Rescue of Munc18-1 and -2 double knockdown reveals the essential functions of interaction between Munc18 and closed syntaxin in PC12 cells.
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Reconciling the regulatory role of Munc18 proteins in SNARE-complex assemblyConformational states of syntaxin-1 govern the necessity of N-peptide binding in exocytosis of PC12 cells and Caenorhabditis elegansPossible roles for Munc18-1 domain 3a and Syntaxin1 N-peptide and C-terminal anchor in SNARE complex formationVesicle fusion probability is determined by the specific interactions of munc18An extended helical conformation in domain 3a of Munc18-1 provides a template for SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex assembly.SNAREpin assembly by Munc18-1 requires previous vesicle docking by synaptotagmin 1.Crucial role of the hydrophobic pocket region of Munc18 protein in mast cell degranulation.Munc18b is a major mediator of insulin exocytosis in rat pancreatic β-cellsAnalysis of familial hemophagocytic lymphohistiocytosis type 4 (FHL-4) mutant proteins reveals that S-acylation is required for the function of syntaxin 11 in natural killer cellsMunc18b Increases Insulin Granule Fusion, Restoring Deficient Insulin Secretion in Type-2 Diabetes Human and Goto-Kakizaki Rat Islets with Improvement in Glucose Homeostasis.Insight into the role of Ca2+-binding protein 5 in vesicle exocytosis.At the junction of SNARE and SM protein function.Dual roles of Munc18-1 rely on distinct binding modes of the central cavity with Stx1A and SNARE complexLow-resolution solution structures of Munc18:Syntaxin protein complexes indicate an open binding mode driven by the Syntaxin N-peptide.Syntaxin N-terminal peptide motif is an initiation factor for the assembly of the SNARE-Sec1/Munc18 membrane fusion complexSyntaxin binding protein 1 is not required for allergic inflammation via IgE-mediated mast cell activationThe syntaxin 4 N terminus regulates its basolateral targeting by munc18c-dependent and -independent mechanismsStructure-function study of mammalian Munc18-1 and C. elegans UNC-18 implicates domain 3b in the regulation of exocytosis.Munc18-1 and Munc18-2 proteins modulate beta-cell Ca2+ sensitivity and kinetics of insulin exocytosis differently.Hemophagocytic lymphohistiocytosis caused by dominant-negative mutations in STXBP2 that inhibit SNARE-mediated membrane fusion.Resolving the function of distinct Munc18-1/SNARE protein interaction modes in a reconstituted membrane fusion assay.Munc18-1 domain-1 controls vesicle docking and secretion by interacting with syntaxin-1 and chaperoning it to the plasma membranePhosphorylation-regulated axonal dependent transport of syntaxin 1 is mediated by a Kinesin-1 adapter.Munc18-1 is a molecular chaperone for α-synuclein, controlling its self-replicating aggregationThe Munc18-1 domain 3a hinge-loop controls syntaxin-1A nanodomain assembly and engagement with the SNARE complex during secretory vesicle priming.Navigation through the Plasma Membrane Molecular Landscape Shapes Random Organelle MovementSurvey of the year 2009: applications of isothermal titration calorimetry.Vacuolar H(+)-ATPase subunits Voa1 and Voa2 cooperatively regulate secretory vesicle acidification, transmitter uptake, and storage.Phosphorylation of Munc18-1 by Dyrk1A regulates its interaction with Syntaxin 1 and X11α.Managing intracellular transport.The nature of the Syntaxin4 C-terminus affects Munc18c-supported SNARE assembly.Protein structure and phenotypic analysis of pathogenic and population missense variants in STXBP1.Calcium-dependent activator protein for secretion 1 (CAPS1) binds to syntaxin-1 in a distinct mode from Munc13-1.A pivotal role for pro-335 in balancing the dual functions of Munc18-1 domain-3a in regulated exocytosis.Revisiting interaction specificity reveals neuronal and adipocyte Munc18 membrane fusion regulatory proteins differ in their binding interactions with partner SNARE Syntaxins.Syntaxins on granules promote docking of granules via interactions with munc18.UNC-18 and Tomosyn Antagonistically Control Synaptic Vesicle Priming Downstream of UNC-13 in Caenorhabditis elegans.BDNF-TrkB Signaling Coupled to nPKCε and cPKCβI Modulate the Phosphorylation of the Exocytotic Protein Munc18-1 During Synaptic Activity at the Neuromuscular Junction.Mechanism of neurotransmitter release coming into focus
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Rescue of Munc18-1 and -2 double knockdown reveals the essential functions of interaction between Munc18 and closed syntaxin in PC12 cells.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 07 October 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Rescue of Munc18-1 and -2 doub ...... closed syntaxin in PC12 cells.
@en
Rescue of Munc18-1 and -2 doub ...... closed syntaxin in PC12 cells.
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label
Rescue of Munc18-1 and -2 doub ...... closed syntaxin in PC12 cells.
@en
Rescue of Munc18-1 and -2 doub ...... closed syntaxin in PC12 cells.
@nl
prefLabel
Rescue of Munc18-1 and -2 doub ...... closed syntaxin in PC12 cells.
@en
Rescue of Munc18-1 and -2 doub ...... closed syntaxin in PC12 cells.
@nl
P2093
P2860
P50
P356
P1476
Rescue of Munc18-1 and -2 doub ...... closed syntaxin in PC12 cells.
@en
P2093
Frederick W Tse
Gayoung A Han
Herbert Y Gaisano
Liping Han
Nancy T Malintan
Shuzo Sugita
Tiandan Jiang
P2860
P304
P356
10.1091/MBC.E09-08-0712
P577
2009-10-07T00:00:00Z