Affinage

TIA1

Cytotoxic granule associated RNA binding protein TIA1 · UniProt P31483

Length
386 aa
Mass
43.0 kDa
Annotated
2026-04-28
100 papers in source corpus 39 papers cited in narrative 39 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TIA1 is a multifunctional RNA-binding protein that nucleates stress granules and regulates both mRNA translation and alternative pre-mRNA splicing. Its three RNA recognition motifs (RRMs) bind U-rich and C-rich RNA sequences — RRM2 provides primary sequence-specific recognition while RRM3 extends binding affinity and RRM1 mediates protein–protein interaction with U1 snRNP component U1-C — and its C-terminal glutamine-rich prion-related domain (PRD) drives concentration-dependent, prion-like self-aggregation required for stress granule nucleation downstream of eIF2α phosphorylation, a process regulated by Zn²⁺, HSP70, and oxidative modification (PMID:10613902, PMID:15371533, PMID:29298433, PMID:26738979). As a translational silencer, TIA1 binds AU-rich elements in the 3′ UTRs of target mRNAs including TNF-α, COX-2, cytochrome c, p53, and 5′TOP transcripts, sequestering them from polysomes into stress granules and channeling them into both 5′→3′ and 3′→5′ mRNA decay pathways (PMID:10921895, PMID:12885872, PMID:16581801, PMID:21979918, PMID:17711853). As a splicing activator, TIA1 binds U-rich intronic sequences downstream of 5′ splice sites and recruits U1 snRNP via direct interaction with U1-C through RRM1 and the Q domain, promoting exon inclusion of targets including Fas exon 6, FGFR2 K-SAM exon, and SMN2 exon 7, with its splicing activity enhanced by FAST kinase phosphorylation (PMID:11106748, PMID:12486009, PMID:16109372, PMID:17135269). Mutations in TIA1's low-complexity domain cause Welander distal myopathy (E384K) and are associated with ALS/FTD (P362L), with disease mutations altering phase-separation dynamics and stress granule persistence, promoting pathological co-aggregation with TDP-43 and tau (PMID:23401021, PMID:28817800, PMID:36112647).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1995 High

    Identifying TIA-1 as a substrate of FAST kinase during Fas-mediated apoptosis established that TIA-1 is post-translationally regulated in a signaling pathway upstream of DNA fragmentation.

    Evidence In vitro kinase assay and temporal phosphorylation analysis relative to apoptosis in Fas-stimulated cells

    PMID:7544399

    Open questions at the time
    • Specific phosphorylation sites on TIA-1 not mapped
    • Functional consequence of phosphorylation on TIA-1 activity not determined
  2. 1996 High

    Determining that RRM2 provides sequence-specific recognition of U-rich RNA while RRM1 lacks detectable RNA binding resolved the division of labor among TIA-1's three RRM domains.

    Evidence SELEX with individual recombinant RRM domains and filter binding assays

    PMID:8576255

    Open questions at the time
    • Role of RRM3 in RNA binding incompletely characterized
    • No structural information on binding mode
  3. 1999 High

    Demonstrating that TIA-1 acts downstream of eIF2α phosphorylation to nucleate stress granules containing untranslated mRNAs established TIA-1 as a core SG assembly factor linking translational arrest to cytoplasmic mRNP remodeling.

    Evidence Phosphomimetic and nonphosphorylatable eIF2α mutants combined with dominant-negative TIA-1 truncation in mammalian cells

    PMID:10613902

    Open questions at the time
    • Mechanism by which eIF2α phosphorylation triggers TIA-1 recruitment unknown
    • Other SG nucleators not yet identified
  4. 2000 High

    Multiple studies converged to establish TIA-1 as both a translational silencer of ARE-containing mRNAs (TNF-α) and a splicing activator that promotes 5′ splice site recognition by U1 snRNP, revealing its dual nuclear/cytoplasmic regulatory functions.

    Evidence TIA-1 knockout macrophages showed increased TNF-α translation without mRNA destabilization; in vitro splicing assays and UV cross-linking showed TIA-1 binds U-rich intronic sequences to facilitate U1 snRNP recruitment on Fas, msl-2, and FGFR2 pre-mRNAs; FRAP showed dynamic TIA-1 shuttling in SGs

    PMID:10921895 PMID:10938105 PMID:11106748 PMID:11121440

    Open questions at the time
    • Protein partner mediating U1 snRNP recruitment not identified
    • Whether translational silencing and splicing regulation share common RNA-binding surfaces unknown
  5. 2002 High

    Mapping the direct interaction between TIA-1 and U1 snRNP protein U1-C to RRM1 and the Q domain resolved how TIA-1 mechanistically bridges pre-mRNA binding (via RRM2/3) and spliceosome recruitment (via RRM1/Q).

    Evidence Co-precipitation and domain dissection with in vitro U1 snRNP recruitment assays

    PMID:12486009

    Open questions at the time
    • Structural basis of TIA-1–U1-C interaction not determined
    • Whether phosphorylation modulates this interaction unknown
  6. 2004 High

    Demonstrating that TIA-1's prion-related domain drives concentration-dependent aggregation required for SG assembly — replaceable by yeast SUP35-NM — established the prion-like mechanism as the biophysical basis of SG nucleation.

    Evidence Domain-swap mutants, protease protection, HSP70 inhibition, and TIA-1 knockout MEFs showing impaired SG formation

    PMID:15371533

    Open questions at the time
    • Whether PRD aggregation is liquid–liquid phase separation versus solid aggregation not distinguished
    • Endogenous regulators of PRD aggregation beyond HSP70 not identified
  7. 2005 High

    Genome-scale target identification and mechanistic dissection showed TIA-1 binds a bipartite U-rich motif in ~3% of transcripts to repress their translation, while in splicing it facilitates cross-exon communication by promoting U2AF recruitment through U1 snRNP positioning.

    Evidence RIP-Chip with RNAi validation for translational targets; in vitro reconstitution of Fas exon 6 splicing showing TIA-1-dependent U2AF enhancement; domain-mapped nucleo-cytoplasmic shuttling

    PMID:16109372 PMID:16227602 PMID:16278295

    Open questions at the time
    • Overlap between splicing and translational target mRNAs not assessed
    • How shuttling dynamics partition TIA-1 between nuclear and cytoplasmic functions unclear
  8. 2007 High

    Establishing that TIA-1-mediated translational silencing channels mRNAs into both 5′→3′ (DCP2) and 3′→5′ (exosome) decay pathways connected SG-dependent translational arrest to mRNA turnover as a unified post-transcriptional regulatory axis.

