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Calcium influx signal

Cox, D. A. and Cohen, M. L. 5-HT2B receptor signaling in the rat stomach fundus dependence on calcium influx, calcium release and protein kinase C. Behav. Brain Res. 73 289-292,1996. [Pg.248]

Rusanescu G., Qi H., Thomas S. M., Brugge J. S., and Halegoua S. (1995). Calcium influx induces neurite growth through a Src-Ras signaling cassette. Neuron 15 1415-1425. [Pg.135]

Kreitzer AC, Malenka RC (2005) Dopamine modulation of state-dependent endocannabinoid release and long-term depression in the striatum. J Neurosci 25(45) 10537—45 Kreitzer AC, Regehr WG (2001) Retrograde inhibition of presynaptic calcium influx by endogenous cannabinoids at excitatory synapses onto purkinje cells. Neuron 29 717-27 Kreitzer AC, Carter AG, Regehr WG (2002) Inhibition of interneuron firing extends the spread of endocannabinoid signaling in the cerebellum. Neuron 34 787-96... [Pg.471]

Fig. 5. Model for elicitor signal transduction leading to Str expression. The model shows the positions of CrBPF-1 in a JA-independent, and ORCAs in a JA-dependent, elicitor signal transduction pathway. Protein phosphorylation and calcium influx are required for elicitor-induced jasmonate biosynthesis, as well as for the induction of CrBPF-1, ORCA2, and ORCA3. ORCA activation additionally depends on jasmonate biosynthesis. The positions of the TATA box, the BA region, and the jasmonate- and elicitor-responsive element (JERE) within the Str promoter are indicated... Fig. 5. Model for elicitor signal transduction leading to Str expression. The model shows the positions of CrBPF-1 in a JA-independent, and ORCAs in a JA-dependent, elicitor signal transduction pathway. Protein phosphorylation and calcium influx are required for elicitor-induced jasmonate biosynthesis, as well as for the induction of CrBPF-1, ORCA2, and ORCA3. ORCA activation additionally depends on jasmonate biosynthesis. The positions of the TATA box, the BA region, and the jasmonate- and elicitor-responsive element (JERE) within the Str promoter are indicated...
A recent report suggested that some kind of transmembrane signaling event, activating a calcium influx, occurs rapidly after ToxB contact with cells and is required for the disruption of actin filaments (Gilbert et al., 1995). However, a calcium influx is required for endocytosis of ToxB (Caspar et al., 1987), which may explain this observation. [Pg.145]


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