Shangbang Gao

This study identifies a membrane potential-independent role for the K2P channel TWK-40 in regulating presynaptic organisation through intracellular potassium levels and interactions with PYK-1 and transcription factors.

This study shows that UBR-1 deficiency in C. elegans causes ivermectin resistance by disrupting glutamate signaling and GluCl function.

This paper develops a biophysically detailed model of C. elegans body-wall muscle cells using experimental data and a simulation-based inference method to estimate parameters and validate the model's accuracy.

This study identifies a master neuron in C. elegans that modulates forward and backward movement through tonic and phasic activity at different timescales.

The paper shows that UBR-1 regulates synaptic strength between GABAergic and glutamatergic signaling in C. elegans by suppressing inhibitory glutamate signaling in DVB neurons.

This study investigates the roles of complexin/CPX-1 and CAPS/UNC-31 in regulating excitatory and inhibitory synaptic release at C. elegans neuromuscular junctions, revealing distinct regulatory patterns and interactions.

The paper investigates the combined effects of two exocytosis-enhancing mutations in C. elegans and finds they disrupt excitatory-inhibitory balance and impair multiple behaviors.

This paper develops a new genetically encoded fluorescent cAMP indicator, G-Flamp1, which shows high sensitivity, brightness, and fast response kinetics for in vivo cAMP imaging.

This study identifies six signaling pathways regulating the proliferation and developmental potential of human neuroepithelial stem cells in vitro.

This study identifies TWK-40, a K2P channel, as essential for regulating rhythmic motor activity in C. elegans by modulating DVB neuron function and Ca2+ oscillations.

The paper identifies cholecystokinin signaling as essential for robust escape steering in C. elegans by modulating motor neuron activity during escape responses.

This study shows that male pheromones in C. elegans enhance hermaphrodite cholinergic synaptic transmission at the neuromuscular junction, affecting locomotion and mating efficiency.

This study shows that overexpressing an open form of syntaxin can rescue exocytosis defects in multiple C. elegans mutants, suggesting a general mechanism to enhance synaptic transmission.

This study shows that an ALS-associated FUS mutation disrupts synaptic vesicle docking and neuromuscular transmission in C. elegans.

This study identifies a gain-of-function mutation in the UNC-2/CaV2α channel in C. elegans that causes hyperactivity and excitation-dominant synaptic transmission by altering cholinergic and GABAergic transmission.

The paper identifies class A motor neurons in C. elegans as intrinsic oscillators driving reverse locomotion without premotor interneurons.