Affinage

TIA1

Cytotoxic granule associated RNA binding protein TIA1 · UniProt P31483

Length
386 aa
Mass
43.0 kDa
Annotated
2026-06-10
100 papers in source corpus 40 papers cited in narrative 40 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TIA-1 is a multidomain RNA-binding protein that couples mRNA recognition to two cellular functions—translational silencing within stress granules and regulation of alternative pre-mRNA splicing (PMID:10613902, PMID:11106748). RNA recognition is mediated by tandem RRMs: RRM2 selectively binds uridylate-rich sequences while RRM1 lacks intrinsic RNA-binding capacity, and RRM3 augments binding to C-rich and 5'TOP sequences (PMID:8576255, PMID:24824036), with crystallographic and NMR/SAXS data showing RRM2-RRM3 collapse into a compact arrangement upon engaging a 10-nucleotide pyrimidine target (PMID:24682828, PMID:28184449). Through these domains TIA-1 binds U-rich bipartite motifs predominantly in 3'UTRs and represses translation of target mRNAs including TNF-alpha, COX-2, cytochrome c, and p53 without altering transcript levels (PMID:10921895, PMID:12885872, PMID:16227602, PMID:16581801, PMID:28904350), and this silencing can be coupled to mRNA decay via both 5'-3' and 3'-5' pathways (PMID:17711853). Upon eIF2alpha phosphorylation and polysome disassembly, TIA-1 nucleates stress granules through prion-like aggregation of its C-terminal glutamine-rich domain, into and out of which it dynamically shuttles (PMID:10613902, PMID:15371533, PMID:11121440); this self-assembly is promoted by tandem RNA binding sites and by Zn2+-induced multimerization, and is inhibited by ROS-mediated oxidation (PMID:29298433, PMID:26738979, PMID:33621982). In the nucleus TIA-1 promotes inclusion of weak 5' splice sites by binding U-rich intronic sequences and recruiting U1 snRNP through a direct interaction between its Q-rich domain and U1-C, facilitating exon definition (e.g. Fas exon 6, SMN2 exon 7) and opposing PTB-mediated skipping (PMID:11106748, PMID:12486009, PMID:16109372, PMID:21189287). TIA-1 activity is modulated by FAST kinase phosphorylation, which enhances U1 snRNP recruitment at the spliceosome (PMID:7544399, PMID:17135269). Disease-associated mutations in the low-complexity/Q-rich domain pathologically alter phase behavior: ALS/FTD mutations (P362L, A381T) enhance beta-sheet-driven self-assembly and delay disassembly of TDP-43-containing stress granules, whereas the Welander distal myopathy mutation E384K alters SG dynamics and SMN2 splicing (PMID:28817800, PMID:36112647, PMID:23401021). TIA-1 also drives toxic tau oligomer formation and accelerates tau misfolding, linking it to tauopathy (PMID:27160897, PMID:33619090).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1995 High

    Established that TIA-1 is a substrate of an apoptotic signaling kinase, providing the first link between TIA-1 and regulated post-transcriptional control during Fas-mediated cell death.

    Evidence in vitro phosphorylation of TIA-1 by immunoprecipitated FAST kinase with temporal epistasis to DNA fragmentation

    PMID:7544399

    Open questions at the time
    • phosphorylation sites not mapped
    • functional consequence of phosphorylation not defined at this stage
  2. 1996 High

    Resolved which domains confer RNA specificity, showing RRM2 drives U-rich binding while RRM1 is non-binding—defining the modular logic of TIA-1 recognition.

    Evidence in vitro SELEX, filter binding, and per-RRM mutational analysis

    PMID:8576255

    Open questions at the time
    • structural basis of specificity not yet resolved
    • in vivo target spectrum unknown
  3. 1999 High

    Placed TIA-1 genetically downstream of eIF2alpha phosphorylation in stress granule assembly, establishing it as an effector of the translational stress response.

    Evidence phosphomimetic/non-phosphorylatable eIF2alpha mutants and dominant-negative TIA-1 truncation with SG microscopy

    PMID:10613902

    Open questions at the time
    • domain responsible for SG nucleation not identified here
    • molecular nature of aggregation undefined
  4. 2000 High

    Defined TIA-1's two parallel functions—translational silencing of specific mRNAs and splice-site selection—answering what TIA-1 actually does to its bound RNAs.

    Evidence TIA-1 knockout macrophages with polysome fractionation (TNF-alpha); in vitro splicing and U1 recruitment assays (Fas, msl-2); FRAP of GFP-TIA-1 in live cells

    PMID:10921895 PMID:11106748 PMID:11121440

    Open questions at the time
    • how silencing and splicing functions are partitioned between compartments unclear
    • global target set not yet defined
  5. 2002 High

    Identified the direct protein-protein contact—Q-domain/U1-C—through which TIA-1 recruits U1 snRNP, providing the mechanism for its splicing-enhancer activity.

