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1 f T cell-restricted intracellular antigen-1 (TIA1).
2 eins (hnRNPA1, TDP43, FUS, EWSR1, RBM14, and TIA1).
3 ranules that contain the RNA binding protein Tia1.
4 scle immunohistochemistry for CD8, CD57, and TIA1.
5 f PDCD4 by the RNA-binding proteins, HuR and TIA1.
6 tress granule-associated RNA-binding protein TIA1.
7 362 G>A (p.E384K) in the RNA-binding protein TIA1, a key component of stress granules.
8                                              TIA1, a protein critical for eukaryotic stress response
9 , knockdown experiments reveal that FAST and TIA1 act independently of one another to promote the inc
10                                   Decreasing TIA1 also inhibited the accumulation of tau oligomers at
11 usion of full-length SMN2 mRNAs by targeting TIA1 and FABP3 expression, which is distinct from other
12 analysis identified novel targets, including TIA1 and FABP3, for further characterization.
13                                  Splicing of TIA1 and its target genes in muscle and myoblast culture
14 ecessary for the binding of splicing factors TIA1 and Pcbp1 and that these proteins appear to act in
15                                              TIA1 and Pcbp1 associate in a complex containing RBM39,
16                                              TIA1 and TIAR are modular proteins with three N-terminal
17 t T-cell-restricted intracellular antigen 1 (TIA1) and TIA1-related (TIAR) proteins as intron-associa
18 , T-cell-restricted intracellular antigen 1 (TIA1), and TIA1-related protein (TIAR).
19                                Both FAST and TIA1 are also found in the nucleus, where TIA1 promotes
20 igomers generated during copartitioning with TIA1 are significantly more toxic than tau aggregates ge
21  of CPSF3 and hnRNP UL1 as facilitators, and TIA1 as repressor of mouse embryonic fibroblasts reprogr
22 h a Q domain is necessary and sufficient for TIA1-associated regulation of SMN2 exon 7 splicing in vi
23 d domains and this oligomeric form of apo fl TIA1, based on NMR chemical shifts.
24                                              Tia1 binds to a subset of transcripts involved in cell s
25  severed, leading to novel foci that contain TIA1 but lack other stress granule-defining components.
26 f T-cell-restricted intracellular antigen 1 (TIA1) but also switching of the expression of the two is
27 ed the cytotoxic granule-associated protein, TIA1, but perforin was detected in only one case.
28   The malignant cells were CD3+/ granzyme B+/TIA1+/CD8-/CD56-/S100-- with variable staining for beta
29 RNA-binding protein TIA1 to form PABPC1-SUMO-TIA1 complex that recruits U-rich mRNAs into SGs, protec
30                        In HeLa cells, mutant TIA1 constructs caused a mild increase in stress granule
31                                              TIA1 contains three RNA recognition motifs (RRMs) and a
32    We also show that increased expression of TIA1 counteracts the inhibitory effect of polypyrimidine
33                                     Reducing TIA1 decreased the number and size of granules co-locali
34         Underscoring the opposing effects of Tia1 deletion and low SMN level on BW gain, both C (+/+)
35               We next examined the effect of Tia1 deletion in novel C (+/+)/Tia1 (-/-) mice.
36                              However, unlike TIA1, FAST does not bind to the IAS1 sequence.
37   We observed early tail necrosis in C (+/+)/Tia1 (-/-) females but not in males.
38 N level on BW gain, both C (+/+) and C (+/+)/Tia1 (-/-) females showed similar BW gain trajectory at
39 al conditions, emphasizing the importance of TIA1 for tau biology.
40              We provide direct evidence that Tia1 forms a prion in yeast.
41 d translation in part due to dissociation of Tia1 from its mRNA targets.
42 d also reveals new insights into how HuR and TIA1 functions are integrated to achieve such regulation
43 separation of tau in the presence of RNA and TIA1 generates abundant tau oligomers.
44 y of WDM biopsies showed a focal increase of TIA1 in atrophic and vacuolated fibers.
45  factor driving stress granule formation via TIA1 in tauopathies.
