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1 y by polymers of the neuron-specific serpin, neuroserpin.
2 rol biosynthesis and the clearance of mutant neuroserpin.
3  and molecular-dynamics simulations on human neuroserpin.
4 0A mutation suppresses these fluctuations in neuroserpin.
5    The closest vertebrate homolog to Spn4 is neuroserpin.
6 und in patients with the Portland variant of neuroserpin.
7 ly regulated by protease inhibitors, such as neuroserpin.
8 erized by intraneuronal inclusions of mutant neuroserpin.
9 hat affected the conformational stability of neuroserpin.
10 bout the trafficking of wild type and mutant neuroserpins.
11                                              Neuroserpin (20 micro L of 16 micro mol/L active neurose
12  and have a surprisingly simple composition; neuroserpin (a serine protease inhibitor) is their predo
13 campi, and unilateral treatment of rats with neuroserpin, a natural inhibitor of tPA in the brain, en
14                We tested the hypothesis that neuroserpin, a natural inhibitor of tPA, reduces tPA-ind
15 E2 ligase and Hrd1 E3 ligase while truncated neuroserpin, a protein that lacks 132 amino acids, is de
16                                              Neuroserpin, a recently identified inhibitor of tissue-t
17 se caused by point mutations in the gene for neuroserpin, a serine protease inhibitor of the nervous
18 n activator inhibitor-1 (PAI-1) but not with neuroserpin, a tPA-specific inhibitor concentrated in gr
19               Neither the wild-type nor S49P neuroserpin accepted the P7-P2 alpha(1)-anti-trypsin or
20                            Administration of neuroserpin after stroke is neuroprotective, seemingly b
21 confirmed that the inclusions were formed of neuroserpin aggregates, and the responsible mutations in
22                                              Neuroserpin also attenuated kainic acid-induced neuronal
23                                              Neuroserpin also decreased apoptotic cell counts in the
24                                              Neuroserpin also effectively inhibited trypsin and nerve
25 onoclonal antibodies that detect polymerized neuroserpin and have used COS-7 cells, stably transfecte
26 odel of FENIB by overexpressing G392E-mutant neuroserpin and in this study we examine trafficking and
27 ification, and characterization of wild-type neuroserpin and neuroserpin containing the S49P mutation
28                    We found that both active neuroserpin and neuroserpin.tPA complexes were internali
29 ss high levels of anti-PA serpins, including neuroserpin and serpin B2, to prevent plasmin generation
30 l model to study the processing of wild type neuroserpin and the Syracuse (S49P) and Portland (S52R)
31  region containing an a helix shared between neuroserpin and the thyroxine-transport protein transthy
32   ProNGF levels correlated with plasminogen, neuroserpin, and VAChT while NGF correlated with MMP9 ac
33 or (tPA) and the serine proteinase inhibitor neuroserpin are both expressed in areas of the brain wit
34                        Mechanisms regulating neuroserpin are not known, and the current studies were
35                                   Mutants of neuroserpin are retained as polymers within the endoplas
36      Here we show that Syracuse and Portland neuroserpin are retained soon after their synthesis in t
37 haracterized by the retention of polymers of neuroserpin as inclusions within the endoplasmic reticul
38 r the LRP-mediated internalization of active neuroserpin, but could not rule out the possibility that
39  to define the cellular pathways involved in neuroserpin catabolism.
40                             Moreover, mutant neuroserpin causes locomotor deficits in the fly allowin
41 haracterization of wild-type neuroserpin and neuroserpin containing the S49P mutation that causes FEN
42 r either treatment with or overexpression of neuroserpin decreases the volume of the ischemic lesion
43         Overexpression of the mutant form of neuroserpin did not stimulate cell death in the HEK-293
44                                 Injection of neuroserpin directly into the brain immediately after in
45                         In the present study neuroserpin expression and its potential therapeutic ben
46  occlusion (MCAO) increases tPA activity and neuroserpin expression in ischemic tissue, and genetic d
47  to sublethal hypoxia/ischemia increases the neuroserpin expression in the hippocampal CA1 layer and
48                                              Neuroserpin expression increased in neurons surrounding
49                                    Wild-type neuroserpin formed SDS-stable complexes with tPA with an
50                            In contrast, S49P neuroserpin formed unstable complexes with an associatio
51 sociated proteases capable of binding active neuroserpin functions in this capacity.
