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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.
9 , knockdown experiments reveal that FAST and TIA1 act independently of one another to promote the inc
11 usion of full-length SMN2 mRNAs by targeting TIA1 and FABP3 expression, which is distinct from other
14 ecessary for the binding of splicing factors TIA1 and Pcbp1 and that these proteins appear to act in
17 t T-cell-restricted intracellular antigen 1 (TIA1) and TIA1-related (TIAR) proteins as intron-associa
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
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
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
32 We also show that increased expression of TIA1 counteracts the inhibitory effect of polypyrimidine
38 N level on BW gain, both C (+/+) and C (+/+)/Tia1 (-/-) females showed similar BW gain trajectory at
42 d also reveals new insights into how HuR and TIA1 functions are integrated to achieve such regulation
46 cing the RBP T-cell intracellular antigen 1 (TIA1) in vivo protects against neurodegeneration and pro
48 of tau with RNA and the RNA binding protein TIA1 is sufficient to drive phase separation of tau at p
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
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
61 nd TIA1 are also found in the nucleus, where TIA1 promotes the inclusion of exons flanked by weak spl
65 n by the Q/N-rich prion domains of Sup35 and Tia1/Pub1 can be visualized as distinctive line structur
68 ite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and rescued b
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
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
79 toxic granule associated RNA binding protein TIA1 (TIA1) stress granule protein and the influence of
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
86 n T-cell-restricted intracellular antigen 1 (TIA1), translation initiation factors, RNA binding prote