    Evidence co-precipitation of recombinant proteins with domain deletions and in vitro U1 recruitment

    PMID:12486009

    Open questions at the time
    • structural detail of the interaction absent
    • regulation of the contact unknown at this stage
  6. 2002 Medium

    Extended TIA-1 RNA recognition to viral templates, showing RRM2-mediated binding to flavivirus minus-strand RNA promotes genome replication.

    Evidence RNA affinity purification, gel-shift, TIAR KO and reconstitution with WNV growth assays

    PMID:12414941

    Open questions at the time
    • mechanism of replication enhancement not resolved
    • single virus family tested
  7. 2004 High

    Pinned SG assembly on prion-like aggregation of the Q-rich PRD, explaining how TIA-1 physically nucleates granules.

    Evidence PRD deletion, swap with yeast SUP35-NM, protease resistance, HSP70 Co-IP, and TIA-1 KO MEFs

    PMID:15371533

    Open questions at the time
    • biophysical nature of aggregation (LLPS vs amyloid) not distinguished
    • regulation of aggregation undefined
  8. 2003 High

    Generalized TIA-1 translational silencing to additional ARE-containing transcripts and a global target motif, with COX-2 implicating TIA-1 loss in cancer.

    Evidence TIA-1 null fibroblasts, RNA pulldown, polysome analysis (COX-2); TIA-1-RNA IP plus microarray and RNAi de-repression (global U-rich motif)

    PMID:12885872 PMID:16227602

    Open questions at the time
    • mechanism of translational block not defined at codon/initiation level
    • how silencing relates to SG sequestration unclear
  9. 2005 High

    Connected splicing enhancement to exon definition and characterized nucleocytoplasmic shuttling, integrating TIA-1's nuclear and cytoplasmic behaviors.

    Evidence in vitro reconstitution of U1/U2AF cross-talk at Fas exon 6; domain-mutant localization with CRM1/Ran-independence

    PMID:16109372 PMID:16278295

    Open questions at the time
    • export receptor for TIA-1 unidentified
    • signals coupling localization to function unknown
  10. 2006 Medium

    Showed FAST kinase phosphorylation tunes TIA-1 splicing activity at the protein-interaction level rather than RNA binding, linking the 1995 kinase substrate finding to function.

    Evidence FAST K siRNA, Fas minigene assays, in vitro phosphorylation with U1 recruitment readout; cytochrome c RIP and polysome work opposing HuR

    PMID:16581801 PMID:17135269

    Open questions at the time
    • phosphosites still unmapped
    • mechanism by which phosphorylation enhances U1 recruitment unresolved
  11. 2007 Medium

    Showed silencing is mechanistically coupled to mRNA decay and that TIA-1 can engage DNA, broadening its regulatory range.

    Evidence tethering assays with DCP2/Rrp46 siRNA epistasis (decay); ChIP and RNP-IP at COL2A1 (DNA/RNA dual binding)

    PMID:17580305 PMID:17711853

    Open questions at the time
    • whether decay is direct or secondary to polysome disassembly unclear
    • physiological significance of DNA binding undefined
  12. 2008 Medium

    Identified RSK2 as a PRD-interacting kinase partner co-regulated with TIA-1 in stress granules, linking SG dynamics to cell survival signaling.

    Evidence reciprocal Co-IP, domain mapping, RSK2 siRNA survival phenotype, nuclear fractionation

    PMID:18775331

    Open questions at the time
    • whether RSK2 phosphorylates TIA-1 not established
    • single-lab finding
  13. 2011 High

    Tied TIA-1 silencing to nutrient sensing, showing it arrests 5'TOP mRNA translation downstream of GCN2/mTOR, and revealed TDP-43 dependence of TIA-1 aggregation.

    Evidence RIP, polysome fractionation, GCN2/mTOR perturbation (5'TOP); TDP-43 knockdown with SG dynamics and mutant analysis

    PMID:21257637 PMID:21979918

    Open questions at the time
    • how 5'TOP recognition is achieved structurally unclear
    • TDP-43/TIA-1 interplay mechanism undefined
  14. 2014 High

    Provided atomic and biophysical structure of the RNA-engaged RRM module and refined RRM3 specificity, explaining how TIA-1 reads pyrimidine-rich targets.

    Evidence NMR solution structure of RRM2-RRM3, SAXS, ITC; STD-NMR/SPR for RRM3 C-rich binding

    PMID:24682828 PMID:24824036

    Open questions at the time
    • RRM1 contribution structurally unresolved
    • PRD structure not addressed
  15. 2014 Medium

    Demonstrated conserved prion behavior of the TIA-1 ortholog and added a flavivirus-restriction/replication role, situating phase behavior in deep evolutionary and antiviral contexts.