52 ic pathway in cells that express polymers of neuroserpin (G392E).
53  the cosegregation of point mutations in the neuroserpin gene (PI12) with the disease in two families
54 oserpin were identified by sequencing of the neuroserpin gene (SERPINI1) in DNA from blood samples or
55 DNA sequence analysis of exons 2 to 9 of the neuroserpin gene in the proband showed the published nor
56 sts that FENIB is caused by mutations in the neuroserpin gene, resulting in intracellular accumulatio
57  (FENIB) is caused by point mutations in the neuroserpin gene.
58 sment by circular dichroism showed that S49P neuroserpin had a lower melting temperature than wild-ty
59     Collectively, these results suggest that neuroserpin has an unusual chaperone selectivity for int
60             Hydrogen exchange indicates that neuroserpin has greater flexibility in the breach region
61 m (ER) retention signal; however, Spn4.1 and neuroserpin have divergent reactive site loops, with Spn
62  revealed that MCAO resulted in reduction of neuroserpin immunoreactivity in the ipsilateral hemisphe
63            Ischemic brains were treated with neuroserpin in combination with recombinant human tPA (n
64                      However, treatment with neuroserpin in combination with tPA significantly (P<0.0
65 pathway, reduced the ubiquitination of G392E neuroserpin in our cell lines and increased the retentio
66 hways, whereas the accumulation of polymeric neuroserpin in the neuronal ER triggers a poorly underst
67                 Familial encephalopathy with neuroserpin inclusion bodies (FENIB) is a progressive ne
68                 Familial encephalopathy with neuroserpin inclusion bodies (FENIB) is an autosomal dom
69                 Familial encephalopathy with neuroserpin inclusion bodies (FENIB) is an autosomal dom
70    The dementia familial encephalopathy with neuroserpin inclusion bodies (FENIB) is caused by point
71    The dementia familial encephalopathy with neuroserpin inclusion bodies (FENIB) is caused by the ac
72 rm of dementia, familial encephalopathy with neuroserpin inclusion bodies (FENIB), has been proposed,
73  disease entity-familial encephalopathy with neuroserpin inclusion bodies (FENIB).
74 , we investigated five families with typical neuroserpin inclusion bodies but with various neurologic
75 minant dementia familial encephalopathy with neuroserpin inclusion bodies or FENIB.
76  a new disease, familial encephalopathy with neuroserpin inclusion bodies, characterized clinically a
77 n diseases, and familial encephalopathy with neuroserpin inclusion bodies.
78 dementia after age 45 years, and presence of neuroserpin inclusions in only a few neurons.
79 ined and the topographic distribution of the neuroserpin inclusions plotted.
80 mpal CA1 layer and cerebral cortex, and that neuroserpin induces ischemic tolerance and decreases the
81 range of in vitro assays to demonstrate that neuroserpin inhibits amyloid formation by several differ
82                   In vitro studies show that neuroserpin inhibits tPA and, to a lesser extent, urokin
83 indicating the requirement of a cofactor for neuroserpin internalization.
84 ther known plasminogen activator inhibitors, neuroserpin is a more effective inactivator of tPA than
85 n together, these data demonstrate that S49P neuroserpin is a poor proteinase inhibitor and readily f
86                                              Neuroserpin is a regulator of neuronal growth and plasti
87                                              Neuroserpin is a secreted protease inhibitor known to in
88  indicate that the neuroprotective effect of neuroserpin is due to inhibition of plasmin-mediated exc
89   Surprisingly, despite the fact that active neuroserpin is internalized by LRP, this form of the mol
90      Taken together, these data suggest that neuroserpin is likely to be a critical regulator of tPA
91                                       Mutant neuroserpin is retained within the endoplasmic reticulum
92 ort here that a polymerogenic mutant form of neuroserpin is secreted from cells but is not toxic in t
93  We observed that a small fraction of mutant neuroserpin is secreted via the ER-to-Golgi pathway, and
94                                              Neuroserpin isolated from inclusion bodies in the brain
95                                  In summary, neuroserpin levels appear to be carefully regulated by L
96  early-onset dementia caused by mutations in neuroserpin, liver cirrhosis and emphysema caused by mut
97                                        Thus, neuroserpin may be a naturally occurring neuroprotective
98 tion between the reactive centre loop of one neuroserpin molecule with beta-sheet A of the next.