    Evidence mRNA tethering assay with siRNA knockdown of DCP2 and Rrp46; polysome-stabilizing drug rescue

    PMID:17711853

    Open questions at the time
    • Whether decay occurs within SGs or upon SG disassembly not resolved
    • Direct recruitment of decay factors by TIA-1 not shown
  9. 2006 High

    Demonstrating that FAST kinase phosphorylation of TIA-1 enhances U1 snRNP recruitment without increasing RNA binding provided the first evidence that a kinase tunes TIA-1's splicing activity through its protein-interaction rather than RNA-binding function.

    Evidence In vitro kinase assay combined with U1 snRNP recruitment and in vivo Fas splicing assays upon FAST knockdown or overexpression

    PMID:17135269

    Open questions at the time
    • Specific phosphorylation sites mediating enhanced U1 recruitment not mapped
    • Structural mechanism of phosphorylation-enhanced U1-C interaction unknown
  10. 2008 High

    Systematic knockdown established that TIA1/TIAL1 regulate ~15% of alternative cassette exons genome-wide via U-rich motifs within 100 nt of 5′ splice sites, and RSK2 was identified as a signaling kinase that co-localizes with TIA-1 in SGs via direct PRD interaction.

    Evidence Double TIA1/TIAL1 siRNA knockdown with RT-PCR of 41 exons; endogenous co-IP and domain mapping for RSK2–TIA-1; live-cell imaging

    PMID:18456862 PMID:18775331

    Open questions at the time
    • Whether RSK2 phosphorylates TIA-1 directly not demonstrated
    • Functional consequence of RSK2–TIA-1 interaction on splicing not tested
  11. 2011 High

    TIA-1/TIAR were shown to arrest translation of 5′TOP mRNAs under amino acid starvation via GCN2/mTOR signaling, extending TIA-1's translational silencing role beyond ARE-containing mRNAs to the global protein biosynthesis machinery.

    Evidence PAR-CLIP/RIP combined with polysome profiling and GCN2/mTOR pathway inhibition

    PMID:21979918

    Open questions at the time
    • How TIA-1 recognizes 5′TOP sequences structurally not resolved
    • Whether TIA-1 directly senses amino acid levels or responds only via eIF2α phosphorylation unclear
  12. 2013 High

    Identification of the dominant E384K mutation in TIA1's Q-rich domain as the cause of Welander distal myopathy linked altered SG dynamics and splicing (SMN2) to a human Mendelian disease, validating the functional importance of the PRD in vivo.

    Evidence Linkage analysis and exome sequencing in WDM families; FRAP showing reduced SG dynamics; RT-PCR showing altered SMN2 splicing in patient muscle

    PMID:23401021

    Open questions at the time
    • Whether E384K disrupts U1-C interaction not tested
    • Animal model of WDM not established
  13. 2014 High

    Structural studies by NMR, SAXS, and SPR resolved how TIA-1's RRMs are independent in solution but form a compact arrangement upon RNA binding, with RRM3 contributing C-rich RNA recognition relevant to 5′TOP mRNA binding.

    Evidence NMR solution structure, ITC, SAXS, SPR, and STD-NMR of individual and tandem RRM domains with various RNA substrates

    PMID:24682828 PMID:24824036

    Open questions at the time
    • No high-resolution structure of full-length TIA-1 with RNA
    • PRD structure in context of full-length protein unknown
  14. 2016 High

    Two discoveries established that tau directly interacts with TIA1's PRD to promote SG formation and tau misfolding, while ROS-mediated oxidation of TIA-1 inhibits SG nucleation and promotes apoptosis, revealing opposing regulatory inputs on TIA-1 phase behavior with implications for neurodegeneration.

    Evidence Reciprocal co-IP from brain tissue with TIA1 KO/KD rescue for tau; H₂O₂ treatment with SG assembly and apoptosis readouts for ROS

    PMID:26738979 PMID:27160897

    Open questions at the time
    • Oxidation sites on TIA-1 not mapped
    • Whether tau–TIA1 interaction occurs in liquid or solid phase in vivo unclear
  15. 2017 High

    ALS/FTD-associated mutations (P362L) in TIA1's LCD were shown to enhance phase transition propensity and delay SG disassembly, trapping TDP-43 in non-dynamic insoluble SGs, while crystal structure of RRM2–DNA complex provided the first atomic resolution view of TIA-1 target recognition.

    Evidence Phase separation assays and FRAP for disease mutations; X-ray crystallography at 2.3 Å for RRM2–DNA; SAXS for RRM23–RNA compact arrangement

    PMID:28184449 PMID:28817800

    Open questions at the time
    • Whether SG persistence is sufficient to cause neurodegeneration in vivo not established
    • No structure of full RRM123–RNA complex
  16. 2018 High

    Zinc was identified as a stress-inducible second messenger promoting TIA-1 multimerization and phase separation, while PAR-CLIP of TIA1/TIAL1 double knockout revealed that loss of TIA1-dependent splicing triggers PKR activation and paradoxical SG formation through PRKRA mis-splicing.

    Evidence In vitro phase separation with recombinant TIA-1 ± Zn²⁺ and TPEN chelation in cells; PAR-CLIP with DKO transcriptomics and PRKRA/PKR rescue

    PMID:29298433 PMID:29429924

    Open questions at the time
    • Zinc-binding sites on TIA-1 not mapped
    • Full catalog of splicing events whose mis-regulation has pathological consequences not complete
  17. 2021 High

    Reconstitution experiments showed that tandem TIA-1 binding sites in target RNAs (including p53 3′UTR) drive phase separation stoichiometrically, and that TIA1+RNA together generate toxic tau oligomers at physiological concentrations, mechanistically linking SG biology to tau toxicity.

    Evidence In vitro phase separation with designed and native RNA sequences; tau oligomer toxicity assays with recombinant TIA1/RNA/tau

    PMID:33619090 PMID:33621982

    Open questions at the time
    • Whether tandem-site-driven phase separation occurs at endogenous TIA-1 concentrations in cells not demonstrated
    • In vivo relevance of TIA1-driven tau oligomerization to tauopathy progression not confirmed
  18. 2022 High

    Structural analysis of disease mutations in TIA1's PLD revealed that ALS mutations P362L and A381T enhance β-sheet formation and condensation respectively, while WDM mutation E384K attenuates self-assembly, providing a structural framework for genotype–phenotype correlations.

