Affinage

THOC5

THO complex subunit 5 · UniProt Q13769

Length
683 aa
Mass
78.5 kDa
Annotated
2026-06-10
31 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

THOC5 is a subunit of the mammalian THO/TREX complex that acts as a selective mRNA export adaptor coupling co-transcriptional 3'-end processing to nuclear export of a defined subset of transcripts rather than bulk mRNA (PMID:19165146, PMID:21525145). It binds directly to a distinct, non-overlapping surface on the Ntf2-like middle domain of the Tap export receptor—allowing simultaneous Tap engagement by THOC5 and the Aly adaptor—and exhibits intrinsic RNA-binding activity within stable THO mRNPs (PMID:19165146). Through direct interaction with the cleavage/polyadenylation machinery, THOC5 governs poly(A) site choice: it loads CFIm68 co-transcriptionally to favor distal polyadenylation sites and recruits CPSF100 to the 3'UTRs of target genes, so that loss of THOC5 yields chromatin-retained transcripts, shortened 3'UTRs, and failed export (PMID:23685434, PMID:25274738). THOC5 is recruited to chromatin near sites of high RNA polymerase II density and, via interaction with CDK12 and THOC6, modulates polymerase II elongation rate and CDK12 recruitment to R-loops, mechanistically linking it to transcription as well as processing (PMID:36590164). The factor is selectively required for export of inducible and immediate-early transcripts—including heat-shock, M-CSF, Wnt, and serum-responsive genes (Hsp70, Ets1, Sox9, Ascl2, Myc, and immediate-early genes)—with over 90% of serum-induced immediate-early genes failing induction upon THOC5 loss (PMID:21525145, PMID:24157873, PMID:24267292, PMID:25274738). THOC5 activity is gated by signaling-dependent phosphorylation: PKC phosphorylates serines 5/6 adjacent to its NLS to drive nuclear-to-cytoplasmic translocation (PMID:15221008), Src-family and leukemogenic tyrosine kinases phosphorylate Y225 to control mRNA-binding and chemokinesis (PMID:23032722, PMID:26919114), and the ATM-p53 pathway suppresses its mRNA-binding after DNA damage (PMID:21937706). Consistent with its role in inducible gene expression, conditional deletion in mice causes rapid apoptosis of hematopoietic progenitors and disrupts intestinal epithelial homeostasis, and its activity is co-opted in leukemia and breast cancer stem-like states (PMID:20051105, PMID:24267292, PMID:34708581).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1999 High

    Established the first molecular handle on THOC5 as a signaling-responsive protein by showing it transiently associates with an activated receptor tyrosine kinase, raising the question of how a cytokine receptor connects to this factor.

    Evidence Co-IP and GST-Fms pulldown with deletion mutagenesis in cell systems

    PMID:10597251

    Open questions at the time
    • Did not define THOC5's downstream nuclear function
    • Functional consequence of the transient Fms binding for differentiation unresolved at this stage
  2. 2004 High

    Answered how THOC5 subcellular distribution is controlled, showing PKC phosphorylation near the NLS shifts it from nucleus to cytoplasm and links this to differentiation signaling.

    Evidence Phosphomimetic/non-phosphorylatable S5/S6 mutants with localization and differentiation assays

    PMID:15221008

    Open questions at the time
    • Did not connect localization control to a specific mRNA export function
    • Endogenous PKC kinase identity in vivo not pinned down
  3. 2006 Medium

    Provided the first link between THOC5 and RNA processing, showing it is needed for production of polyadenylated C/EBPalpha mRNA and is part of the THO complex during lineage decisions.

    Evidence Overexpression/knockdown with Northern blot, RT-PCR, and Co-IP in C2C12 cells

    PMID:16909111

    Open questions at the time
    • Mechanism of processing/export selectivity undefined
    • Direct vs indirect effect on C/EBPalpha not separated
  4. 2008 High

    Defined THOC5 as a partner-import platform by showing it directly binds and chaperones THOC7 into the nucleus, clarifying THO complex assembly.

    Evidence Co-IP, domain-mapping deletion mutagenesis, and co-localization imaging

    PMID:19059247

    Open questions at the time
    • Structural basis of the THOC5-THOC7 interface not resolved
    • Whether nuclear import of THOC7 is required for export function untested
  5. 2008 Medium

    Connected THOC5 to oncogenic signaling and survival, showing leukemogenic tyrosine kinases phosphorylate it to elevate PIP3 and suppress apoptosis, and that it associates with C/EBPbeta to drive myeloid maturation.