    Evidence yeast Pub1 prion assays with Sup35 cooperation; TBEV replicon and KO MEF assays; WNV binding-site mutagenesis with viral RNA quantitation

    PMID:18768985 PMID:24696465 PMID:24981173

    Open questions at the time
    • whether viral roles are restriction or pro-replication is context-dependent and unresolved
    • ortholog prion mechanism not directly demonstrated for human TIA-1
  16. 2016 Medium

    Established redox control of SG nucleation and identified tau as a brain interactor whose toxicity depends on TIA-1, opening the neurodegeneration axis.

    Evidence H2O2 oxidation with SG/apoptosis assays; brain Co-IP, TIA-1 KO/KD with tau misfolding readouts

    PMID:26738979 PMID:27160897

    Open questions at the time
    • oxidized residues not mapped
    • direct vs indirect tau interaction not fully resolved
  17. 2017 High

    Defined disease mutation mechanism (LCD mutations enhance phase transition and trap TDP-43) and added p53 silencing plus multi-protein splicing roles, unifying biophysics, splicing, and disease.

    Evidence patient mutations with in vitro LLPS, FRAP, TDP-43 solubility and neuropathology (P362L); p53 RIP/polysome in B cells; RBM39/Pcbp1/TIA-1 splicing complex reconstitution

    PMID:28193846 PMID:28817800 PMID:28904350

    Open questions at the time
    • link between altered SG dynamics and neuronal death not fully causal
    • in vivo consequences of mutations not modeled
  18. 2018 High

    Identified Zn2+ as a physiological multimerization trigger and used double knockout to reveal that TIA-1/TIAL1 loss drives mis-splicing-induced PKR activation and spontaneous SGs.

    Evidence recombinant LLPS with ZnCl2/TPEN and in-cell Zn2+ release; CRISPR DKO with PAR-CLIP, RNA-seq, PRKRA/EIF2AK2 epistasis rescue

    PMID:29298433 PMID:29429924

    Open questions at the time
    • zinc-binding site on TIA-1 not localized
    • physiological relevance of the PKR feedback loop in vivo unclear
  19. 2021 Medium

    Showed tandem RNA binding sites tune TIA-1 phase separation/fibrillization and that TIA-1 directly drives toxic tau oligomer formation, defining how RNA stoichiometry and tau converge on pathological assemblies.

    Evidence in vitro LLPS/fibril assays with designed tandem-site RNA/DNA and SAXS; reconstituted tau-TIA-1 phase separation with oligomer toxicity assays

    PMID:33619090 PMID:33621982

    Open questions at the time
    • in-cell relevance of tandem-site tuning not shown
    • structure of toxic tau-TIA-1 species undefined
  20. 2022 High

    Resolved at residue resolution how PLD physicochemistry governs assembly and how ALS vs WDM mutations act oppositely—ALS mutations enhancing amyloid, WDM mutation attenuating stickiness.

    Evidence NMR, molecular dynamics, 3D electron crystallography, and aggregation assays of PLD with multiple disease mutations

    PMID:36112647

    Open questions at the time
    • link to full-length cellular phase behavior partly indirect
    • therapeutic targeting of PLD not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TIA-1's distinct activities—splice-site selection, translational silencing, and stress-granule/aggregate formation—are coordinated, compartment-resolved, and pharmacologically targetable in disease remains unresolved.
  • no integrated model coupling RNA binding stoichiometry to in-cell phase behavior
  • phosphorylation/oxidation/zinc inputs not mapped to defined residues in vivo
  • no demonstration that modulating TIA-1 phase transition rescues neurodegeneration in animal models

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 6 GO:0045182 translation regulator activity 5 GO:0140110 transcription regulator activity 4 GO:0003677 DNA binding 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0031410 cytoplasmic vesicle 3 GO:0005634 nucleus 2 GO:0005829 cytosol 2
Pathway
R-HSA-8953854 Metabolism of RNA 5 R-HSA-1643685 Disease 4 R-HSA-392499 Metabolism of proteins 4 R-HSA-8953897 Cellular responses to stimuli 4
Partners
MAPTPCBP1RBM39RSK2SAM68TDP-43TIAL1U1-C
Complex memberships
U1 snRNP-associated spliceosomal complexstress granule