    Evidence NMR, molecular dynamics simulations, and 3D electron crystallography of PLD peptides

    PMID:36112647

    Open questions at the time
    • Full-length PLD structure in phase-separated state not determined
    • Whether therapeutic modulation of PLD assembly is feasible unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural basis of how TIA-1 simultaneously coordinates RNA binding, U1-C interaction, and prion-like self-assembly in the context of the full-length protein remains unresolved, as does the in vivo mechanism by which disease mutations in the PLD differentially drive myopathy versus ALS/FTD.
  • No full-length TIA-1 structure in complex with RNA and protein partners
  • Animal models linking specific TIA1 mutations to neurodegenerative disease phenotypes are lacking
  • How cells distinguish reversible TIA-1 phase separation from pathological solidification is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 5 GO:0140110 transcription regulator activity 5 GO:0140098 catalytic activity, acting on RNA 3 GO:0003677 DNA binding 2
Localization
GO:0031410 cytoplasmic vesicle 6 GO:0005634 nucleus 3 GO:0005829 cytosol 3
Pathway
R-HSA-392499 Metabolism of proteins 6 R-HSA-8953854 Metabolism of RNA 5 R-HSA-8953897 Cellular responses to stimuli 4 R-HSA-168256 Immune System 2 R-HSA-5357801 Programmed Cell Death 2
Partners
ELAVL1FASTKKHDRBS1MAPTRPS6KA3TDP43TIAL1U1C
Complex memberships
U1 snRNP (via U1-C)stress granules

