Pages that link to "Q44931369"

The following pages link to Dominant-negative calcium channel suppression by truncated constructs involves a kinase implicated in the unfolded protein response. (Q44931369):

Displaying 46 items.

• Neuronal precursor cell-expressed developmentally down-regulated 4-1 (NEDD4-1) controls the sorting of newly synthesized Ca(V)1.2 calcium channels (Q24595139) (← links)
• BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells (Q24652441) (← links)
• The ducky(2J) mutation in Cacna2d2 results in reduced spontaneous Purkinje cell activity and altered gene expression (Q24676262) (← links)
• The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential (Q26781422) (← links)
• Genetic disruption of voltage-gated calcium channels in psychiatric and neurological disorders (Q26783154) (← links)
• Dominant-negative suppression of Cav2.1 currents by alpha(1)2.1 truncations requires the conserved interaction domain for beta subunits (Q30429315) (← links)
• Beta-subunits promote the expression of Ca(V)2.2 channels by reducing their proteasomal degradation (Q30498795) (← links)
• Dissection of synaptic excitability phenotypes by using a dominant-negative Shaker K channel subunit. (Q30856646) (← links)
• CaV2.1 channelopathies (Q33537218) (← links)
• The GPA-dependent, spherostomatocytosis mutant AE1 E758K induces GPA-independent, endogenous cation transport in amphibian oocytes (Q33655576) (← links)
• Age-related homeostatic midchannel proteolysis of neuronal L-type voltage-gated Ca²⁺ channels. (Q33736402) (← links)
• Regulation of high-voltage-activated Ca(2 ) channel function, trafficking, and membrane stability by auxiliary subunits (Q33763700) (← links)
• GABA(A) receptor alpha1 subunit mutation A322D associated with autosomal dominant juvenile myoclonic epilepsy reduces the expression and alters the composition of wild type GABA(A) receptors (Q34074424) (← links)
• Identification of the alpha2-delta-1 subunit of voltage-dependent calcium channels as a molecular target for pain mediating the analgesic actions of pregabalin (Q34579804) (← links)
• The tail of the cardiac sodium channel (Q35156520) (← links)
• Regulation of voltage-gated calcium channels by proteolysis (Q35166587) (← links)
• Large genomic deletions in CACNA1A cause episodic ataxia type 2 (Q35204801) (← links)
• A naturally occurring truncated Cav1.2 α1-subunit inhibits Ca2 current in A7r5 cells (Q37234587) (← links)
• Proteolytic maturation of α2δ represents a checkpoint for activation and neuronal trafficking of latent calcium channels (Q37388710) (← links)
• The inhibition of functional expression of calcium channels by prion protein demonstrates competition with α2δ for GPI-anchoring pathways (Q37584850) (← links)
• Differential upregulation in DRG neurons of an α2δ-1 splice variant with a lower affinity for gabapentin after peripheral sensory nerve injury (Q37706465) (← links)
• Neuronal P/Q-type calcium channel dysfunction in inherited disorders of the CNS. (Q37976377) (← links)
• Ubiquitin Ligase RNF138 Promotes Episodic Ataxia Type 2-Associated Aberrant Degradation of Human Cav2.1 (P/Q-Type) Calcium Channels (Q38717597) (← links)
• Mutation Spectrum in the CACNA1A Gene in 49 Patients with Episodic Ataxia. (Q38752492) (← links)
• From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms (Q39301735) (← links)
• Pure haploinsufficiency for Dravet syndrome Na(V)1.1 (SCN1A) sodium channel truncating mutations (Q39431641) (← links)
• The increased trafficking of the calcium channel subunit alpha2delta-1 to presynaptic terminals in neuropathic pain is inhibited by the alpha2delta ligand pregabalin (Q39753024) (← links)
• The alpha(2)delta subunit augments functional expression and modifies the pharmacology of Ca(V)1.3 L-type channels (Q39792719) (← links)
• A destructive interaction mechanism accounts for dominant-negative effects of misfolded mutants of voltage-gated calcium channels. (Q39988648) (← links)
• Inhibition of recombinant N-type Ca(V) channels by the gamma 2 subunit involves unfolded protein response (UPR)-dependent and UPR-independent mechanisms. (Q40155766) (← links)
• The calcium channel alpha2delta-2 subunit partitions with CaV2.1 into lipid rafts in cerebellum: implications for localization and function. (Q40240262) (← links)
• The GABRG2 mutation, Q351X, associated with generalized epilepsy with febrile seizures plus, has both loss of function and dominant-negative suppression (Q40395726) (← links)
• A truncated isoform of pyroglutamyl aminopeptidase II produced by exon extension has dominant-negative activity. (Q40462905) (← links)
• How do T-type calcium channels control low-threshold exocytosis? (Q41876708) (← links)
• N terminus is key to the dominant negative suppression of Ca(V)2 calcium channels: implications for episodic ataxia type 2. (Q41960046) (← links)
• Three-dimensional structure of CaV3.1: comparison with the cardiac L-type voltage-gated calcium channel monomer architecture (Q41975039) (← links)
• A CaV2.1 N-terminal fragment relieves the dominant-negative inhibition by an Episodic ataxia 2 mutant (Q42426246) (← links)
• Calcium currents are enhanced by α2δ-1 lacking its membrane anchor (Q42565287) (← 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)
• Inhibition of synaptic transmission and G protein modulation by synthetic CaV2.2 Ca2 channel peptides (Q43612129) (← links)
• Dominant-negative effects of human P/Q-type Ca2 channel mutations associated with episodic ataxia type 2. (Q46818398) (← links)
• Alternative splicing generates a smaller assortment of CaV2.1 transcripts in cerebellar Purkinje cells than in the cerebellum. (Q48702276) (← links)
• Voltage-gated calcium channels, calcium signaling, and channelopathies (Q59530617) (← links)
• Expression of Rem2, an RGK family small GTPase, reduces N-type calcium current without affecting channel surface density (Q81375760) (← links)
• Alternative Splicing at N Terminus and Domain I Modulates CaV1.2 Inactivation and Surface Expression (Q88615653) (← links)
• Zebrafish as a Model System for the Study of Severe CaV2.1 (α1A) Channelopathies (Q89963752) (← links)