Evidence

Reading pass · 40 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). A phosphomimetic eIF-2alpha mutant (S51D) induces SG assembly, a non-phosphorylatable mutant (S51A) prevents it, and a TIA-1 mutant lacking RNA-binding domains acts as a transdominant inhibitor of SG formation, placing TIA-1 downstream of eIF-2alpha in the pathway. Phosphomimetic/non-phosphorylatable eIF-2alpha mutant transfection, dominant-negative TIA-1 truncation mutant, fluorescence microscopy of SG assembly The Journal of cell biology High 10613902
2004 Stress granule assembly is mediated by prion-like aggregation of TIA-1's glutamine-rich prion-related domain (PRD). The PRD is required for SG recruitment and exhibits concentration-dependent aggregation inhibited by HSP70; substitution of the PRD with the yeast prion domain SUP35-NM reconstitutes SG assembly. MEFs lacking TIA-1 show impaired SG formation with normal eIF2alpha phosphorylation, confirming TIA-1 acts downstream of eIF2alpha. Truncation/deletion mutants, PRD domain swap with yeast SUP35-NM, TIA-1 knockout MEFs, protease resistance assay, HSP70 co-immunoprecipitation Molecular biology of the cell High 15371533
2000 TIA-1 and PABP-I dynamically and continuously shuttle in and out of stress granules, as demonstrated by FRAP of GFP-tagged proteins in live cells. Drugs that stabilize polysomes (emetine) dissolve preformed SGs, while drugs that destabilize polysomes (puromycin) promote SG assembly, indicating SGs and polysomes exist in equilibrium. GFP-tagged TIA-1 live-cell imaging, FRAP, pharmacological manipulation (emetine, puromycin) The Journal of cell biology High 11121440
2000 TIA-1 functions as a translational silencer of TNF-alpha. In TIA-1 knockout macrophages, TNF-alpha protein production is significantly increased without change in transcript levels or half-life, but with increased polysome association of TNF-alpha mRNA, indicating TIA-1 inhibits translation rather than mRNA stability. Homologous recombination knockout mice, polysome fractionation, LPS stimulation of macrophages, intracellular flow cytometry, ELISA The EMBO journal High 10921895
2000 TIA-1 regulates alternative pre-mRNA splicing by binding U-rich sequences downstream of 5' splice sites and facilitating U1 snRNP recruitment, demonstrated for Drosophila msl-2 and human Fas pre-mRNAs. In vitro splicing assays, UV cross-linking, immunoprecipitation, overexpression in cultured cells, U1 snRNP recruitment assays Molecular cell High 11106748
1996 RNA binding specificity of TIA-1 is mediated primarily by RRM2, which selectively binds uridylate-rich sequences; replacing uridylates with cytidines abolishes binding. RRM3 can bind a broad population of cellular RNAs, while RRM1 does not bind RNA due to negatively charged residues in the RNP1 octamer. In vitro SELEX (selection/amplification from random RNA pools), filter binding assays, mutational analysis of individual RRM domains The Journal of biological chemistry High 8576255
2002 TIA-1 interacts directly with the U1 snRNP protein U1-C via its Q-rich domain (enhanced by RRM1), and RRM2+3 are required for pre-mRNA binding. This direct TIA-1/U1-C interaction facilitates recruitment of U1 snRNP to weak 5' splice sites. Co-precipitation assays with recombinant proteins, domain deletion analysis, in vitro U1 snRNP recruitment assays The EMBO journal High 12486009
2005 TIA-1 promotes Fas exon 6 inclusion by enhancing U1 snRNP binding to the 5' splice site of intron 6, which in turn facilitates U2AF binding to the 3' splice site of intron 5 (exon definition). This opposes PTB-mediated exon skipping via an exonic splicing silencer. In vitro splicing assays, U1 snRNP and U2AF binding assays, PTB competition experiments, reporter minigene transfection Molecular cell High 16109372
1995 Fas-activated serine/threonine kinase (FAST) is activated during Fas-mediated apoptosis and directly phosphorylates TIA-1. FAST dephosphorylation and concomitant activation precedes TIA-1 phosphorylation and DNA fragmentation, placing FAST upstream of TIA-1 in Fas apoptotic signaling. Kinase activation assays, phosphorylation of TIA-1 by immunoprecipitated FAST kinase in vitro, temporal analysis relative to DNA fragmentation The Journal of experimental medicine High 7544399
2003 TIA-1 binds the AU-rich element in the COX-2 mRNA 3'UTR and functions as a translational silencer of COX-2. TIA-1 null fibroblasts produce significantly more COX-2 protein without changes in transcription or mRNA turnover; colon cancer cells with COX-2 overexpression show defective TIA-1 binding. RNA binding studies, TIA-1 null fibroblasts (KO mice), COX-2 transcript stability assays, polysome analysis, in vitro RNA pulldown The Journal of experimental medicine High 12885872
2005 TIA-1 associates with a broad set of target mRNAs containing a U-rich bipartite motif (30-37 nt) predominantly in the 3'UTR, and represses their translation. The motif was identified by immunoprecipitation of TIA-1-RNA complexes followed by microarray analysis; RNAi knockdown of TIA-1 de-represses target mRNA translation. Immunoprecipitation of TIA-1-RNA complexes, microarray analysis, RT-PCR validation, biotinylated RNA pulldown/Western blot, RNAi knockdown Molecular and cellular biology High 16227602