Evidence

Reading pass · 39 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 TIA-1 acts downstream of eIF-2alpha phosphorylation to promote assembly of stress granules (SGs) harboring untranslated mRNAs. A phosphomimetic eIF-2alpha mutant (S51D) induces SG assembly, a nonphosphorylatable mutant (S51A) prevents it, and a TIA-1 mutant lacking RNA-binding domains acts as a transdominant inhibitor of SG formation. Transfection of phosphomimetic/nonphosphorylatable eIF-2alpha mutants in mammalian cells; dominant-negative TIA-1 truncation mutant; colocalization with poly(A)+ RNA The Journal of cell biology High 10613902
2004 Prion-like aggregation of TIA-1's glutamine-rich prion-related domain (PRD) mediates stress granule assembly. The PRD shows concentration-dependent aggregation inhibited by HSP70, resistance to protease digestion, and sequestration of HSP70/HSP27/HSP40. Substitution of the PRD with the yeast prion aggregation domain SUP35-NM reconstitutes SG assembly. TIA-1 knockout MEFs show impaired SG formation despite normal eIF2alpha phosphorylation. Truncation/domain-swap mutants, HSP70 overexpression, protease protection assay, TIA-1 knockout MEFs, live cell imaging Molecular biology of the cell High 15371533
2000 TIA-1 and PABP-I dynamically shuttle in and out of stress granules (FRAP analysis). Drugs that stabilize polysomes (emetine) inhibit SG assembly and dissolve preformed SGs, while drugs that destabilize polysomes (puromycin) promote SG assembly, demonstrating that SGs and polysomes exist in equilibrium. TIA-1ΔRRM transdominant inhibitor of SG assembly promotes expression of reporter genes, suggesting SGs regulate mRNA translation. FRAP of GFP-tagged TIA-1 and PABP-I in live cells; polysome-stabilizing/destabilizing drugs; reporter gene assay The Journal of cell biology High 11121440
2000 TIA-1 functions as a translational silencer of TNF-alpha mRNA by binding its AU-rich element (ARE) in the 3'UTR. TIA-1 knockout macrophages produce significantly more TNF-alpha protein without changes in transcript half-life, but with increased association of TNF-alpha mRNA with polysomes. Homologous recombination knockout mice; polysome fractionation; ELISA; mRNA half-life analysis The EMBO journal High 10921895
2000 TIA-1 is an alternative pre-mRNA splicing regulator that binds U-rich sequences downstream of 5' splice sites to facilitate 5' splice site recognition by U1 snRNP. TIA-1 regulates splicing of Drosophila msl-2 and human Fas pre-mRNAs, and shows functional similarity to the S. cerevisiae splicing factor Nam8. In vitro splicing assays; UV cross-linking; specific immunoprecipitation; overexpression in cultured cells Molecular cell High 11106748
1996 RRM2 of TIA-1 is the domain that mediates specific binding to uridylate-rich RNA sequences, as determined by in vitro SELEX. RRM3 binds a broad population of cellular RNAs but not U-rich sequences selected by full-length protein; RRM1 has no detectable RNA-binding activity. In vitro selection/amplification (SELEX) from random RNA pools; filter binding assays; mutational analysis of individual RRM domains The Journal of biological chemistry High 8576255
2002 TIA-1 directly interacts with U1 snRNP protein U1-C via its N-terminal region (RRM1 and Q-rich domain) to facilitate U1 snRNP recruitment to 5' splice sites. RRMs 2 and 3 are necessary and sufficient for pre-mRNA binding, while RRM1 and the Q domain are required for U1 snRNP association. Co-precipitation experiments; domain dissection; in vitro U1 snRNP recruitment assays The EMBO journal High 12486009
2000 TIA-1 activates 5' splice site usage of the K-SAM alternative exon of FGF receptor 2 by binding to U-rich sequence IAS1 immediately downstream of the 5' splice site in a U1 snRNP-dependent manner. A TIA-1-MS2 coat protein fusion can substitute for wild-type TIA-1 when IAS1 is replaced by an MS2 operator near the 5' splice site. In vitro splicing assays; UV cross-linking/immunoprecipitation; overexpression in cultured cells; tethering assay with TIA-1-MS2 fusion Molecular and cellular biology High 10938105
1995 Fas-activated serine/threonine kinase (FAST) is rapidly activated upon Fas ligation and directly phosphorylates TIA-1. Phosphorylation of TIA-1 precedes DNA fragmentation during Fas-mediated apoptosis, placing FAST and TIA-1 in a signaling cascade upstream of apoptotic DNA fragmentation. Kinase activity assay; immunoprecipitation; phosphorylation time-course relative to DNA fragmentation The Journal of experimental medicine High 7544399
2003 TIA-1 functions as a translational silencer of COX-2 by binding its ARE in the 3'UTR. TIA-1 null fibroblasts produce significantly more COX-2 protein without changes in COX-2 transcription or mRNA turnover. Colon cancer cells that overexpress COX-2 show defective TIA-1 binding to COX-2 mRNA in vitro and in vivo. RNA binding studies; TIA-1 null fibroblasts; Western blotting; RNA-binding IP; reporter assays The Journal of experimental medicine High 12885872
2005 TIA-1 promotes Fas exon 6 inclusion by facilitating U1 snRNP binding to the exon 6 5' splice site, which in turn enhances U2AF binding to the upstream 3' splice site. PTB promotes exon skipping by binding an exonic splicing silencer and inhibiting U2AF and U2 snRNP recruitment. U1 snRNP recognition of the 5' splice site is required for both TIA-1-mediated U2AF enhancement and PTB-mediated U2AF inhibition. In vitro splicing assays; RNA-protein interaction studies; U1 snRNP/U2AF binding assays; functional reporters Molecular cell High 16109372
2005 TIA-1 immunoprecipitation followed by microarray analysis identified a U-rich, 30-37 nt bipartite RNA motif preferentially in 3'UTRs as the TIA-1 binding signature. TIA-1 binds ~3% of the UniGene transcripts. RNAi knockdown of TIA-1 revealed that TIA-1 represses translation of bound target mRNAs. RIP-Chip (immunoprecipitation of TIA-1-RNA complexes + microarray); biotinylated RNA pulldown/Western blot; RNA interference Molecular and cellular biology High 16227602
2006 TIA-1 functions as a translational repressor of cytochrome c mRNA, opposing the translational activator HuR. Silencing TIA-1 dramatically increases cytochrome c translation, while silencing HuR reduces it. During ER stress, reduced HuR binding and altered TIA-1 activity contribute to decreased cytochrome c translation. RNA interference (siRNA knockdown); polysome fractionation; metabolic labeling of nascent protein; RIP Molecular and cellular biology High 16581801