    Evidence Mass spectrometry phosphosite identification, PIP3/PtdInsP3 and apoptosis assays, Co-IP, ectopic expression

    PMID:18373705 PMID:19015024

    Open questions at the time
    • Mechanistic link between phosphorylation, PIP3 elevation, and mRNA function unclear
    • Direct vs indirect C/EBPbeta interaction not fully validated
  6. 2009 High

    Resolved how THOC5 interfaces with the export machinery, demonstrating direct binding to a Tap surface distinct from Aly and selective requirement for HSP70 mRNA export but not bulk export.

    Evidence Reciprocal in vitro binding (GST pulldown), Co-IP, RNA-binding assays, and knockdown export assays

    PMID:19165146

    Open questions at the time
    • Did not define the full set of THOC5-dependent transcripts
    • Determinants of transcript selectivity unknown
  7. 2010 High

    Established the in vivo physiological essentiality of THOC5, showing its loss triggers rapid hematopoietic progenitor apoptosis and destabilizes THO complex partner THOC1.

    Evidence Interferon-inducible conditional knockout mouse with bone marrow transplant rescue and flow cytometry

    PMID:20051105

    Open questions at the time
    • Which essential target mRNAs underlie progenitor survival not identified
    • Cell-type specificity of dependence not mapped
  8. 2011 High

    Defined THOC5 as a selective export factor for ~10 spliced transcripts and showed Hsp70 export is THOC5-dependent only under heat stress, framing it as a stress/inducible-mRNA export factor.

    Evidence Cre-lox conditional KO MEFs with cytoplasmic transcriptome analysis and RIP

    PMID:21525145

    Open questions at the time
    • Sequence/structural features marking THOC5-dependent transcripts unknown
    • Stage at which selectivity is imposed not defined
  9. 2011 High

    Answered how DNA damage modulates THOC5, showing the ATM-p53 pathway suppresses its mRNA-binding via its C-terminal domain, linking export to the damage response.

    Evidence RIP, ATM inhibitor (KU55933), ATM/p53 siRNA epistasis, and C-terminal/PEST mutants

    PMID:21937706

    Open questions at the time
    • Whether ATM directly phosphorylates THOC5 not established
    • The C-terminal regulatory residues not pinpointed
  10. 2012 High

    Identified Y225 as a tyrosine-kinase-controlled switch for THOC5 mRNA-binding and cell motility, dysregulated in CML and drug-targetable.

    Evidence MS phosphosite mapping, Y225 mutagenesis, in vitro kinase/phosphatase (Src/CD45) assays, chemokinesis assays, primary CML cells

    PMID:23032722

    Open questions at the time
    • How Y225 phosphorylation alters RNA contacts mechanistically unclear
    • Full set of Y225-dependent transcripts not enumerated
  11. 2013 High

    Mechanistically united THOC5 with co-transcriptional 3'-end processing and inducible gene programs, showing it loads CFIm68 to set poly(A) site choice and is needed for processing/export of M-CSF and Wnt target mRNAs.

    Evidence Co-IP, ChIP-seq, microarray, inducible conditional KO, RIP across multiple studies

    PMID:23685434 PMID:24157873 PMID:24267292

    Open questions at the time
    • Direct vs bridged nature of THOC5-CFIm68 contact not crystallographically defined
    • How processing defect is mechanistically coupled to export block not fully separated
  12. 2014 High

    Extended the processing role to immediate-early gene induction, showing THOC5 recruits CPSF100 to target 3'UTRs and is required for serum induction of >90% of immediate-early genes.

    Evidence MS interactome with THOC5 bait, chromatin association assays, transcriptomics, serum stimulation with knockdown

    PMID:25274738

    Open questions at the time
    • Order of CFIm68 vs CPSF100 recruitment not resolved
    • Determinants targeting THOC5 to IEG loci unknown
  13. 2016 Medium

    Generalized the Y225 switch to other leukemogenic receptors, showing MPL W515L drives Y225 phosphorylation to dysregulate MYC transport and chemokinesis.

    Evidence Quantitative proteomics, Y225 mutagenesis, chemokinesis assays, primary CD34+ patient cells

    PMID:26919114

    Open questions at the time
    • Direct kinase responsible for Y225 in this context not confirmed
    • Mechanism linking Y225 to MYC mRNA selectivity unclear
  14. 2021 Medium

    Implicated THOC5 in cancer stemness, showing it is required for THOC2-dependent export of SOX2/NANOG mRNAs and radioresistance in triple-negative breast cancer.

