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1                                              hnRNP H and F are alternative splicing factors for numer
2                                              hnRNP H does not appear to mediate splicing control or s
3                                              hnRNP H family proteins bind to the enhancer as well; th
4                                              hnRNP H is required for interaction of U1 snRNP with the
5 nce was also specifically bound by hnRNP A1, hnRNP H, ASF/SF2 and SRp40, but not by 9G8.
6 to this element were identified as hnRNP A1, hnRNP H, hnRNP F, and SF2/ASF by site-specific cross-lin
7                           Antibodies against hnRNP H immunoprecipitated cross-linked p55 and induced
8  that the sequence GGGA is recognized by all hnRNP H family proteins.
9 ds only hnRNP H/H' to a binding site for all hnRNP H family members.
10  expression level, suggesting that Chtop and hnRNP H regulate intron 2 retention of Chtop mRNA antago
11 g of each factor demonstrated that SRSF1 and hnRNP H antagonistically modulate splicing by binding ex
12 nt on the antagonistic activities of 9G8 and hnRNPs H and F.
13 s from in vitro splicing reactions with anti-hnRNP H antibody indicated that hnRNP H remains bound to
14 sis of purified p58 protein identified it as hnRNP H.
15 ction and identified by mass spectrometry as hnRNP H.
16     The c-src DCS has been shown to assemble hnRNP H, not hnRNP F, from HeLa cell extracts, and we sh
17 physical and functional interactions between hnRNP H, CUG-BP1 and MBNL1 dictate IR splicing in normal
18 el G-rich elements tested were found to bind hnRNP H/H' protein and the processing of selected signal
19                 Sequences capable of binding hnRNP H protein with varying affinities may play a role
20 RNA interference was used to knock down both hnRNP H and hnRNP F.
21 endent suppressor complex consisting of both hnRNP H and CUG-BP1, which is required to maximally inhi
22 down and cDNA expression, we found that both hnRNP H and F activate the HRAS cassette exon.
23 n that affects the spatial location of bound hnRNP H with respect to the exon 6D splicing determinant
24 otifs, some resembling known motifs bound by hnRNPs H and A1.
25 nalyses of ENCODE RNA-seq datasets confirmed hnRNP H regulation of HRAS splicing.
26 tracts revealed large assemblages containing hnRNP H, H', and F but deficient in CstF-64 in memory B-
27 polyadenylation, since viral RNAs containing hnRNP H-specific mutations were spliced and polyadenylat
28 n normal myoblasts, overexpression of either hnRNP H or CUG-BP1 results in the formation of an RNA-de
29                      These results establish hnRNP H and hnRNP F as being repressors of exon inclusio
30 C repeat RNA in vitro is the splicing factor hnRNP H, and that this interaction is linked to G-Q form
31 e previously identified an auxiliary factor, hnRNP H/H', which stimulates 3'-end processing through a
32 nce that interacts with the splicing factors hnRNP H and SC35.
33  protein mutation suggests the potential for hnRNP H to antagonize polyadenylation.
34    Despite being described as a receptor for hnRNP H, the ESS2p element is sequestered by base pairin
35     Thus, we identified a potential role for hnRNP H in basal and dynamic mitochondrial function that
36 diction indicated multiple binding sites for hnRNP H and hnRNP F within these cis-regulatory elements
37       Much less is known, however, about how hnRNP H and hnRNP F silence exons.
38                                     However, hnRNP H binding to the SRE acts as an enhancer of exon 6
39  mutant DMPK-derived RNA and have identified hnRNP H as an abundant candidate.
40                   In this study, we identify hnRNP H and hnRNP F proteins as being novel silencers of
41 lysis identified a corresponding decrease in hnRNP H protein in 114 kb congenic mice.
42 urprisingly, there was a twofold increase in hnRNP H protein in the striatal synaptosome of H1(+/-) m
43 deling ribonucleoprotein complexes including hnRNP H, H2, H3, F, A2/B1, K, L, DDX5, DDX17, and DHX9.
44  dampen the inhibitory activity of increased hnRNP H levels on IR splicing in normal myoblasts.
45 elevated in DM1 myoblasts and that increased hnRNP H levels in normal myoblasts results in the inhibi
46 ns, which correlates with elevated insoluble hnRNP H/G-Q aggregates.
47 eptide sequencing reveal that this factor is hnRNP H, a member of the heterogeneous nuclear ribonucle
48 rate dysregulated splicing of multiple known hnRNP H-target transcripts in C9 patient brains, which c
49 taining this sequence to a substrate lacking hnRNP H binding activity is sufficient to promote bindin
50 ric complex containing the proteins hnRNP M, hnRNP H, hnRNP C, Matrin3, NF110/NFAR-2, NF45, and DDX5,
51                      However, the ability of hnRNP H mutations to suppress the read-through caused by
52                                   Binding of hnRNP H correlates with the ESS activity.
53                      The specific binding of hnRNP H requires not only a CUG repeat expansion but als
54 onjunction with si-RNA mediated depletion of hnRNP H contributes to partial rescue of the IR splicing
55 e splicing reactions or partial depletion of hnRNP H from nuclear extract activates exon 7 splicing i
56 rk enrichment, consistent with the effect of hnRNP H on HRAS splicing.
57                        The identification of hnRNP H as a factor capable of binding and possibly modu
58                   Partial immunodepletion of hnRNP H from the nuclear extract partially inactivated t
59                       Immunoprecipitation of hnRNP H cross-linked to the N1 enhancer RNA, as well as
60                           The involvement of hnRNP H in the activity of an ESS may represent a protot
61 blasts demonstrates that increased levels of hnRNP H, H2, H3, F, and DDX5 independently dysregulate s
62                                      Loss of hnRNP H/F altered cell cycle progression and induced apo
63 s of the enhancer complex in the presence of hnRNP H-specific antibodies, confirmed that hnRNP H is a
64 emingly contrasting functional properties of hnRNP H appear to be caused by a change in the RNA secon
65 that may also explain the dual properties of hnRNP H in splicing regulation.