2006 FAST kinase synergizes with TIA-1/TIAR to regulate Fas alternative splicing. FAST K depletion causes skipping of Fas exon 6; FAST K overexpression enhances exon 6 inclusion dependent on TIA-1/TIAR. In vitro phosphorylation of TIA-1 by FAST K enhances U1 snRNP recruitment without increasing TIA-1 pre-mRNA binding. siRNA depletion; overexpression; in vitro splicing assays; in vitro kinase assay; U1 snRNP recruitment assay The Journal of biological chemistry High 17135269
2007 TIA-1-mediated translational silencing promotes mRNA decay. Tethering TIA-1 to a reporter mRNA promotes its decay. TIA-1-mediated decay requires both 5'-3' (DCP2) and 3'-5' (exosome component Rrp46) decay pathways and is inhibited by drugs stabilizing polysomes (emetine, cycloheximide), indicating polysome disassembly is prerequisite. Gene array analysis; mRNA tethering assay; siRNA knockdown of decay pathway components; polysome-stabilizing drug treatment The Journal of biological chemistry High 17711853
2008 Systematic analysis showed TIA1/TIAL1 bind U-rich motifs within 100 nt downstream of 5' splice sites to regulate approximately 15% of alternative cassette exons. Simultaneous knockdown of TIA1 and TIAL1 increased skipping of 88% of alternatively spliced exons associated with U-rich motifs but did not affect 97% of exons lacking such motifs. Computational motif analysis; simultaneous siRNA knockdown of TIA1 and TIAL1; RT-PCR validation of 41 alternative exons Genome research High 18456862
2008 RSK2 kinase directly interacts with the prion-related domain of TIA-1 via its N-terminal kinase domain, co-localizing in stress granules. RSK2 and TIA-1 co-sequestration is codependent. Mitogen releases RSK2 from SGs for nuclear import in a TIA-1-dependent manner. Nuclear RSK2 promotes proliferation through cyclin D1 induction. Endogenous Co-IP; domain interaction mapping; siRNA silencing; live-cell imaging; nuclear fractionation Molecular cell High 18775331
2011 TIA-1 and TIAR are positive regulators of SMN2 exon 7 splicing in an intronic context where U-rich motifs are separated from the 5' splice site by overlapping inhibitory elements. Any single RRM in combination with the Q domain is necessary and sufficient for TIA1-dependent regulation. Increased TIA1 expression counteracts inhibitory effects of PTB on SMN exon 7 splicing. In vivo splicing assays with domain mutants; RNAi; epistasis with PTB Molecular and cellular biology High 21189287
2011 TIA-1 and TIAR bind to the 5' end of 5'TOP mRNAs (encoding protein biosynthesis factors) under amino acid starvation, arresting their translation at the initiation step. This requires GCN2 kinase activation and mTOR pathway inactivation. Upon starvation, 5'TOP mRNAs are released from polysomes and accumulate in stress granules in a TIA-1/TIAR-dependent manner. PAR-CLIP/RIP; polysome profiling; stress granule colocalization; GCN2/mTOR pathway inhibition Genes & development High 21979918
2014 NMR, ITC, and SAXS structural analysis of TIA-1 revealed that RRM2 adopts a canonical RRM fold while RRM3 is preceded by a non-canonical helix α0. All three RRMs are largely independent in the absence of RNA, but RNA binding induces a compact arrangement. RRM2,3 binds pyrimidine-rich FAS pre-mRNA or poly-U9 RNA with nanomolar affinity. RRM1 has little intrinsic RNA binding affinity. NMR solution structure; ITC; SAXS; RNA binding assays Nucleic acids research High 24682828
2016 TIA-1 oxidation by reactive oxygen species (ROS/H2O2) inhibits stress granule assembly. When cells face both SG-inducing ER stress and oxidative stress simultaneously, oxidized TIA1 cannot nucleate SGs, promoting apoptosis. This mechanism is proposed to underlie neuronal cell death in neurodegenerative diseases. ROS treatment (H2O2); stress granule assembly assays; apoptosis measurements; TIA1 redox state analysis Nature communications High 26738979
2017 ALS/FTD-associated mutations in the TIA1 low-complexity domain (e.g., P362L) significantly increase TIA1's propensity to undergo phase transition. In live cells, TIA1 LCD mutations delay stress granule disassembly, promote accumulation of non-dynamic SGs harboring TDP-43, and cause TDP-43 in SGs to become less mobile and insoluble. Genetics (mutation burden analysis); phase separation assays; FRAP in live cells; TDP-43 solubility fractionation; neuropathology Neuron High 28817800
2018 PAR-CLIP of TIA1 and TIAL1 shows both proteins bind target sites with identical specificity in 3' UTRs and introns proximal to 5' and 3' splice sites. Double knockout of TIA1/TIAL1 increases target mRNA abundance and causes accumulation of aberrantly spliced mRNAs subject to NMD. Loss of PRKRA by mis-splicing triggers EIF2AK2/PKR activation and SG formation; ectopic PRKRA or EIF2AK2 knockout rescued this phenotype. PAR-CLIP; double knockout; transcriptomics; rescue by ectopic cDNA or second KO Molecular cell High 29429924
2018 Recombinant TIA-1 undergoes rapid multimerization and phase separation in the presence of divalent zinc (Zn2+), reversible by the zinc chelator TPEN. Arsenite treatment of cells releases Zn2+ before stress granule formation, and TPEN inhibits TIA-1-positive SG formation. Zn2+ functions as a stress-inducible second messenger promoting TIA-1 multimerization and SG localization. In vitro phase separation assays with recombinant TIA-1; zinc chelation (TPEN); live-cell imaging; zinc release measurement Cell reports High 29298433
2005 TIA-1 and TIAR continuously shuttle between cytoplasm and nucleus via distinct RRM-domain-mediated mechanisms. RRM2 and the first half of the auxiliary region mediate nuclear accumulation; RRM3 mediates nuclear export. Nuclear accumulation is Ran-GTP-dependent and transcription-dependent; nuclear export is independent of CRM1 and Ran-GTP. GFP-tagged domain mutants; nuclear/cytoplasmic fractionation; inhibitor treatments (transcription inhibitors, RanGTP depletion, leptomycin B); fluorescence microscopy Journal of cell science High 16278295
2016 Tau interacts with TIA1 in brain tissue and the brain-protein interactome of TIA1 includes ribosomal proteins and other RBPs. Tau is required for normal TIA1-protein interactions. Tau expression accelerates stress granule formation, while TIA1 knockdown or knockout inhibits tau misfolding and associated toxicity in hippocampal neurons. TIA1 overexpression induces tau misfolding and neurodegeneration. Co-IP from brain tissue; TIA1 interactome (mass spectrometry); TIA1 KO/KD in cultured neurons; TIA1 overexpression; tau misfolding assays; neurotoxicity assays Cell reports High 27160897
