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1  proximal to the loci for gelsolin and alpha-fodrin.
2 orin 5 (AQP5) and 120-kDa fragments of alpha-fodrin.
3 estricting access of either Sharpin or alpha-fodrin.
4  occurs to a lesser extent than does that of fodrin.
5 clonal Abs recognizing the full-length alpha-fodrin.
6 caspase-3, but did not recognize full-length fodrin.
7 r-like pattern and was colocalized with beta-fodrin.
8 e commensurately higher levels of ankyrin or fodrin.
9 els and nerves, contain only alpha- and beta-fodrin.
10           Disruption of ELF (embryonic liver fodrin), a Smad4 adaptor protein, modulates TGF-beta sig
11                                              Fodrin, a component of the cortical cytoskeleton, also u
12                               Degradation of fodrin, a cytoskeletal linker molecule that attaches CD4
13 ti-ZO-1 antibodies confirmed its identity as fodrin, a protein believed to link membrane and other pr
14 s shows that IPF alpha is derived from alpha fodrin, a protein implicated in several diverse cellular
15 n astrocytes exposed to acidic medium, alpha-fodrin, a selective endogenous substrate of calpain, was
16 e-deficient mouse suggested a role for alpha-fodrin, a ubiquitous Ag, in the disease process.
17             Inhibition of calpain stabilized fodrin, a well characterized calpain substrate.
18 stem, frequently eliciting anti-150-kd alpha-fodrin Abs in addition to the previously reported anti-1
19               Exon 17b peptides also promote fodrin-actin complex formation.
20 ggest that insulin induces remodeling of the fodrin-actin network, which is required for the fusion o
21 essary and sufficient to induce formation of fodrin-actin-4.1R ternary complexes.
22 al properties of neuronal cells by promoting fodrin/actin association.
23 tive SAB domains of 4.1 homologs to sediment fodrin/actin was also investigated.
24           4.1G-SAB stimulates association of fodrin/actin, although with an approximately 2-fold redu
25 his antibody recognized cleavage products of fodrin after digestion by caspase-3, but did not recogni
26 n, but immune reactivity against SS-A, SS-B, fodrin, alpha- amylase, and carbonic anhydrase have been
27 sult, adult muscle fibers contain only alpha-fodrin (alphaII) and the muscle isoform of beta-spectrin
28                    We report here that alpha-fodrin, an abundant membrane-associated cytoskeletal pro
29 a caspase-cleavage site-directed antibody to fodrin, an abundant neuronal cytoskeleton protein.
30 Ank 2), and the cytoskeletal proteins, alpha-fodrin and beta-spectrin, also selectively co-immunoprec
31 -8 h) and their respective substrates, alpha-fodrin and Bid.
32 cur in vivo in a supramolecular complex with fodrin and F-actin.
33 e inhibitor, Ac-DEVD-CHO, strongly inhibited fodrin and lamin B1 cleavage, as well as nuclear morphol
34  apoptotic events, including the cleavage of fodrin and lamin B1.
35 s to degrade specific membrane/cytoskeletal (fodrin and leukocyte function-associated molecule 1) and
36 ith these apoptotic stimuli reveal that both fodrin and poly(ADP-ribose) polymerase proteolysis are i
37 d that t-SNAREs, NSF, actin, vimentin, alpha-fodrin and the calcium channels alpha1c and beta3 are as
38 e is the interaction between TJ proteins and fodrin and/or other cytoskeletal proteins.
39  using antibodies to non-erythroid spectrin (fodrin) and Golgi-spectrin (beta I sigma *) revealed tha
40 ovel beta-spectrin elf (embryonic liver beta-fodrin), and here we report the analysis of elf3, the lo
41 teins of the membrane cytoskeleton (ankyrin, fodrin, and actin) and analyzed by confocal imaging.
42 eins, including actin, myosin II, myosin 1G, fodrin, and an actin- and membrane-binding protein calle
43 isoform, PM Ca(2+) pump type 1 (PMCA1), beta-fodrin, and Ank 3.
44 poly(ADP-ribose) polymerase (PARP) and alpha-fodrin, and DNA degradation.