99            Last, we used rationally designed neuroserpin mutants to demonstrate a direct involvement
100  and thrombotic proteases, whereas mammalian neuroserpin (NSP) inhibits only thrombolytic proteases.
101               In the central nervous system, neuroserpin (NSP) is a serpin thought to regulate t-PA e
102 her than plasminogen and that the effects of neuroserpin on seizure progression and neuronal cell sur
103                                         Like neuroserpin, one of the Spn4 proteins (Spn4.1) features
104 eath, and this effect is abrogated by either neuroserpin or the NMDA receptor antagonist MK-801.
105 ns are known that are responsible for mutant neuroserpin polymerization and accumulation as inclusion
106 dings provide strong support for the role of neuroserpin polymerization in the formation of the intra
107 ur cell lines and increased the retention of neuroserpin polymers in both HeLa cells and primary neur
108 ase-causing mutation and the accumulation of neuroserpin polymers in cell and fly models of the disea
109 ating primary hippocampal neurons with G392E neuroserpin polymers, we did not detect cytotoxicity or
110                            We show here that neuroserpin Portland (Ser52Arg), which causes a severe f
111  in keeping with the reactive centre loop of neuroserpin Portland being partially inserted into beta-
112 everity of dementia in FENIB associated with neuroserpin Portland.
113 otein consisted of residues 20 to 410 of the neuroserpin precursor deduced from its cDNA sequence ind
114   The increased mobility of these regions in neuroserpin relative to alpha(1)-antitrypsin provides a
115                     The degradation of G392E neuroserpin results from SREBP-dependent activation of t
116 xin-induced cell death and is independent of neuroserpin's ability to inhibit tPA activity.
117 to alpha(1)-antitrypsin provides a basis for neuroserpin's increased tendency toward the formation of
118 ese findings have led to the hypothesis that neuroserpin's neuroprotection is mediated by inhibition
119 e in the proband showed the published normal neuroserpin sequence except for the presence of both ade
120 ion and that intracerebral administration of neuroserpin significantly reduced this proteolysis.
121        An affinity-purified antibody against neuroserpin specifically labels the Collins bodies, conf
122 ellular handling of all four mutant forms of neuroserpin that cause FENIB.
123 hila models to show that the G392E mutant of neuroserpin that forms polymers is degraded by UBE2j1 E2
124 ttern of seizure spreading and a response to neuroserpin that is similar to that of wild-type animals
125 ogen activator tPA was lower in HA-NCI while neuroserpin, the CNS tPA inhibitor, was higher in AD and
126    We found that both active neuroserpin and neuroserpin.tPA complexes were internalized by mouse cor
127 d uPA activity were significantly reduced in neuroserpin-treated animals.
128 re progression is significantly delayed, and neuroserpin treatment does not further delay seizure spr
129  Inhibition of tPA within the hippocampus by neuroserpin treatment does not prevent seizure onset but
130     Like other members of the serpin family, neuroserpin undergoes a large conformational change as p
131  Ser52 was found indicating that only mutant neuroserpin was present in the inclusion bodies.
132 oserpin (20 micro L of 16 micro mol/L active neuroserpin) was intracisternally injected 3 hours and t
133 or the serine proteinase inhibitor (serpin), neuroserpin, was isolated from a human whole brain cDNA
134 aggregates, and the responsible mutations in neuroserpin were identified by sequencing of the neurose
135                    Both mutant and wild type neuroserpin were partially degraded by proteasomes.
136 rages 4.6 A but becomes as large as 7.5 A in neuroserpin while it remains stable at approximately 3.5
137 elix F away from the face of beta-sheet A in neuroserpin while no such movement is evident in alpha(1
138 pins such as alpha(1)-antitrypsin, wild-type neuroserpin will polymerize under near-physiological con
139     Chemical characterization of the variant neuroserpin will significantly enhance the understanding
140 pha(1)-antitrypsin within hepatocytes and of neuroserpin within neurons to cause cirrhosis and dement
141 NIB) is caused by the accumulation of mutant neuroserpin within neurons, but little is known about th

 
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