2002 TIA-1 and TIAR bind specifically to the 3' terminal stem-loop of West Nile virus minus-strand RNA (WNV 3'(-)SL RNA) via RRM2. The Kd for TIA-1 RRM2 interaction is 1.12 × 10^-7 M. WNV growth is reduced in TIAR knockout cells and reconstitution with TIAR rescues growth efficiency. RNA affinity purification; peptide sequencing; competition gel mobility-shift assays; recombinant domain binding assays; viral growth in KO cells Journal of virology High 12414941
2013 Welander distal myopathy (WDM) is caused by a dominant E384K mutation in the Q-rich domain of TIA1 (located in the region that interacts with U1-C splicing factor). Mutant TIA1 causes increased stress granule abundance and slower FRAP recovery in HeLa cells. WDM patient muscle shows focal TIA1 accumulation and increased splicing of SMN2 alternative exons. Linkage analysis; whole-genome/exome sequencing; FRAP; high-content SG quantification; RT-PCR splicing analysis; immunofluorescence of patient biopsies Annals of neurology High 23401021
2007 TIA-1 binds to AU-rich cis elements in COL2A1 intron 2 and modulates alternative splicing of exon 2. TIA-1 also interacts with the corresponding genomic DNA sequence (preferring single-stranded over double-stranded DNA), confirmed by ChIP assay. Active transcription by RNA polymerase disrupts TIA-1 DNA binding. Minigene splicing assay; RNP immunoprecipitation; chromatin immunoprecipitation (ChIP); competition binding assays The Journal of biological chemistry Medium 17580305
2021 TIA1 interaction with RNA and the combination of TIA1 + RNA is sufficient to drive phase separation of tau at physiological concentrations without crowding agents. Phase separation of tau in the presence of RNA and TIA1 generates tau oligomers that are significantly more toxic than tau aggregates generated by RNA alone or artificial crowding agents. Tau selectively copartitions with TIA1 but not G3BP1 under physiological conditions. In vitro phase separation assays with recombinant proteins; tau oligomer toxicity assays; selectivity comparison with other RBPs Proceedings of the National Academy of Sciences of the United States of America High 33619090
2022 NMR, molecular dynamics simulations, and 3D electron crystallography revealed that ALS mutations P362L and A381T in TIA1's prion-like domain enhance self-assembly by inducing β-sheet interactions and highly condensed assembly, respectively, increasing the likelihood of irreversible amyloid fibrillization. The WDM mutation E384K attenuates sticky properties. The dynamic structures of the PLD are synergistically determined by physicochemical properties of amino acids in units of five residues. NMR; molecular dynamics simulations; 3D electron crystallography; biochemical aggregation assays Proceedings of the National Academy of Sciences of the United States of America High 36112647
2009 Sam68 is recruited into stress granules under oxidative stress through direct complex formation with TIA-1. Sam68 domains aa269-321 and the KH domain are both essential for SG recruitment. Sam68 knockdown does not affect SG assembly, indicating it is not a core SG component but is recruited via TIA-1. Co-immunoprecipitation; domain mutants; siRNA knockdown; immunofluorescence colocalization Experimental cell research Medium 19615357
2014 TIA1 interacts with annexin A7 (ANXA7) as identified by yeast two-hybrid screening. ANXA7, acting as a GTPase, modulates TIA1 phosphorylation. Promoting ANXA7-TIA1 interaction inhibits TIA1 phosphorylation and promotes processing of pro-autophagic factor FLJ11812 and ATG13 expression in endothelial cells. Yeast two-hybrid; co-immunoprecipitation; pharmacological ANXA7 inhibitor (ABO); Western blotting The international journal of biochemistry & cell biology Low 25461769
2011 TDP-43 contributes to SG assembly and maintenance under oxidative stress, and differentially regulates TIA-1 and G3BP. Absence of TDP-43 disrupts controlled aggregation of TIA-1, slowing SG formation. Disease-associated TDP-43(R361S) is a loss-of-function mutation for SG formation and alters TIA-1 and G3BP levels. siRNA knockdown of TDP-43; TDP-43 disease mutant overexpression; immunofluorescence; Western blotting; SG quantification Human molecular genetics Medium 21257637
2017 TIA1 binds p53 mRNA in activated B lymphocytes and controls its translational silencing and stress granule localization. Upon DNA damage, TIA1 dissociates from p53 mRNA, which relocates from stress granules to polysomes for cap-independent translation. This is an ATM-dependent mechanism extended globally to key DNA damage response modulators. RIP; polysome fractionation; stress granule colocalization; ATM inhibition; global mRNA translation profiling Nature communications High 28904350
2021 Full-length TIA-1 undergoes liquid-liquid phase separation in vitro induced by single-stranded RNA or DNA in a multisite, sequence-specific manner. Tandem binding sites (not single sites) are required to enhance TIA-1 phase separation, tuned by protein:binding site stoichiometry. Tandem TIA-1 binding sites in the p53 mRNA 3'UTR efficiently enhance TIA-1 phase separation, identifying them as potential SG nucleation sites. In vitro phase separation assays; fibril formation assays; SAXS; biotinylated RNA pulldown; designed and native RNA sequences Nucleic acids research High 33621982
2022 Intracellular tau accumulation inhibits autophagosome formation by binding the prion-related domain of TIA1 (PRD-TIA1), increasing intracellular amino acid levels, and activating mTORC1 signaling (increased p-4EBP1, p-p70S6K1, p-ULK1). Blocking tau-TIA1 interaction by overexpressing PRD-TIA1, TIA1 shRNA knockdown, or tau PROTAC degradation attenuates autophagy impairment. Co-immunoprecipitation; immunofluorescence; HPLC for amino acid measurement; mTORC1 activity assay; autophagosome formation (LC3 puncta/TEM); shRNA; overexpression; PROTAC Military Medical Research Medium 35799293
2014 TIA-1 RRM3 binds C-rich and U-rich RNA sequences with micromolar affinity (demonstrated by NMR STD and SPR). In combination with RRM2 and in full-length TIA-1, RRM3 significantly enhances binding to C-rich RNAs, consistent with its role in binding 5'TOP mRNA sequences. NMR saturation transfer difference (STD-NMR); surface plasmon resonance (SPR); biotinylated RNA pulldown RNA biology High 24824036
2017 Crystal structure of TIA-1 RRM2 in complex with DNA determined to 2.3 Å resolution, providing the first atomic resolution structure of any TIA protein RRM in complex with oligonucleotide. SAXS shows TIA-1 RRM23 adopts a compact structure upon complex formation with target RNA or DNA, with both RRMs engaging the 10-nt target sequence. X-ray crystallography (2.3 Å); SAXS; SPR binding assays Nucleic acids research High 28184449

