G Protein βγ Subunit-Mediated Presynaptic Inhibition: Regulation of Exocytotic Fusion Downstream of Ca2+ Entry

By T. Blackmer, E. C. Larsen, Michiko Takahashi, T. Martin, S. Alford, Heidi E. Hamm. Science, 2001

240 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8b5328794c06c2d06650b4db3e4bcfe4814855cd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. T. Sakaba
2. E. Neher
3. Heidi E. Hamm

In Molecular Biology

1. T. Sakaba
2. E. Neher
3. Heidi E. Hamm
4. Anita M. Preininger

Citations in the corpus

• Gβγ acts at the C terminus of SNAP-25 to mediate presynaptic inhibition (2005, background): “However, a number of studies have identified modulatory pathways in which G proteins do not target classical effectors or Ca 2+ entr”
• Multiple roles of calcium ions in the regulation of neurotransmitter release. (2008, background): “Quite a number of additional mechanisms have been postulated to influence the Ca-triggered exocytosis, such as modulation by cAMP (Trudeau et al., 1997), inositolpolyphosphates (Illies et al., 2007), and bg subunits of G proteins (Blackmer et al., 2001, 2005; Gerachshenko et al., 2005).”
• Insights into G protein structure, function, and regulation. (2003, background): “G can inhibit neurotransmitter release independently of second messenger formation and ion channel modulation, perhaps by direct interaction with the exocytotic fusion machinery, because both syntaxin 1B and SNAP25B are G binding partners (132).”
• G protein βγ directly regulates SNARE protein fusion machinery for secretory granule exocytosis (2005, background): “Studies of presynaptic inhibition in the nervous system also have shown modes of inhibition not accounted for by second messengers or ion channel modulatio”
• Inhibition of Olfactory Receptor Neuron Input to Olfactory Bulb Glomeruli Mediated by Suppression of Presynaptic Calcium Influx (2005, background): “In other systems, activation of metabotropic receptors (such as GABAB receptors) can modulate release by affecting vesicle release machinery directly (Blackmer et al. 2001).”
• Modulation of glycine-activated ion channel function by G-protein βγ subunits (2003, background): “It has been previously shown that the action of Gβγ on cellular effectors can be potently and selectively blocked by the regulatory domains of several Gβγ-associated proteins, such as the C-terminal regions of G protein–coupled receptor kinases (GRKs”