ライフサイエンスコーパス: TIA1

1 f T cell-restricted intracellular antigen-1 (TIA1).

2 ranules that contain the RNA binding protein Tia1.

3 scle immunohistochemistry for CD8, CD57, and TIA1.

4 f PDCD4 by the RNA-binding proteins, HuR and TIA1.

5 362 G>A (p.E384K) in the RNA-binding protein TIA1, a key component of stress granules.

6 , knockdown experiments reveal that FAST and TIA1 act independently of one another to promote the inc

7 Decreasing TIA1 also inhibited the accumulation of tau oligomers at

8 Splicing of TIA1 and its target genes in muscle and myoblast culture

9 ecessary for the binding of splicing factors TIA1 and Pcbp1 and that these proteins appear to act in

10 TIA1 and Pcbp1 associate in a complex containing RBM39,

11 TIA1 and TIAR are modular proteins with three N-terminal

12 t T-cell-restricted intracellular antigen 1 (TIA1) and TIA1-related (TIAR) proteins as intron-associa

13 , T-cell-restricted intracellular antigen 1 (TIA1), and TIA1-related protein (TIAR).

14 Both FAST and TIA1 are also found in the nucleus, where TIA1 promotes

15 h a Q domain is necessary and sufficient for TIA1-associated regulation of SMN2 exon 7 splicing in vi

16 Tia1 binds to a subset of transcripts involved in cell s

17 severed, leading to novel foci that contain TIA1 but lack other stress granule-defining components.

18 f T-cell-restricted intracellular antigen 1 (TIA1) but also switching of the expression of the two is

19 ed the cytotoxic granule-associated protein, TIA1, but perforin was detected in only one case.

20 The malignant cells were CD3+/ granzyme B+/TIA1+/CD8-/CD56-/S100-- with variable staining for beta

21 In HeLa cells, mutant TIA1 constructs caused a mild increase in stress granule

22 We also show that increased expression of TIA1 counteracts the inhibitory effect of polypyrimidine

23 Reducing TIA1 decreased the number and size of granules co-locali

24 Underscoring the opposing effects of Tia1 deletion and low SMN level on BW gain, both C (+/+)

25 We next examined the effect of Tia1 deletion in novel C (+/+)/Tia1 (-/-) mice.

26 However, unlike TIA1, FAST does not bind to the IAS1 sequence.

27 We observed early tail necrosis in C (+/+)/Tia1 (-/-) females but not in males.

28 N level on BW gain, both C (+/+) and C (+/+)/Tia1 (-/-) females showed similar BW gain trajectory at

29 We provide direct evidence that Tia1 forms a prion in yeast.

30 d translation in part due to dissociation of Tia1 from its mRNA targets.

31 d also reveals new insights into how HuR and TIA1 functions are integrated to achieve such regulation

32 y of WDM biopsies showed a focal increase of TIA1 in atrophic and vacuolated fibers.

33 cing the RBP T-cell intracellular antigen 1 (TIA1) in vivo protects against neurodegeneration and pro

34 TIA1 is reported to be downregulated in obese patients,

35 We show that female Tia1-knockout (Tia1 (-/-)) mice gain significant body we

36 ation analyses showed an increased burden of TIA1 LCD mutations in ALS patients compared to controls

37 the effect of Tia1 deletion in novel C (+/+)/Tia1 (-/-) mice.

38 We show that female Tia1-knockout (Tia1 (-/-)) mice gain significant body weight (BW) durin

39 Postmortem neuropathology of five TIA1 mutations carriers showed a consistent pathological

40 In live cells, TIA1 mutations delayed stress granule (SG) disassembly a

41 The identification of TIA1 mutations in ALS/FTD reinforces the importance of R

42 TIA1 mutations significantly increased the propensity of

43 competitive mode of binding between HuR and TIA1 on the PDCD4 transcript in the cytoplasm, suggestin

44 tivation in which a coordinated effort among TIA1, Pcbp1, and RBM39 stabilizes or increases U2 snRNP

45 These data provide in vivo evidence that TIA1 plays a key role in mediating toxicity and further

46 nd TIA1 are also found in the nucleus, where TIA1 promotes the inclusion of exons flanked by weak spl

47 We show that FAST, like TIA1, promotes the inclusion of exon IIIb of the FGFR2 m

48 ns significantly increased the propensity of TIA1 protein to undergo phase transition.

49 Moreover, Tia1/Pub1 acts cooperatively with release factor Sup35/e

50 n by the Q/N-rich prion domains of Sup35 and Tia1/Pub1 can be visualized as distinctive line structur

51 Tia1/Pub1 is a stress granule component carrying a Q/N-r

52 ite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and rescued b

53 T-cell-restricted intracellular antigen 1 (TIA1) regulates SMN exon 7 splicing.

54 estricted intracellular antigen 1 (TIA1) and TIA1-related (TIAR) proteins as intron-associated positi

55 -restricted intracellular antigen 1 (TIA-1), TIA1-related protein (TIAR), and RasGAP-SH3 domain bindi

56 stricted intracellular antigen 1 (TIA1), and TIA1-related protein (TIAR).

57 he PDCD4 transcript, knockdown of HuR and/or TIA1 results in a significant decrease in steady-state P

58 Both FAST and TIA1 target a U-rich intronic sequence (IAS1) adjacent t

59 development and exacerbation of the C (+/+)/Tia1 (-/-) testis transcriptome.

60 WDM is caused by mutated TIA1 through a dominant pathomechanism probably involvin

61 Our findings expand the scope of TIA1/TIAR in genome-wide regulation of alternative splic

62 We show that TIA1/TIAR stimulate exon recognition in an entirely nove

63 to stress granules, where it interacts with TIA1 to modulate the process of stress-induced translati

64 ry approaches reveal binding of both HuR and TIA1 to the PDCD4 transcript.

65 ng the antiviral proteins, such as PCBP2 and TIA1, to form SG-like structures.

66 n T-cell-restricted intracellular antigen 1 (TIA1), translation initiation factors, RNA binding prote

67 Depletion of TIA1 via small interfering RNAs (siRNAs), but not deplet

68 Mutant TIA1 was characterized by cell biological studies on HeL