PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19793988-1 2009 The soluble N-ethylmaleimide-sensitive fusion (NSF) attachment protein (SNAP) receptor (SNARE) protein syntaxin 1A forms nano-sized clusters (membrane rafts) on the plasma membrane (PM) that are in equilibrium with freely diffusing syntaxin molecules. Ethylmaleimide 12-28 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 47-50 12164547-8 2002 Several presynaptic thiol-containing proteins (e.g. SNAP-25, NSF) are critically involved in formation of SNARE (soluble N-ethylmaleimide (NEM)-sensitive fusion protein receptor) complexes that mediate membrane fusion processes such as exocytosis and turnover of plasmalemmal proteins and other constituents. Ethylmaleimide 121-137 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 61-64 12244131-1 2002 N-ethylmaleimide (NEM)-sensitive factor (NSF), a regulator of soluble NSF attachment protein receptors (SNAREs), is required for vesicular transport in many eukaryotic cells. Ethylmaleimide 0-16 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 41-44 12244131-1 2002 N-ethylmaleimide (NEM)-sensitive factor (NSF), a regulator of soluble NSF attachment protein receptors (SNAREs), is required for vesicular transport in many eukaryotic cells. Ethylmaleimide 0-16 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 70-73 18272689-5 2008 NSF interacts directly with MuSK with nanomolar affinity, and treatment of muscle cells with the NSF inhibitor N-ethylmaleimide, mutation of NSF, or suppression of NSF expression all inhibited agrin-induced AChR clustering. Ethylmaleimide 111-127 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 97-100 18272689-5 2008 NSF interacts directly with MuSK with nanomolar affinity, and treatment of muscle cells with the NSF inhibitor N-ethylmaleimide, mutation of NSF, or suppression of NSF expression all inhibited agrin-induced AChR clustering. Ethylmaleimide 111-127 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 97-100 18272689-5 2008 NSF interacts directly with MuSK with nanomolar affinity, and treatment of muscle cells with the NSF inhibitor N-ethylmaleimide, mutation of NSF, or suppression of NSF expression all inhibited agrin-induced AChR clustering. Ethylmaleimide 111-127 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 97-100 11680900-4 2001 Furthermore, N-ethylmaleimide treatment abolished the NSF/CD28 interaction completely, and blocked CD28 association with a tyrosine phosphorylated 103 kDa protein in the activated cells. Ethylmaleimide 13-29 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 54-57 11301340-0 2001 Unraveling the mechanism of the vesicle transport ATPase NSF, the N-ethylmaleimide-sensitive factor. Ethylmaleimide 66-82 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 57-60 10402460-2 1999 A cell-free system that reconstructs these events has revealed that cisternal regrowth requires interplay between soluble factors and soluble N-ethylmaleimide (NEM)-sensitive fusion protein (NSF) attachment protein receptors (SNAREs) via two intersecting pathways controlled by the ATPases, p97 and NSF. Ethylmaleimide 142-158 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 191-194 10954749-8 2000 The activation of Rab3A protects NSF from N-ethylmaleimide inhibition and precludes the exchange of the endogenous protein with recombinant dominant negative mutants of NSF. Ethylmaleimide 42-58 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 33-36 10716927-4 2000 However, this activity of NSF is resistant to inactivation by N-ethylmaleimide and does not depend on the presence of alpha-SNAP (soluble NSF-attachment protein). Ethylmaleimide 62-78 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 26-29 10571232-1 1999 We investigated whether the interaction between the N-ethyl-maleimide-sensitive fusion protein (NSF) and the AMPA receptor (AMPAR) subunit GluR2 is involved in synaptic plasticity in the CA1 region of the hippocampus. Ethylmaleimide 52-69 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 96-99 10402460-2 1999 A cell-free system that reconstructs these events has revealed that cisternal regrowth requires interplay between soluble factors and soluble N-ethylmaleimide (NEM)-sensitive fusion protein (NSF) attachment protein receptors (SNAREs) via two intersecting pathways controlled by the ATPases, p97 and NSF. Ethylmaleimide 142-158 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 299-302 10402460-2 1999 A cell-free system that reconstructs these events has revealed that cisternal regrowth requires interplay between soluble factors and soluble N-ethylmaleimide (NEM)-sensitive fusion protein (NSF) attachment protein receptors (SNAREs) via two intersecting pathways controlled by the ATPases, p97 and NSF. Ethylmaleimide 160-163 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 191-194 10402460-2 1999 A cell-free system that