45 in complex, consisting of alpha-fodrin, beta-fodrin, and the muscle isoform of beta-spectrin.
46 we identified betaII-spectrin (also known as fodrin) as a schwannomin-binding protein.
47         Little is known about the anti-alpha-fodrin autoantibody response on a molecular level.
48 topes on the 150-kd cleaved product of alpha-fodrin become exposed to the immune system, frequently e
49 g intensities of Na/K-ATPase, ankyrin-3, and fodrin become more similar during development until they
50 orm of spectrin complex, consisting of alpha-fodrin, beta-fodrin, and the muscle isoform of beta-spec
51                   Antibodies to Ank 2, alpha-fodrin, beta-spectrin and IP(3)R-1 all co-immunoprecipit
52 ort that beta-spectrin (betaI) replaces beta-fodrin (betaII) at the sarcolemma as skeletal muscle fib
53 bstrate for mu-calpain is alpha II spectrin (fodrin, brain spectrin), which is cleaved between Tyr117
54 antibody was shown to cross-react with alpha-fodrin breakdown products.
55 ellular ATP induced DNA fragmentation, alpha-fodrin breakdown, and elevated levels of caspase-3-type
56                These include alpha- and beta-fodrin, calmodulin-dependent protein kinases, ADP-ribosy
57                    In vitro analysis of this fodrin caspase-cleavage product (CCP) antibody demonstra
58  formation, double-labeling experiments with fodrin CCP and PHF-1 were performed.
59  was a significant corresponding increase in fodrin CCP immunolabeling (r = 0.84).
60  from controls and AD were immunostained for fodrin (CCPs).
61 activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology.
62 pitope recognized became exposed after alpha-fodrin cleavage.
63 ibution indicates that this vimentin-plectin-fodrin complex provides a continuous linkage from the nu
64 tic cells, although no specific initiator of fodrin degradation has been identified.
65                In the absence of CD45, or if fodrin degradation is prevented, galectin-1-induced cell
66 ic uptake by macrophages of T cells in which fodrin degradation is prevented, relative to T cells in
67                  In this study, we show that fodrin degradation occurs during galectin-1 T cell death
68 and DNA degradation proceed, indicating that fodrin degradation occurs via a distinct pathway compare
69 , relative to T cells in which CD45-mediated fodrin degradation occurs.
70  T cell death and that CD45 is essential for fodrin degradation to occur.
71                We found that embryonic liver fodrin (ELF), a beta-Spectrin originally identified in e
72 ad2, Smad4 and Smad adaptor, embryonic liver fodrin (ELF), are prominent tumor suppressors in gastroi
73 receptor type II (TBRII) and embryonic liver fodrin (ELF).
74  the minimal sequences required to stimulate fodrin/F-actin association.
75 d production of 150 kD calpain-cleaved alpha-fodrin fragment, expression of IEGs, reactive astroglios
76 tion of actin and the translocation of alpha-fodrin from the cytoplasm to the plasma membrane.
77                             Both ankyrin and fodrin had complex subcellular distribution patterns, al
78                                              Fodrin has a highly punctate distribution in resting cel
79                        The anti-150-kd alpha-fodrin hmAbs may serve as valuable reagents for the stud
80 w of two SS donors and a panel of anti-alpha-fodrin IgGs was isolated by selection on alpha-fodrin im
81 drin IgGs was isolated by selection on alpha-fodrin immunoblots.
82      AKAP75 is co-localized with F-actin and fodrin in the cortical cytoskeleton.
83 icited to a 120-kd fragment of cleaved alpha-fodrin in the majority of SS patients, but generally not
84 oteolytic degradation of both GFAP and alpha-fodrin in these samples.
