Papers using
synapsin I
antibodies
Autolytic transition of mu-calpain upon activation as resolved by antibodies distinguishing between the pre- and post-autolysis forms.Okazawa Hitoshi, In PLoS ONE, 1991
... Temecula, CA), mouse anti-Tuj1 (1∶2000, Covance, Princeton, NJ), rabbit anti-GFAP (1∶500, DAKO, Carpinteria, CA), rabbit anti-Synapsin I (1∶500, Millipore), mouse anti-Cux1 (1∶100, Abnova, Taipei, Taiwan), rabbit anti-Satb2 ...
Papers on
synapsin I
Ganglioside GQ1b induces dopamine release through the activation of Pyk2.Chen et al., Beijing, China. In Mol Cell Neurosci, Jan 2016
Further studies revealed that activated Pyk2 stimulated ERK1/2 and p-38, while only the ERK1/2 activation was indispensable for GQ1b induced DA release, which interacted with Synapsin I directly and led to its phosphorylation, then depolymerization of F-actin, thus contributed to DA release.
Glutamate Release.Ueda et al., Charlottesville, United States. In Neurochem Res, Dec 2015
Glutamate-loaded vesicles undergo removal of Synapsin I by CaM kinase II-mediated phosphorylation, transforming to the release-ready pool.
Epilepsy associated with autism and attention deficit hyperactivity disorder: is there a genetic link?Curatolo et al., Roma, Italy. In Brain Dev, 2014
The majority of the candidate genes are involved in synaptic formation/remodeling/maintenance (NRX1, CNTN4, DCLK2, CNTNAP2, TRIM32, ASTN2, CTNTN5, SYN1), neurotransmission (SYNGAP1, GABRG1, CHRNA7), or DNA methylation/chromatin remodeling (MBD5).
Glutamatergic neurotransmission in the synapsin I and II double knock-out mouse.Walaas et al., Oslo, Norway. In Semin Cell Dev Biol, 2011
We here briefly describe the important characteristics of the synapsin proteins, and review recent studies on transgenic mice devoid of the gene products encoded by the synapsin I and II genes, where both neurochemical, cell biological and electrophysiological methods have been employed.
RIM1alpha is required for presynaptic long-term potentiation.Malenka et al., Stanford, United States. In Nature, 2002
Studies of knockout mice have shown that the synaptic vesicle protein Rab3A is required for mossy fibre LTP, but the protein kinase A substrates rabphilin, synapsin I and synapsin II are dispensable.