Pages that link to "Q30784526"

The following pages link to Identification and characterization of novel human Ca(v)2.2 (alpha 1B) calcium channel variants lacking the synaptic protein interaction site. (Q30784526):

Displaying 25 items.

• Alternative splicing of the voltage-gated Ca2+ channel beta4 subunit creates a uniquely folded N-terminal protein binding domain with cell-specific expression in the cerebellar cortex (Q24307212) (← links)
• Synaptic targeting of N-type calcium channels in hippocampal neurons (Q24614506) (← links)
• The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential (Q26781422) (← links)
• Expression and pharmacology of endogenous Cav channels in SH-SY5Y human neuroblastoma cells (Q34639654) (← links)
• Functional diversity in neuronal voltage-gated calcium channels by alternative splicing of Ca(v)alpha1. (Q34976636) (← links)
• Functional roles of cytoplasmic loops and pore lining transmembrane helices in the voltage-dependent inactivation of HVA calcium channels. (Q35157838) (← links)
• Functional interactions between presynaptic calcium channels and the neurotransmitter release machinery. (Q35172802) (← links)
• The impact of splice isoforms on voltage-gated calcium channel alpha1 subunits (Q35596481) (← links)
• Novel splice variants of rat CaV2.1 that lack much of the synaptic protein interaction site are expressed in neuroendocrine cells (Q35676370) (← links)
• Neuronal calcium channels: splicing for optimal performance (Q36026611) (← links)
• Analgesic conotoxins: block and G protein-coupled receptor modulation of N-type (Ca(V) 2.2) calcium channels (Q36159142) (← links)
• Overexpressed Ca(v)beta3 inhibits N-type (Cav2.2) calcium channel currents through a hyperpolarizing shift of ultra-slow and closed-state inactivation (Q36412553) (← links)
• Venom peptides as a rich source of cav2.2 channel blockers (Q36807192) (← links)
• Cumulative inactivation of N-type CaV2.2 calcium channels modified by alternative splicing (Q37682852) (← links)
• The neuronal splicing factor Nova controls alternative splicing in N-type and P-type CaV2 calcium channels (Q37819803) (← links)
• Trafficking and stability of voltage-gated calcium channels (Q37941517) (← links)
• Targeting voltage-gated calcium channels: developments in peptide and small-molecule inhibitors for the treatment of neuropathic pain (Q38020929) (← links)
• The Role of Calcium Channels in Epilepsy (Q38686593) (← links)
• Molecular characterization of a two-domain form of the neuronal voltage-gated P/Q-type calcium channel alpha(1)2.1 subunit (Q40683514) (← links)
• Differential role of N-type calcium channel splice isoforms in pain. (Q42514056) (← links)
• Alternative splicing in the synaptic protein interaction site of rat Ca(v)2.2 (alpha (1B)) calcium channels: changes induced by chronic inflammatory pain (Q43492318) (← links)
• Interactions with PDZ proteins are required for L-type calcium channels to activate cAMP response element-binding protein-dependent gene expression. (Q44419008) (← links)
• Alternative splicing of a beta4 subunit proline-rich motif regulates voltage-dependent gating and toxin block of Cav2.1 Ca2+ channels. (Q44856248) (← links)
• Maturation of rat cerebellar Purkinje cells reveals an atypical Ca2+ channel current that is inhibited by omega-agatoxin IVA and the dihydropyridine (-)-(S)-Bay K8644. (Q48359638) (← links)
• Agonist-independent modulation of N-type calcium channels by ORL1 receptors. (Q54733725) (← links)