85         To determine whether caspases cleave fodrin in vivo, tissue sections from controls and AD wer
86 not with the 120-kd fragment or intact alpha-fodrin, indicating that the epitope recognized became ex
87                                 We show that fodrin interacts with the t-soluble N-ethylmaleimide-sen
88               The cytoskeletal protein alpha-fodrin is cleaved during this apoptotic process, and a s
89                           Moreover, purified fodrin is cleaved in vitro by CPP32 (but not by ICE) int
90 tin-binding protein, alphaII-spectrin (alpha-fodrin) is cleaved into 150-, 115-, and 110-kDa fragment
91 uitously expressed autoantigens (e.g., alpha-fodrin, La, and nuclear mitotic apparatus protein) and t
92 iating apoptotic events, including gelsolin, fodrin, laminB, and DFF45/ICAD, was delayed or absent.
93 but not low E-/P-cadherin cells, ankyrin and fodrin levels varied among cells, with a subset of cells
94                         Rather, AKAP75 (like fodrin) may be associated with a multiprotein complex th
95 ructural proteins including vimentin, actin, fodrin, moesin, and lamin B in resting peripheral blood
96  Included among these 11 proteins were alpha-fodrin (nonerythroid spectrin) and actin.
97           Membrane skeleton proteins include fodrin (nonerythroid spectrin), myosin-IIA, myosin-IG, a
98 henotype in vitro, including gelsolin, PAK2, fodrin, nuclear lamins and the inhibitory subunit of DNA
99 similar to those of other substrates such as fodrin or MAP2 that may be "natural" substrates for the
100 n is inherently different from hydrolysis of fodrin or MAP2, which are much less accessible as substr
101                                              Fodrin or nonerythroid spectrin is an abundant component
102 muscle contains spectrin (or spectrin I) and fodrin (or spectrin II), members of the spectrin superge
103                                  The 120 kDa fodrin peptide is associated with caspase-3 activation d
104  (one component of SSA), La (SSB), and alpha-fodrin protein, common autoantigens in Sjogren's syndrom
105                                     However, fodrin proteolysis can be distinguished from poly(ADP-ri
106                  These findings suggest that fodrin proteolysis in vivo may reflect the activity of m
107                Strikingly, CPP32 activation, fodrin proteolysis, and PS externalization were all inhi
108 ited ATP-induced DNA fragmentation and alpha-fodrin proteolysis, but had no effect on ATP-induced SAP
109 m Fas-induced apoptosis but does not prevent fodrin proteolysis, indicating that cleavage of this pro
110 n D neither inhibits GLUT4 translocation nor fodrin redistribution in adipocytes.
111          In contrast, the bulk of AKAP75 and fodrin remain associated with the cortical region of cyt
112           Third, Na/K-ATPase, ankyrin-3, and fodrin specifically colocalize at the basal-lateral plas
113 t 25% of SS sera exhibited this 150-kd alpha-fodrin specificity.
114 reased production of the 120-kDa fragment of fodrin suggesting enhanced caspase-3 activity, an increa
115 of plasma membrane Ca2+-ATPase isoform 1 and fodrin; the degradation is attenuated by buffering [Ca2+
116 s to the uropod associated with vimentin and fodrin; their spatial distribution indicates that this v
117  and insulin causes a dramatic remodeling of fodrin to a more diffuse pattern.
118 nsporter 4 (GLUT4) translocation, and causes fodrin to partially redistribute from the plasma membran
119                           Importantly, alpha-fodrin translocation was prevented by LXA(4) but actin r
120              Calpain-mediated proteolysis of fodrin was also detected, indicating that calpain is act
121 f calpain specific target substrates such as fodrin was significantly reduced in these mice.
122           This study demonstrated that alpha-fodrin was uniquely cleaved during cytotoxic lymphocyte
123 ific degradation of the endogenous substrate fodrin) was marginally increased at 4 h and significantl
124          The sublamellar structural protein, fodrin, was metabolized to products consistent with calp
125  AQP5 and cleaved 120-kDa fragments of alpha-fodrin were found in tears and lacrimal gland lysates, r
126 n and calpain-specific degradation products (fodrin) were increased by 90.1% and 52.7%, respectively,
127 alpha3, and IP(3)R-1 in neurons and of alpha-fodrin with NCX1 and SERCA2 in astrocytes.
128 tion and association of ELF (embryonic liver fodrin) with Smad3 and Smad4 resulting in nuclear transl

 
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