Direct Interaction of Rab4 with Syntaxin 4
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چکیده
منابع مشابه
Direct interaction of the rat unc-13 homologue Munc13-1 with the N terminus of syntaxin.
unc-13 mutants in Caenorhabditis elegans are characterized by a severe deficit in neurotransmitter release. Their phenotype is similar to that of the C. elegans unc-18 mutation, which is thought to affect synaptic vesicle docking to the active zone. This suggests a crucial role for the unc-13 gene product in the mediation or regulation of synaptic vesicle exocytosis. Munc13-1 is one of three cl...
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برهمکنش dnaتیموس گاوی طبیعی (ct-dna) با اتیلن دی آمین تترااستات (edta)در بافرtris-hcl با 8/7 ph ( دراین ph،edta به نمک دی سدیم تبدیل می شود) وسسامول در بافر tris-hcl با4/7 ph مورد بررسی قرار گرفته است. edta و سسامول استفاده فراوانی در تکنولوژی غذایی و صنعت شیمیایی دارند. مدل اتصال dna مربوط بهedta بوسیله اسپکتروفتومتری جذب، دورنگ نمایی حلقوی(cd)، ویسکومتری وژل الکتروفورز بررسی شده است. طیفuv ...
15 صفحه اولDirect Interaction of Endogenous Kv Channels with Syntaxin Enhances Exocytosis by Neuroendocrine Cells
K(+) efflux through voltage-gated K(+) (Kv) channels can attenuate the release of neurotransmitters, neuropeptides and hormones by hyperpolarizing the membrane potential and attenuating Ca(2+) influx. Notably, direct interaction between Kv2.1 channels overexpressed in PC12 cells and syntaxin has recently been shown to facilitate dense core vesicle (DCV)-mediated release. Here, we focus on endog...
متن کاملK+ channel facilitation of exocytosis by dynamic interaction with syntaxin.
Kv channels inhibit release indirectly by hyperpolarizing membrane potential, but the significance of Kv channel interaction with the secretory apparatus is not known. The Kv2.1 channel is commonly expressed in the soma and dendrites of neurons, where it could influence the release of neuropeptides and neurotrophins, and in neuroendocrine cells, where it could influence hormone release. Here we...
متن کاملUNC-13 Interaction with Syntaxin Is Required for Synaptic Transmission
Neurotransmitter secretion at synapses is controlled by several processes-morphological docking of vesicles at release sites, priming of docked vesicles to make them fusion competent, and calcium-dependent fusion of vesicles with the plasma membrane . In worms, flies, and mice, mutants lacking UNC-13 have defects in vesicle priming . Current models propose that UNC-13 primes vesicles by stabili...
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ژورنال
عنوان ژورنال: Journal of Biological Chemistry
سال: 2001
ISSN: 0021-9258
DOI: 10.1074/jbc.m003883200