular effectors that accomplish structural an...
متن کاملThe adhesion-GPCR BAI1 regulates synaptogenesis by controlling the recruitment of the Par3/Tiam1 polarity complex to synaptic sites.
Excitatory synapses are polarized structures that primarily reside on dendritic spines in the brain. The small GTPase Rac1 regulates the development and plasticity of synapses and spines by modulating actin dynamics. By restricting the Rac1-guanine nucleotide exchange factor Tiam1 to spines, the polarity protein Par3 promotes synapse development by spatially controlling Rac1 activation. However...
متن کاملDifferential regulation of the Rac1 GTPase–activating protein (GAP) BCR during oxygen/glucose deprivation in hippocampal and cortical neurons
Brain ischemia causes oxygen and glucose deprivation (OGD) in neurons, triggering a cascade of events leading to synaptic accumulation of glutamate. Excessive activation of glutamate receptors causes excitotoxicity and delayed cell death in vulnerable neurons. Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are more vulnerable to injury than their cortical counterparts, bu...
متن کامل