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 RNA-binding proteins TIA-1 and TIAR link the phosphorylation of eIF-2 alpha to the assembly of mammalian stress granules. The Journal of cell biology 1066 10613902
2004 Stress granule assembly is mediated by prion-like aggregation of TIA-1. Molecular biology of the cell 829 15371533
2000 Dynamic shuttling of TIA-1 accompanies the recruitment of mRNA to mammalian stress granules. The Journal of cell biology 665 11121440
2017 TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics. Neuron 505 28817800
2000 TIA-1 is a translational silencer that selectively regulates the expression of TNF-alpha. The EMBO journal 435 10921895
2011 TAR DNA-binding protein 43 (TDP-43) regulates stress granule dynamics via differential regulation of G3BP and TIA-1. Human molecular genetics 336 21257637
2005 Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition. Molecular cell 291 16109372
2016 Interaction of tau with the RNA-Binding Protein TIA1 Regulates tau Pathophysiology and Toxicity. Cell reports 271 27160897
2007 Interaction of TIA-1/TIAR with West Nile and dengue virus products in infected cells interferes with stress granule formation and processing body assembly. Proceedings of the National Academy of Sciences of the United States of America 255 17502609
2000 The apoptosis-promoting factor TIA-1 is a regulator of alternative pre-mRNA splicing. Molecular cell 253 11106748
2002 Visibly stressed: the role of eIF2, TIA-1, and stress granules in protein translation. Cell stress & chaperones 217 12380690
2017 Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo. Nature neuroscience 205 29273772
2005 Identification and functional outcome of mRNAs associated with RNA-binding protein TIA-1. Molecular and cellular biology 204 16227602
2012 Contrasting pathology of the stress granule proteins TIA-1 and G3BP in tauopathies. The Journal of neuroscience : the official journal of the Society for Neuroscience 199 22699908
1996 Individual RNA recognition motifs of TIA-1 and TIAR have different RNA binding specificities. The Journal of biological chemistry 196 8576255
2002 The splicing regulator TIA-1 interacts with U1-C to promote U1 snRNP recruitment to 5' splice sites. The EMBO journal 189 12486009
2011 Translational coregulation of 5'TOP mRNAs by TIA-1 and TIAR. Genes & development 182 21979918
2000 The RNA-binding protein TIA-1 is a novel mammalian splicing regulator acting through intron sequences adjacent to a 5' splice site. Molecular and cellular biology 177 10938105
1992 Identification and functional characterization of a TIA-1-related nucleolysin. Proceedings of the National Academy of Sciences of the United States of America 173 1326761
2003 Regulation of cyclooxygenase-2 expression by the translational silencer TIA-1. The Journal of experimental medicine 170 12885872
2006 Translational control of cytochrome c by RNA-binding proteins TIA-1 and HuR. Molecular and cellular biology 167 16581801
2004 Arthritis suppressor genes TIA-1 and TTP dampen the expression of tumor necrosis factor alpha, cyclooxygenase 2, and inflammatory arthritis. Proceedings of the National Academy of Sciences of the United States of America 164 14769925
2002 Cell proteins TIA-1 and TIAR interact with the 3' stem-loop of the West Nile virus complementary minus-strand RNA and facilitate virus replication. Journal of virology 156 12414941
2017 miR-19a promotes colorectal cancer proliferation and migration by targeting TIA1. Molecular cancer 154 28257633
1995 Fas-activated serine/threonine kinase (FAST) phosphorylates TIA-1 during Fas-mediated apoptosis. The Journal of experimental medicine 153 7544399
2008 Codependent functions of RSK2 and the apoptosis-promoting factor TIA-1 in stress granule assembly and cell survival. Molecular cell 131 18775331
2013 Welander distal myopathy is caused by a mutation in the RNA-binding protein TIA1. Annals of neurology 123 23401021
2003 The proximal region of the 3'-untranslated region of cyclooxygenase-2 is recognized by a multimeric protein complex containing HuR, TIA-1, TIAR, and the heterogeneous nuclear ribonucleoprotein U. The Journal of biological chemistry 123 12855701
2016 TIA1 oxidation inhibits stress granule assembly and sensitizes cells to stress-induced apoptosis. Nature communications 121 26738979
2021 TIA1 potentiates tau phase separation and promotes generation of toxic oligomeric tau. Proceedings of the National Academy of Sciences of the United States of America 118 33619090
1997 TIA-1 expression in lymphoid neoplasms. Identification of subsets with cytotoxic T lymphocyte or natural killer cell differentiation. The American journal of pathology 117 9176382
2001 TIA-1 and TIAR activate splicing of alternative exons with weak 5' splice sites followed by a U-rich stretch on their own pre-mRNAs. The Journal of biological chemistry 115 11514562
2002 Distinct bone marrow findings in T-cell granular lymphocytic leukemia revealed by paraffin section immunoperoxidase stains for CD8, TIA-1, and granzyme B. Blood 101 11756181
2018 The TIA1 RNA-Binding Protein Family Regulates EIF2AK2-Mediated Stress Response and Cell Cycle Progression. Molecular cell 95 29429924
2013 Welander distal myopathy caused by an ancient founder mutation in TIA1 associated with perturbed splicing. Human mutation 94 23348830
1993 Expression of perforin, granzyme A and TIA-1 by human uterine CD56+ NK cells implies they are activated and capable of effector functions. Human reproduction (Oxford, England) 94 7512092
2018 TIA1 regulates the generation and response to toxic tau oligomers. Acta neuropathologica 88 30465259
2008 A systematic analysis of intronic sequences downstream of 5' splice sites reveals a widespread role for U-rich motifs and TIA1/TIAL1 proteins in alternative splicing regulation. Genome research 87 18456862
2018 TIA-1 Self-Multimerization, Phase Separation, and Recruitment into Stress Granules Are Dynamically Regulated by Zn2. Cell reports 86 29298433
1996 Structure, tissue distribution and genomic organization of the murine RRM-type RNA binding proteins TIA-1 and TIAR. Nucleic acids research 86 8871565
2018 TIA1 variant drives myodegeneration in multisystem proteinopathy with SQSTM1 mutations. The Journal of clinical investigation 81 29457785
1997 Cytotoxicity and apoptosis in human renal allografts: identification, distribution, and quantitation of cells with a cytotoxic granule protein GMP-17 (TIA-1) and cells with fragmented nuclear DNA. Laboratory investigation; a journal of technical methods and pathology 78 9166283
2014 Structure, dynamics and RNA binding of the multi-domain splicing factor TIA-1. Nucleic acids research 75 24682828
2006 Fas-activated serine/threonine kinase (FAST K) synergizes with TIA-1/TIAR proteins to regulate Fas alternative splicing. The Journal of biological chemistry 72 17135269
2010 TIA1 prevents skipping of a critical exon associated with spinal muscular atrophy. Molecular and cellular biology 71 21189287
2005 Identification of the sequence determinants mediating the nucleo-cytoplasmic shuttling of TIAR and TIA-1 RNA-binding proteins. Journal of cell science 71 16278295
2004 Herpes simplex virus 1 induces cytoplasmic accumulation of TIA-1/TIAR and both synthesis and cytoplasmic accumulation of tristetraprolin, two cellular proteins that bind and destabilize AU-rich RNAs. Journal of virology 71 15280467
2014 Alternative splicing of TIA-1 in human colon cancer regulates VEGF isoform expression, angiogenesis, tumour growth and bevacizumab resistance. Molecular oncology 70 25224594
2014 Functional role of Tia1/Pub1 and Sup35 prion domains: directing protein synthesis machinery to the tubulin cytoskeleton. Molecular cell 66 24981173
2014 The stress granule component TIA-1 binds tick-borne encephalitis virus RNA and is recruited to perinuclear sites of viral replication to inhibit viral translation. Journal of virology 64 24696465