66                        The possible roles of hnRNP H in NRS function are discussed.
67 icate C9 expansion-mediated sequestration of hnRNP H as a significant contributor to neurodegeneratio
68                               Suppression of hnRNP H expression by RNAi rescued nuclear retention of
69                   Furthermore, expression of hnRNPs H, F, 2H9, A1, and A2 and SR proteins SF2 and SRp
70 g virus, we altered the expression levels of hnRNPs H, F, 2H9, GRSF1, A1, A2, and A3 and SR proteins
71                            Overexpression of hnRNPs H and F blocked 9G8-mediated splicing both in viv
72  of the DCS from a substrate that binds only hnRNP H/H' to a binding site for all hnRNP H family memb
73 iscovered a role for the RNA binding protein hnRNP H in methamphetamine reward and reinforcement.
74 y heterogeneous nuclear ribonuclear protein (hnRNP)H/F.
75  a splicing-suppressing RNA-binding protein, hnRNP H.
76  enhances the binding of two other proteins, hnRNP H and KSRP, to the DCS RNA.
77 RS binds serine/arginine-rich (SR) proteins, hnRNP H and the U1/U11 snRNPs, and appears to inhibit sp
78 n of antibodies that specifically recognizes hnRNP H to the splicing reactions or partial depletion o
79 n be restored by the addition of recombinant hnRNP H, indicating that hnRNP H is an important factor
80 reversed by addition of purified recombinant hnRNP H.
81 lity shift assays indicated that recombinant hnRNP H specifically interacts with the p55 binding site
82 steady-state levels of the splice regulator, hnRNP H, are elevated in DM1 myoblasts and that increase
83     Heterogeneous nuclear ribonucleoprotein (hnRNP) H and F are members of a closely related subfamil
84 ich heterogeneous nuclear ribonucleoprotein (hnRNP) H and F regulate proteolipid protein (PLP)/DM20 a
85 the heterogeneous nuclear ribonucleoprotein (hnRNP) H protein family to determine their RNA binding s
86 the heterogeneous nuclear ribonucleoprotein (hnRNP) H protein family, H, H', F, and 2H9, are involved
87     Heterogeneous nuclear ribonucleoprotein (hnRNP) H, polypyrimidine tract binding protein (PTB), an
88 he heterogeneous nuclear ribonucleoproteins (hnRNPs) H and F bind to and compete for the same element
89 nylation signals identified potential G-rich hnRNP H/H' binding sites at similar downstream locations
90 the context of the wild-type viral sequence, hnRNP H acts as a repressor of exon 6D inclusion indepen
91 to the mechanisms linking increased synaptic hnRNP H with decreased methamphetamine-induced dopamine
92 rked increase in basal level of synaptosomal hnRNP H and mitochondrial proteins that decreased in res
93  hnRNP H-specific antibodies, confirmed that hnRNP H is a protein component of the splicing enhancer
94 s with the p55 binding site, confirming that hnRNP H is p55.
95 ly, in vitro binding assays demonstrate that hnRNP H can interact with the related protein hnRNP F, s
96 onstitution assays we have demonstrated that hnRNP H/H' can stimulate processing of two additional mo
97                  These results indicate that hnRNP H participates in exclusion of exon 7 in nonmuscle
98 ns with anti-hnRNP H antibody indicated that hnRNP H remains bound to the src pre-mRNA after the asse
99 tion of recombinant hnRNP H, indicating that hnRNP H is an important factor for N1 splicing.
100                    In addition, we show that hnRNP H accelerates intron 2 splicing of Chtop mRNA in a
101                                 We show that hnRNP H and hnRNP F proteins are present in a complex wi
102 depletion-- reconstitution studies show that hnRNP H is essential for enhancer activity.
103                        Finally, we show that hnRNP H/F are transcription-dependent shuttling proteins
104  from the HIV-1 tat gene and have shown that hnRNP H family members are required for efficient splici
105       Collectively, the results suggest that hnRNP H and F are GYR domain-dependent shuttling protein
106                       Our data indicate that hnRNPs H, H', F, 2H9, and GRSF-1 bind the consensus moti
107 the related protein hnRNP F, suggesting that hnRNPs H and F may exist as a heterodimer in a single en
108                                          The hnRNP H protein family members activated splicing of the
109 ith RNA-seq revealed that exons carrying the hnRNP H-binding GGGGG motif are predisposed to be skippe
110 to the point mutation region may convert the hnRNP H-U1 snRNP complex into a splicing enhancer.
111 ee RNA-binding motifs and is a member of the hnRNP H family of RNA-binding proteins.
112  (GST) pulldown assays demonstrated that the hnRNP H NLS interacts with the import receptor transport
113 ermined to be a common property of all three hnRNP H/H' binding sites.
114 bind to degenerative binding motifs, whereas hnRNP H strictly requires an uninterrupted stretch of po
115  NRS did not affect polyadenylation, whereas hnRNP H strongly inhibited polyadenylation.
116                  We propose a model in which hnRNP H and SR proteins compete for binding to the NRS.
117 pansion, and more frequently colocalize with hnRNP H.
118 context it cannot form a stable complex with hnRNP H.
119             By selectively coordinating with hnRNP H/F and U proteins, AKAP95 appears to mainly promo
120 tissue-specific splicing by interacting with hnRNP H protein subfamily.
121  MBNL1 show RNA-independent interaction with hnRNP H and dampen the inhibitory activity of increased

 
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