reconstructs these events has revealed that cisternal regrowth requires interplay between soluble factors and soluble N-ethylmaleimide (NEM)-sensitive fusion protein (NSF) attachment protein receptors (SNAREs) via two intersecting pathways controlled by the ATPases, p97 and NSF. Ethylmaleimide 160-163 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 299-302 10399941-1 1999 Here, we show that disruption of N-ethylmaleimide-sensitive fusion protein- (NSF-) GluR2 interaction by infusion into cultured hippocampal neurons of a blocking peptide (pep2m) caused a rapid decrease in the frequency but no change in the amplitude of AMPA receptor-mediated miniature excitatory postsynaptic currents (mEPSCs). Ethylmaleimide 33-49 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 77-80 10387016-7 1999 This interaction leads to a stimulation of Sec18p D1 domain ATPase activity, with kinetics similar to those of alpha-SNAP stimulation of NSF, although differences in temperature and N-ethylmaleimide sensitivity were observed between NSF and Sec18p. Ethylmaleimide 182-198 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 233-236 10085240-1 1999 The tSNARE (the target-membrane soluble NSF-attachment protein receptor, where NSF is N-ethylmaleimide-sensitive fusion protein) synaptosomal-associated protein of 25 kDa (SNAP-25) is expressed in pancreatic B-cells and its cleavage by botulinum neurotoxin E (BoNT/E) abolishes stimulated secretion of insulin. Ethylmaleimide 86-102 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 40-43 10085240-1 1999 The tSNARE (the target-membrane soluble NSF-attachment protein receptor, where NSF is N-ethylmaleimide-sensitive fusion protein) synaptosomal-associated protein of 25 kDa (SNAP-25) is expressed in pancreatic B-cells and its cleavage by botulinum neurotoxin E (BoNT/E) abolishes stimulated secretion of insulin. Ethylmaleimide 86-102 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 79-82 9614185-1 1998 The importance of soluble N-ethyl maleimide (NEM)-sensitive fusion protein (NSF) attachment protein (SNAP) receptors (SNAREs) in synaptic vesicle exocytosis is well established because it has been demonstrated that clostridial neurotoxins (NTs) proteolyze the vesicle SNAREs (v-SNAREs) vesicle-associated membrane protein (VAMP)/brevins and their partners, the target SNAREs (t-SNAREs) syntaxin 1 and SNAP25. Ethylmaleimide 26-43 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 76-79 9878078-10 1999 N-ethylmaleimide and botulinum toxin types A and B caused cells to accumulate increased number of vesicles suggesting that exocytosis was regulated by NSF-dependent SNARE mechanism. Ethylmaleimide 0-16 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 151-154 10212832-8 1998 A general hypothesis called the SNARE hypothesis (soluble NSF attachment protein receptors where NSF stands for N-ethylmaleimide-sensitive fusion protein) postulates that the specificity of secretory vesicle targeting is generated by complexes that form between membrane proteins on the transport vesicle (v-SNARE"s) and membrane proteins located on the target membrane (t-SNARE"s). Ethylmaleimide 112-128 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 58-61 10212832-8 1998 A general hypothesis called the SNARE hypothesis (soluble NSF attachment protein receptors where NSF stands for N-ethylmaleimide-sensitive fusion protein) postulates that the specificity of secretory vesicle targeting is generated by complexes that form between membrane proteins on the transport vesicle (v-SNARE"s) and membrane proteins located on the target membrane (t-SNARE"s). Ethylmaleimide 112-128 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 97-100 1601890-1 1992 Soluble N-ethylmaleimide-sensitive fusion attachment proteins (SNAPs) are required for the binding of N-ethylmaleimide-sensitive fusion protein (NSF) to Golgi membranes and are, therefore, required for intra-Golgi transport. Ethylmaleimide 8-24 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 102-143 7553850-4 1995 We now provide evidence that the sequential stack formation from VGMs reflects two distinct fusion processes: the first event is N-ethyl-maleimide (NEM)-sensitive factor (NSF) dependent, and the second fusion event requires an NSF-like NEM-sensitive ATPase called p97. Ethylmaleimide 129-146 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 171-174 8051162-1 1994 N-Ethylmaleimide-sensitive factor (NSF) was originally characterized as the protein that restores in vitro protein transport activity of the Golgi membranes inactivated by N-ethylmaleimide. Ethylmaleimide 172-188 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 0-33 8051162-1 1994 N-Ethylmaleimide-sensitive factor (NSF) was originally characterized as the protein that restores in vitro protein transport activity of the Golgi membranes inactivated by N-ethylmaleimide. Ethylmaleimide 