2006 TIA-1 functions as a translational repressor of cytochrome c mRNA by binding its 3'UTR (proximal region), opposing the translational activator HuR. TIA-1 silencing dramatically increases cytochrome c translation; following ER stress, cytochrome c mRNA exits polysomes and translation declines. RNA-binding protein immunoprecipitation, siRNA knockdown, polysome fractionation, metabolic labeling of nascent cytochrome c protein Molecular and cellular biology Medium 16581801
2006 FAST kinase synergizes with TIA-1/TIAR to promote Fas exon 6 inclusion. Depletion of FAST K causes exon 6 skipping; FAST K overexpression effects are suppressed by TIA-1/TIAR depletion. In vitro phosphorylation of TIA-1 by FAST K enhances U1 snRNP recruitment without increasing TIA-1 pre-mRNA binding, suggesting phosphorylation modulates protein-protein interactions at the spliceosome. siRNA depletion of FAST K, Fas minigene reporter assays, in vitro phosphorylation of TIA-1 by FAST K, U1 snRNP recruitment assays The Journal of biological chemistry Medium 17135269
2007 TIA-1-induced translational silencing promotes mRNA decay via both the 5'-3' (DCP2-dependent) and 3'-5' (exosome Rrp46-dependent) decay pathways. TIA-1-mediated decay requires polysome disassembly (inhibited by cycloheximide/emetine but not puromycin); tethering TIA-1 to a reporter mRNA promotes its decay. siRNA knockdown of decay pathway components (DCP2, Rrp46), reporter mRNA tethering assay, polysome-stabilizing/destabilizing drugs, gene array analysis in TIA-1 KO macrophages The Journal of biological chemistry Medium 17711853
2008 RSK2 directly interacts with the prion-related domain (PRD) of TIA-1 via its N-terminal kinase domain and co-localizes in stress granules in a codependent manner. Silencing RSK2 decreases cell survival under stress. Mitogen releases RSK2 from SGs for nuclear import, and nuclear accumulation of RSK2 depends on TIA-1. Co-immunoprecipitation of endogenous proteins, domain mapping with RSK2 N-terminal kinase domain, siRNA knockdown of RSK2, live-cell imaging of SG colocalization, nuclear fractionation Molecular cell Medium 18775331
2011 TIA-1 and TIAR bind the 5' end of 5'TOP mRNAs upon amino acid starvation (requiring GCN2 activation and mTOR inactivation) and arrest translation at the initiation step, causing 5'TOP mRNA polysome release and accumulation in stress granules. RNA immunoprecipitation, polysome fractionation, siRNA knockdown of TIA-1/TIAR, GCN2 inhibition, mTOR inhibition/activation, stress granule microscopy Genes & development High 21979918
2002 TIA-1 (and TIAR) bind specifically to the 3' terminal stem-loop of West Nile virus minus-strand RNA via RRM2. WNV growth is less efficient in TIAR knockout cells but not in cells lacking other RNA virus susceptibility factors; reconstitution of TIAR restored WNV growth, suggesting TIA-1/TIAR facilitate flavivirus genome RNA replication. RNA affinity column purification, UV cross-linking/immunoprecipitation, recombinant protein competition gel-shift assays, TIAR KO cell lines, reconstitution experiments, virus growth assays Journal of virology Medium 12414941
2014 TIA-1 binds tick-borne encephalitis virus (TBEV) RNA in infected cells and is recruited to perinuclear sites of viral replication, depleting SGs. TIA-1 inhibits TBEV at the level of first-round viral translation, as TIA-1 KO fibroblasts show increased luciferase activity from a TBEV replicon at early time points. RNA immunoprecipitation in TBEV-infected cells, siRNA knockdown, TIA-1 KO MEFs, TBEV-luciferase replicon assay, immunofluorescence microscopy Journal of virology Medium 24696465
2014 TIA-1 NMR solution structure (RRM2-RRM3) reveals 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 adopt a compact arrangement upon RNA binding. RRM2,3 binds pyrimidine-rich RNA with nanomolar affinity; RRM1 has little intrinsic RNA binding affinity. NMR spectroscopy (solution structure of RRM2-RRM3), SAXS, isothermal titration calorimetry (ITC), RNA binding assays Nucleic acids research High 24682828
2016 TIA-1 oxidation by reactive oxygen species (H2O2) inhibits stress granule assembly. When cells face concurrent ER stress and oxidative stress, ROS-oxidized TIA1 cannot form SGs, leading to enhanced apoptosis. This demonstrates that TIA1's SG-nucleating activity is redox-regulated. H2O2 treatment combined with ER stress (tunicamycin), SG formation assays by immunofluorescence, TIA1 oxidation biochemical analysis, cell viability/apoptosis assays Nature communications Medium 26738979
2016 Tau interacts with TIA1 in brain tissue, and tau regulates the distribution of TIA1 and accelerates stress granule formation. Conversely, TIA1 knockdown or knockout inhibits tau misfolding and associated toxicity in cultured hippocampal neurons, while TIA1 overexpression induces tau misfolding and neurodegeneration. Co-immunoprecipitation from brain tissue, TIA1 interactome analysis (MS), TIA1 KO/KD in hippocampal neurons, tau misfolding assays, pharmacological SG inhibition Cell reports Medium 27160897