1999 The expression of TIA-1+ cytolytic-type granules and other cytolytic lymphocyte-associated markers in CD30+ anaplastic large cell lymphomas (ALCL): correlation with morphology, immunophenotype, ultrastructure, and clinical features. Human pathology 63 10029454
2011 Poliovirus unlinks TIA1 aggregation and mRNA stress granule formation. Journal of virology 62 21957303
2007 Two isoforms of the T-cell intracellular antigen 1 (TIA-1) splicing factor display distinct splicing regulation activities. Control of TIA-1 isoform ratio by TIA-1-related protein. The Journal of biological chemistry 61 17488725
2007 T-cell intracellular antigen-1 (TIA-1)-induced translational silencing promotes the decay of selected mRNAs. The Journal of biological chemistry 61 17711853
2009 Amyotrophic lateral sclerosis-linked mutant SOD1 sequesters Hu antigen R (HuR) and TIA-1-related protein (TIAR): implications for impaired post-transcriptional regulation of vascular endothelial growth factor. The Journal of biological chemistry 58 19805546
2007 The number of tumour-infiltrating TIA-1+ cytotoxic T cells but not FOXP3+ regulatory T cells predicts outcome in diffuse large B-cell lymphoma. British journal of haematology 57 17456059
2017 Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells. Nature communications 56 28904350
1996 Mechanisms of lysis by activated cytotoxic cells expressing perforin and granzyme-B genes and the protein TIA-1 in muscle biopsies of myositis. The Journal of rheumatology 54 8823683
1998 Intraepidermal lymphocytes in psoriatic lesions are activated GMP-17(TIA-1)+CD8+CD3+ CTLs as determined by phenotypic analysis. Journal of cutaneous pathology 53 9521496
1997 Assessment of cytotoxic T-lymphocyte phenotype using the specific markers granzyme B and TIA-1 in cervical neoplastic lesions. British journal of cancer 50 9374383
2017 Tumoral immune-infiltrate (IF), PD-L1 expression and role of CD8/TIA-1 lymphocytes in localized osteosarcoma patients treated within protocol ISG-OS1. Oncotarget 47 29340095
2008 Mutation of mapped TIA-1/TIAR binding sites in the 3' terminal stem-loop of West Nile virus minus-strand RNA in an infectious clone negatively affects genomic RNA amplification. Journal of virology 45 18768985
2017 Clinical and neuropathological features of ALS/FTD with TIA1 mutations. Acta neuropathologica communications 43 29216908
2014 Post-transcriptional regulation of programmed cell death 4 (PDCD4) mRNA by the RNA-binding proteins human antigen R (HuR) and T-cell intracellular antigen 1 (TIA1). The Journal of biological chemistry 42 25519906
2014 Dysregulated expression of lipid storage and membrane dynamics factors in Tia1 knockout mouse nervous tissue. Neurogenetics 41 24659297
2010 TIAR and TIA-1 mRNA-binding proteins co-aggregate under conditions of rapid oxygen decline and extreme hypoxia and suppress the HIF-1α pathway. Journal of molecular cell biology 40 20980400
2022 ALS mutations in the TIA-1 prion-like domain trigger highly condensed pathogenic structures. Proceedings of the National Academy of Sciences of the United States of America 36 36112647
2017 TIA-1 Is a Functional Prion-Like Protein. Cold Spring Harbor perspectives in biology 36 28003185
2007 Nuclear protein TIA-1 regulates COL2A1 alternative splicing and interacts with precursor mRNA and genomic DNA. The Journal of biological chemistry 36 17580305
1994 Intron-exon organization and chromosomal localization of the human TIA-1 gene. Journal of immunology (Baltimore, Md. : 1950) 35 8176212
2011 Three RNA recognition motifs participate in RNA recognition and structural organization by the pro-apoptotic factor TIA-1. Journal of molecular biology 34 22154808
2018 Myopathy With SQSTM1 and TIA1 Variants: Clinical and Pathological Features. Frontiers in neurology 31 29599744
2003 TIA-1 or TIAR is required for DT40 cell viability. The Journal of biological chemistry 31 12533540
1999 Assessment and diagnostic utility of the cytotoxic T-lymphocyte phenotype using the specific markers granzyme-B and TIA-1 in esophageal mucosal biopsies. Human pathology 31 10208460
2021 Tandem RNA binding sites induce self-association of the stress granule marker protein TIA-1. Nucleic acids research 30 33621982
2020 Reduction of the RNA Binding Protein TIA1 Exacerbates Neuroinflammation in Tauopathy. Frontiers in neuroscience 30 32327969
2014 HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA. International journal of molecular sciences 30 24566137
2001 Identification of TIA-1+ and granzyme B+ cytotoxic T cells in lichen sclerosus et atrophicus. Dermatology (Basel, Switzerland) 30 11385223
1992 Evidence of cytotoxic T-cell destruction of epidermal cells in human graft-vs-host disease. Immunohistology with monoclonal antibody TIA-1. Archives of pathology & laboratory medicine 30 1616423
2017 TIA1 is a gender-specific disease modifier of a mild mouse model of spinal muscular atrophy. Scientific reports 27 28775379
2006 Control of the ATP synthase beta subunit expression by RNA-binding proteins TIA-1, TIAR, and HuR. Biochemical and biophysical research communications 27 16890199
1993 The developmentally-regulated Drosophila gene rox8 encodes an RRM-type RNA binding protein structurally related to human TIA-1-type nucleolysins. Nucleic acids research 27 8396236
2009 Sam68 relocalization into stress granules in response to oxidative stress through complexing with TIA-1. Experimental cell research 25 19615357
2000 TIA-1 positive tumor-infiltrating lymphocytes in nevi and melanomas. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 25 10658910
2018 Potential use of TIA-1, MFF, microRNA-200a-3p, and microRNA-27 as a novel marker for hepatocellular carcinoma. Biochemical and biophysical research communications 24 29496454
2018 Suberanilohydroxamic acid prevents TGF-β1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation. Biochimica et biophysica acta. Gene regulatory mechanisms 24 29555582
2018 miR-487a promotes progression of gastric cancer by targeting TIA1. Biochimie 24 30144499
2014 TIA1 interacts with annexin A7 in regulating vascular endothelial cell autophagy. The international journal of biochemistry & cell biology 24 25461769
2022 Intracellular accumulation of tau inhibits autophagosome formation by activating TIA1-amino acid-mTORC1 signaling. Military Medical Research 23 35799293
2010 Transcriptional down-regulation of IGFBP-3 in human hepatocellular carcinoma cells is mediated by the binding of TIA-1 to its AT-rich element in the 3'-untranslated region. Cancer letters 23 20599318
2017 Protein 4.1R Exon 16 3' Splice Site Activation Requires Coordination among TIA1, Pcbp1, and RBM39 during Terminal Erythropoiesis. Molecular and cellular biology 22 28193846
2014 The binding of TIA-1 to RNA C-rich sequences is driven by its C-terminal RRM domain. RNA biology 22 24824036
2021 Disease-associated mutations affect TIA1 phase separation and aggregation in a proline-dependent manner. Brain research 21 34310938
2021 Amyotrophic lateral sclerosis (ALS) linked mutation in Ubiquilin 2 affects stress granule assembly via TIA-1. CNS neuroscience & therapeutics 21 34750982
2020 ALS-Linked Mutant SOD1 Associates with TIA-1 and Alters Stress Granule Dynamics. Neurochemical research 21 33025330
2019 Genetic Perturbation of TIA1 Reveals a Physiological Role in Fear Memory. Cell reports 21 30865887
2001 TIA-1 regulates the production of tumor necrosis factor alpha in macrophages, but not in lymphocytes. Arthritis and rheumatism 21 11762949
2023 Liquid Droplet Aging and Seeded Fibril Formation of the Cytotoxic Granule Associated RNA Binding Protein TIA1 Low Complexity Domain. Journal of the American Chemical Society 20 36638831
2017 TIA-1 RRM23 binding and recognition of target oligonucleotides. Nucleic acids research 20 28184449
1996 Expression of TIA-1 and TIA-2 in T cell malignancies and T cell lymphocytosis. Journal of clinical pathology 20 8655683