172-188 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 35-38 8051162-11 1994 Their ATPase activities were sensitive to N-ethylmaleimide and dependent on their protein concentrations, as observed in wild-type NSF. Ethylmaleimide 42-58 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 131-134 1441755-1 1992 We have sequenced a gene that encodes a 377 amino acid putative protein with an ATPase motif typical of the protein family including SEC18p (NSF = N-ethyl maleimide-sensitive fusion protein; vesicle-mediated endoplasmic reticulum to Golgi protein transfer), PAS1p (peroxisome assembly), CDC48p (VCP = valosin-containing protein; cell cycle) and TBP1 (Tat-binding protein). Ethylmaleimide 147-164 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 141-144 1601890-1 1992 Soluble N-ethylmaleimide-sensitive fusion attachment proteins (SNAPs) are required for the binding of N-ethylmaleimide-sensitive fusion protein (NSF) to Golgi membranes and are, therefore, required for intra-Golgi transport. Ethylmaleimide 8-24 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 145-148 3390865-1 1988 An N-ethylmaleimide-sensitive transport component (NSF) has been purified on the basis of its ability to support transport between Golgi cisternae. Ethylmaleimide 5-19 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 51-54 1999460-5 1991 Cytosol fractions immunodepleted of greater than or equal to 90% of NSF protein, or heated to 37 degrees C to inactivate greater than or equal to 93% of NSF activity, were fully able to restore transport to NEM-treated reaction mixtures. Ethylmaleimide 207-210 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 68-71 2140770-4 1990 The particle has a N-ethylmaleimide (NEM)-inhibitable Mg2(+)-ATPase activity, and its amino acid sequence, as deduced from cDNA clones, displays considerable homology to the mammalian NEM-sensitive fusion protein (NSF) and yeast Sec18p believed to be essential for vesicle fusion in secretory processes, indicating that these three proteins belong to the same multigene family. Ethylmaleimide 19-35 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 184-212 2140770-4 1990 The particle has a N-ethylmaleimide (NEM)-inhibitable Mg2(+)-ATPase activity, and its amino acid sequence, as deduced from cDNA clones, displays considerable homology to the mammalian NEM-sensitive fusion protein (NSF) and yeast Sec18p believed to be essential for vesicle fusion in secretory processes, indicating that these three proteins belong to the same multigene family. Ethylmaleimide 37-40 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 184-212 2140770-4 1990 The particle has a N-ethylmaleimide (NEM)-inhibitable Mg2(+)-ATPase activity, and its amino acid sequence, as deduced from cDNA clones, displays considerable homology to the mammalian NEM-sensitive fusion protein (NSF) and yeast Sec18p believed to be essential for vesicle fusion in secretory processes, indicating that these three proteins belong to the same multigene family. Ethylmaleimide 37-40 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 214-217 2541136-1 1989 An N-ethylmaleimide (NEM)-sensitive fusion protein (NSF) has recently been purified on the basis of its ability to restore transport to NEM-inactivated Golgi membranes in a cell-free transport system. Ethylmaleimide 3-19 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 52-55 2541136-1 1989 An N-ethylmaleimide (NEM)-sensitive fusion protein (NSF) has recently been purified on the basis of its ability to restore transport to NEM-inactivated Golgi membranes in a cell-free transport system. Ethylmaleimide 21-24 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 52-55 28635948-5 2017 Inhibitors of N-ethylmaleimide sensitive factor (NSF), N-ethylmaleimide (NEM) or interfering peptides, prevent de-priming in munc18-1/2SWAP or munc13-1 null synapses, but not in CAPS-1/2 null, another priming-deficient mutant. Ethylmaleimide 14-30 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 49-52 30617180-2 2019 Inactive SNARE bundles are reactivated by hexameric N-ethylmaleimide-sensitive factor, vesicle-fusing ATPase (Sec18/NSF)-driven disassembly that enables a new round of membrane fusion. Ethylmaleimide 52-68 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 116-119 26758690-0 2016 LRRK2 phosphorylates pre-synaptic N-ethylmaleimide sensitive fusion (NSF) protein enhancing its ATPase activity and SNARE complex disassembling rate. Ethylmaleimide 34-50 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 69-72 23322694-10 2013 Herein, we discuss the role of syntaxin-11 in soluble NSF (N-ethylmaleimide sensitive fusion) attachment protein receptors complex formation leading to cytotoxic lymphocyte degranulation and its importance in maintaining immune homeostasis. Ethylmaleimide 59-75 N-ethylmaleimide sensitive factor, vesicle fusing ATPase Homo sapiens 54-57