2017 ALS/FTD-associated mutations in the TIA1 low-complexity domain (LCD), including P362L, increase TIA1's propensity to undergo phase transition, delay SG disassembly, promote accumulation of non-dynamic SGs harboring TDP-43, and render TDP-43 less mobile and insoluble. Patient-derived genetic analysis, phase separation assays in vitro, live-cell SG dynamics (FRAP), TDP-43 mobility and solubility assays, postmortem neuropathology Neuron High 28817800
2018 Recombinant TIA-1 undergoes rapid multimerization and phase separation in the presence of divalent zinc (Zn2+), reversible by the zinc chelator TPEN. In arsenite-stressed cells, Zn2+ is released before SG formation, and TPEN inhibits formation and maintenance of TIA-1-positive SGs, identifying Zn2+ as a physiological second messenger for TIA-1 multimerization. Recombinant TIA-1 phase separation assay with ZnCl2, TPEN chelation rescue, Zn2+ release measurement in arsenite-treated cells, immunofluorescence SG assays Cell reports Medium 29298433
2018 Double knockout of TIA1 and TIAL1 increases target mRNA abundance proportional to binding site number and causes accumulation of aberrantly spliced mRNAs subject to NMD. Loss of PRKRA by mis-splicing activates PKR (EIF2AK2) and triggers spontaneous SG formation; ectopic PRKRA cDNA or EIF2AK2 knockout in DKO cells rescues this phenotype. CRISPR double KO of TIA1/TIAL1, PAR-CLIP for target site mapping, RNA-seq for splicing/abundance, ectopic PRKRA cDNA rescue, EIF2AK2 KO epistasis Molecular cell High 29429924
2005 TIA-1 and TIAR continuously shuttle between nucleus and cytoplasm in a transcription-dependent manner. RRM2 and the first half of the auxiliary region mediate nuclear accumulation; RRM3 mediates nuclear export. Both RRMs contribute to localization through their RNA-binding capacity. Nuclear export is Ran-GTP-independent and CRM1-independent. Domain truncation/mutation analysis, leptomycin B (CRM1 inhibitor) treatment, Ran-GTP depletion, transcription inhibitors, fluorescence microscopy of GFP-tagged constructs Journal of cell science Medium 16278295
2007 TIA-1 binds to AU-rich sequences in COL2A1 intron 2, modulates alternative splicing of COL2A1 exon 2, and also interacts with the equivalent single-stranded DNA sequence in vivo (confirmed by chromatin immunoprecipitation), suggesting a dual role at both transcription and pre-mRNA splicing levels. Minigene splicing assays, RNP immunoprecipitation for pre-mRNA binding, chromatin immunoprecipitation (ChIP) with RNase step, competition assays for DNA vs RNA binding The Journal of biological chemistry Medium 17580305
2008 TIA-1 and TIAR binding sites in the West Nile virus 3' minus-strand stem-loop RNA were mapped to short AU sequences (UAAUU) in internal loops. Infectious clone RNAs with deleted/substituted binding sites showed decreased TIAR/TIA-1 binding efficiency correlated with decreased intracellular genomic RNA levels and virus production, implicating TIA-1/TIAR binding in asymmetric amplification of genomic RNA from the minus-strand template. Infectious clone RNA mutagenesis, in vitro protein binding assays, plaque assays, intracellular RNA quantification by qRT-PCR Journal of virology Medium 18768985
2009 Sam68 is recruited to stress granules under oxidative stress through direct complex formation with TIA-1. Domains aa269-321 and the KH domain of Sam68 are essential for SG recruitment, but Sam68 knockdown does not impair SG assembly. Co-immunoprecipitation of Sam68 and TIA-1, domain deletion mapping, siRNA knockdown of Sam68, immunofluorescence of SG markers under oxidative stress Experimental cell research Low 19615357
2010 TIA1 prevents skipping of SMN2 exon 7 in a novel context where intronic U-rich motifs are separated from the 5' splice site by overlapping inhibitory elements. Any single RRM combined with the Q domain is sufficient for TIA1-associated regulation of SMN2 exon 7 splicing in vivo. TIA1 counteracts the inhibitory effect of PTB on SMN exon 7 splicing. In vivo splicing assays with TIA1/TIAR expression, domain deletion/chimeric protein analysis, co-expression with PTB, RT-PCR of endogenous SMN2 exon 7 splicing Molecular and cellular biology Medium 21189287
2011 TDP-43 differentially regulates key SG components: controlled aggregation of TIA-1 is disrupted in the absence of TDP-43, resulting in slowed SG formation. TDP-43 also regulates G3BP mRNA levels. The disease mutation TDP-43(R361S) is a loss-of-function mutation for SG formation and alters TIA-1 and G3BP levels. TDP-43 siRNA knockdown, oxidative stress/heat shock/thapsigargin-induced SG assays, immunofluorescence, Western blot for TIA-1 and G3BP, TDP-43 mutant expression Human molecular genetics Medium 21257637