46 cing the RBP T-cell intracellular antigen 1 (TIA1) in vivo protects against neurodegeneration and pro
47                                              TIA1 is reported to be downregulated in obese patients,
48  of tau with RNA and the RNA binding protein TIA1 is sufficient to drive phase separation of tau at p
49                          We show that female Tia1-knockout (Tia1 (-/-)) mice gain significant body we
50 ation analyses showed an increased burden of TIA1 LCD mutations in ALS patients compared to controls
51 reduced stress granule formation and reduced TIA1 levels in immortalized cells and in MAPT mutant neu
52 the effect of Tia1 deletion in novel C (+/+)/Tia1 (-/-) mice.
53           We show that female Tia1-knockout (Tia1 (-/-)) mice gain significant body weight (BW) durin
54            Postmortem neuropathology of five TIA1 mutations carriers showed a consistent pathological
55                               In live cells, TIA1 mutations delayed stress granule (SG) disassembly a
56                        The identification of TIA1 mutations in ALS/FTD reinforces the importance of R
57                                              TIA1 mutations significantly increased the propensity of
58  competitive mode of binding between HuR and TIA1 on the PDCD4 transcript in the cytoplasm, suggestin
59 tivation in which a coordinated effort among TIA1, Pcbp1, and RBM39 stabilizes or increases U2 snRNP
60     These data provide in vivo evidence that TIA1 plays a key role in mediating toxicity and further
61 nd TIA1 are also found in the nucleus, where TIA1 promotes the inclusion of exons flanked by weak spl
62                      We show that FAST, like TIA1, promotes the inclusion of exon IIIb of the FGFR2 m
63 ns significantly increased the propensity of TIA1 protein to undergo phase transition.
64                                    Moreover, Tia1/Pub1 acts cooperatively with release factor Sup35/e
65 n by the Q/N-rich prion domains of Sup35 and Tia1/Pub1 can be visualized as distinctive line structur
66                                              Tia1/Pub1 is a stress granule component carrying a Q/N-r
67 transcription factors such as GADD45A, SOX9, TIA1, RBBP9, and FOXM1 implicated.
68 ite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and rescued b
69   T-cell-restricted intracellular antigen 1 (TIA1) regulates SMN exon 7 splicing.
70 estricted intracellular antigen 1 (TIA1) and TIA1-related (TIAR) proteins as intron-associated positi
71 -restricted intracellular antigen 1 (TIA-1), TIA1-related protein (TIAR), and RasGAP-SH3 domain bindi
72 stricted intracellular antigen 1 (TIA1), and TIA1-related protein (TIAR).
73 he PDCD4 transcript, knockdown of HuR and/or TIA1 results in a significant decrease in steady-state P
74 nder mild conditions, full-length (fl) mouse TIA1 spontaneously oligomerizes to form a metastable col
75 granule associated RNA binding protein TIA1 (TIA1) stress granule protein and the influence of a dise
76                                Both FAST and TIA1 target a U-rich intronic sequence (IAS1) adjacent t
77  development and exacerbation of the C (+/+)/Tia1 (-/-) testis transcriptome.
78                     WDM is caused by mutated TIA1 through a dominant pathomechanism probably involvin
79 toxic granule associated RNA binding protein TIA1 (TIA1) stress granule protein and the influence of
80             Our findings expand the scope of TIA1/TIAR in genome-wide regulation of alternative splic
81                                 We show that TIA1/TIAR stimulate exon recognition in an entirely nove
82 ed PABPC1 interacts with RNA-binding protein TIA1 to form PABPC1-SUMO-TIA1 complex that recruits U-ri
83  to stress granules, where it interacts with TIA1 to modulate the process of stress-induced translati
84 ry approaches reveal binding of both HuR and TIA1 to the PDCD4 transcript.
85 ng the antiviral proteins, such as PCBP2 and TIA1, to form SG-like structures.
86 n T-cell-restricted intracellular antigen 1 (TIA1), translation initiation factors, RNA binding prote
87            Tau selectively copartitions with TIA1 under physiological conditions, emphasizing the imp
88                                 Depletion of TIA1 via small interfering RNAs (siRNAs), but not deplet
89                                       Mutant TIA1 was characterized by cell biological studies on HeL
90            We present a micellar model of fl TIA1 wherein RRM2 and RRM3 are colocalized, ordered, hyd