2013 Welander distal myopathy (WDM) is caused by the E384K mutation in TIA1's Q-rich domain. Mutant TIA1 causes increased SG abundance and slower FRAP kinetics in HeLa cells, consistent with altered SG dynamics. The E384K mutation is in the domain that interacts with U1-C splicing factor, and WDM patients have increased SMN2 exon 7 skipping. Genetic sequencing/linkage analysis, Western blot and immunofluorescence of WDM muscle biopsies, high-content SG quantification in HeLa cells, FRAP, RT-PCR of SMN2 splicing Annals of neurology Medium 23401021
2014 In yeast, Tia1/Pub1 forms a prion and cooperates with Sup35/eRF3 to establish a two-protein self-propagating state along tubulin cytoskeleton. A tubulin-associated complex containing Pub1 and Sup35 oligomers (plus TUB1 mRNA and translation machinery) depends on prion domains; PUB1 disruption leads to cytoskeletal defects. Yeast prion assays, fluorescence microscopy of line structures along tubulin, genetic disruption of PUB1, co-purification of Pub1/Sup35/TUB1 mRNA complex Molecular cell Medium 24981173
2014 TIA-1 RRM3 binds both C-rich and U-rich sequences with micromolar affinity, and in the context of full-length TIA-1, RRM3 significantly enhances binding to C-rich RNA (including 5'TOP sequences), as demonstrated by STD-NMR and biotinylated RNA pulldown. STD-NMR, surface plasmon resonance (SPR), biotinylated RNA pulldown/Western blot with full-length TIA-1 and isolated domains RNA biology Medium 24824036
2017 Crystal structure of TIA-1 RRM2 in complex with DNA at 2.3 Å resolution provides the first atomic-resolution structure of any TIA protein RRM with oligonucleotide. SAXS shows TIA-1 RRM23 adopts a compact structure upon complex formation with target RNA or DNA; both RRMs engage the 10-nt target sequence. X-ray crystallography (2.3 Å), SAXS, in vitro binding assays, site-directed mutagenesis (Lys274) Nucleic acids research High 28184449
2021 TIA1 interaction with RNA and the presence of TIA1 protein together are sufficient to drive phase separation of tau at physiological concentrations without crowding agents. Phase separation of tau with TIA1 generates abundant tau oligomers that are significantly more toxic than tau aggregates formed with RNA alone, identifying a mechanism for generating toxic tau species. In vitro phase separation assay with recombinant proteins and RNA, tau oligomer toxicity assays, comparison with other RBPs (G3BP1) and crowding agents (PEG) Proceedings of the National Academy of Sciences of the United States of America Medium 33619090
2021 Tandem RNA binding sites (not single sites) are required to enhance TIA-1 phase separation. Single-stranded RNA and DNA with tandem binding sites efficiently promote both liquid-liquid phase separation and amyloid-like fibril formation of full-length TIA-1 in vitro; this is finely tuned by protein:binding site stoichiometry. In vitro phase separation assays with designed and native RNA/DNA sequences, fibril formation assays, SAXS for conformational analysis Nucleic acids research Medium 33621982
2022 NMR analysis and molecular dynamics simulations reveal that TIA1 PLD dynamic structure is determined by physicochemical properties in 5-residue units. ALS mutations P362L and A381T enhance self-assembly by inducing β-sheet interactions and highly condensed assemblies (promoting irreversible amyloid fibrillization), while WDM mutation E384K attenuates sticky properties. NMR analysis, molecular dynamics simulations, 3D electron crystallography, biochemical aggregation assays Proceedings of the National Academy of Sciences of the United States of America High 36112647
2017 TIA1 (Tia1) controls translational silencing of p53 mRNA and its localization to stress granules in activated B lymphocytes. Upon DNA damage, p53 mRNA is released from TIA1-containing stress granules and associates with polyribosomes for CAP-independent translation. Tia1 dissociation from mRNA targets is part of the ATM-dependent DNA damage response. RIP (TIA1), polyribosome fractionation, stress granule isolation, RNA granule localization imaging, knockout/knockdown analysis in primary B cells, global translation profiling Nature communications Medium 28904350
2014 TIA1 interacts with annexin A7 (ANXA7), and this interaction regulates TIA1 phosphorylation. Treatment with ABO (ANXA7 inhibitor) promotes TIA1-ANXA7 interaction and inhibits TIA1 phosphorylation in HUVECs, leading to increased expression of ATG13 (pro-autophagy) via FLJ11812 processing. Yeast two-hybrid screening, co-immunoprecipitation, ABO treatment, Western blot for phospho-TIA1, autophagy marker quantification The international journal of biochemistry & cell biology Low 25461769
2017 TIA1 N-terminal region coordinates with Pcbp1 and RBM39 to activate 3' splice site of protein 4.1R exon 16. TIA1 and Pcbp1 bind a UUUUCCCCCC motif between branch point and 3' splice site; together with RBM39, they promote U2 snRNP recruitment and spliceosome A complex formation via RBM39-U2AF65-SF3b155 interactions. In vitro splicing assays, RNA binding/UV cross-linking, RNAi knockdown, co-immunoprecipitation of RBM39/TIA1/Pcbp1 complex, U2 snRNP recruitment assays Molecular and cellular biology Medium 28193846

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 1074 10613902
2004 Stress granule assembly is mediated by prion-like aggregation of TIA-1. Molecular biology of the cell 832 15371533
2000 Dynamic shuttling of TIA-1 accompanies the recruitment of mRNA to mammalian stress granules. The Journal of cell biology 670 11121440
2017 TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics. Neuron 507 28817800
2000 TIA-1 is a translational silencer that selectively regulates the expression of TNF-alpha. The EMBO journal 437 10921895
2011 TAR DNA-binding protein 43 (TDP-43) regulates stress granule dynamics via differential regulation of G3BP and TIA-1. Human molecular genetics 337 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 275 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 207 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 178 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 166 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
2016 TIA1 oxidation inhibits stress granule assembly and sensitizes cells to stress-induced apoptosis. Nature communications 125 26738979
2013 Welander distal myopathy is caused by a mutation in the RNA-binding protein TIA1. Annals of neurology 124 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
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 122 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 96 29429924
2013 Welander distal myopathy caused by an ancient founder mutation in TIA1 associated with perturbed splicing. Human mutation 95 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) 95 7512092
2018 TIA1 regulates the generation and response to toxic tau oligomers. Acta neuropathologica 90 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
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 TIA-1 Self-Multimerization, Phase Separation, and Recruitment into Stress Granules Are Dynamically Regulated by Zn2. Cell reports 85 29298433
2018 TIA1 variant drives myodegeneration in multisystem proteinopathy with SQSTM1 mutations. The Journal of clinical investigation 83 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
1993 Cytotoxic effector cell granules recognized by the monoclonal antibody TIA-1 are present in CD8+ lymphocytes in lymph nodes of human immunodeficiency virus-1-infected patients. The American journal of pathology 72 8506945
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 67 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
2017 Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells. Nature communications 57 28904350
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
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
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 48 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 37 36112647
2007 Nuclear protein TIA-1 regulates COL2A1 alternative splicing and interacts with precursor mRNA and genomic DNA. The Journal of biological chemistry 37 17580305
2017 TIA-1 Is a Functional Prion-Like Protein. Cold Spring Harbor perspectives in biology 36 28003185
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
2020 Reduction of the RNA Binding Protein TIA1 Exacerbates Neuroinflammation in Tauopathy. Frontiers in neuroscience 32 32327969
2021 Tandem RNA binding sites induce self-association of the stress granule marker protein TIA-1. Nucleic acids research 31 33621982
2018 Myopathy With SQSTM1 and TIA1 Variants: Clinical and Pathological Features. Frontiers in neurology 31 29599744
2014 HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA. International journal of molecular sciences 31 24566137
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
2001 Identification of TIA-1+ and granzyme B+ cytotoxic T cells in lichen sclerosus et atrophicus. Dermatology (Basel, Switzerland) 30 11385223
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
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 25 29496454
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
2022 Intracellular accumulation of tau inhibits autophagosome formation by activating TIA1-amino acid-mTORC1 signaling. Military Medical Research 24 35799293
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
2021 Amyotrophic lateral sclerosis (ALS) linked mutation in Ubiquilin 2 affects stress granule assembly via TIA-1. CNS neuroscience & therapeutics 22 34750982
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
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
2021 Dynamics of alternative splicing during somatic cell reprogramming reveals functions for RNA-binding proteins CPSF3, hnRNP UL1, and TIA1. Genome biology 20 34082786
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
2017 Mutation analysis of the TIA1 gene in Chinese patients with amyotrophic lateral sclerosis and frontotemporal dementia. Neurobiology of aging 19 29370934
2001 TIA1 and mast cell tryptase in food allergy of children: increase of intraepithelial lymphocytes expressing TIA1 associates with allergy. Journal of pediatric gastroenterology and nutrition 19 11176318

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