    Evidence siRNA knockdown, xenograft assays, protein expression analysis

    PMID:34708581

    Open questions at the time
    • Direct THOC5 binding to SOX2/NANOG transcripts not shown here
    • Whether processing or export step is rate-limiting undefined
  15. 2022 High

    Revealed a transcription-elongation arm of THOC5 function, showing chromatin-associated THOC5 interacts with CDK12, DDX5/17, and THOC6 to set polymerase II elongation rate and recruit CDK12 to R-loops.

    Evidence Depletion plus in vivo elongation rate measurement, ChIP-seq, chromatin Co-IP, R-loop analysis; plus M-CSF-dependent shuttling and FICD binding in osteoclast precursors

    PMID:35688054 PMID:36590164

    Open questions at the time
    • Causal hierarchy between elongation control, R-loop resolution, and processing not resolved
    • Structural basis of CDK12-THOC5-THOC6 assembly unknown
  16. 2024 Medium

    Linked THOC5 to oncogenic splicing-factor mutation, showing SF3B1 K700E weakens SF3B1-THOC5 interaction and impairs export of THOC5-bound mRNAs, rescuable by THOC5 overexpression.

    Evidence Co-IP (mutant vs WT SF3B1), RIP, nuclear export assays, THOC5 overexpression rescue

    PMID:39259498

    Open questions at the time
    • Whether SF3B1-THOC5 contact is direct not established
    • Identity of the affected transcript set incompletely defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • What molecular features mark a transcript as THOC5-dependent, and how phosphorylation, processing, elongation, and export selectivity are mechanistically integrated, remains unresolved.
  • No structural model of THOC5 in the THO/TREX complex with its processing/export partners
  • Cis-determinants of THOC5 target selectivity unknown
  • Causal ordering of elongation control vs 3'-processing vs export not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 5 GO:0060090 molecular adaptor activity 3 GO:0140098 catalytic activity, acting on RNA 3
Localization
GO:0005634 nucleus 4 GO:0000228 nuclear chromosome 3 GO:0005829 cytosol 3 GO:0005654 nucleoplasm 2
Pathway
R-HSA-8953854 Metabolism of RNA 4 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-9609507 Protein localization 3 R-HSA-8953897 Cellular responses to stimuli 2
Partners
ALYREFCDK12CPSF2/CPSF100CPSF6/CFIM68SF3B1TAP/NXF1THOC1THOC7
Complex memberships
THO/TREX complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 THOC5 binds to a distinct, non-overlapping surface on the middle (Ntf2-like) domain of the Tap export receptor, allowing simultaneous binding of both THOC5 and the adaptor protein Aly to Tap-p15. THOC5 exhibits in vitro RNA-binding activity and associates with HSP70 mRNPs in vivo as a component of the stable THO complex. Nuclear export of HSP70 mRNA specifically requires both THOC5 and Aly, but THOC5 is not required for bulk mRNA export. Co-immunoprecipitation, in vitro binding assays (GST pulldown), RNA-binding assays, in vivo mRNA export assays with knockdown The EMBO journal High 19165146
1999 THOC5/FMIP (MW ~78 kDa) binds transiently via its N-terminal 144 residues to the cytoplasmic domain of activated (ligand-stimulated) c-Fms tyrosine kinase receptor. Binding is followed by rapid tyrosine phosphorylation of FMIP within the binding domain, which drastically reduces its association with Fms. No binding was observed with the cytoplasmic domains of c-Kit, TrkA, c-Met, or the insulin receptor. Co-immunoprecipitation, GST-Fms fusion protein pulldown, deletion mutagenesis Oncogene High 10597251
2004 THOC5/FMIP is phosphorylated by protein kinase C (PKC) on serines 5 and 6, adjacent to its nuclear localization signal (NLS). This NLS is essential for predominantly nuclear localization. PKC-mediated phosphorylation on S5/S6 causes translocation of THOC5 from nucleus to cytosol. Phosphomimetic mutations (SS5,6EE) promoted cytoplasmic localization and enhanced M-CSF-mediated survival/differentiation, while non-phosphorylatable mutant (SS5,6AA) remained nuclear even in the presence of activated PKCα. Site-directed mutagenesis (phosphomimetic and non-phosphorylatable mutants), subcellular fractionation/localization imaging, functional differentiation assay Oncogene High 15221008
2008 THOC7 lacks a typical nuclear localization signal (NLS) and resides mainly in the cytoplasm on its own, but directly binds to the N-terminal portion (residues 1-199) of THOC5/FMIP via THOC7 residues 50-137. This interaction is required for THOC5-dependent nuclear transport of THOC7: in the presence of THOC5, THOC7 is transported into the nucleus; a THOC7 mutant lacking the FMIP-binding site fails to co-localize with FMIP. Co-immunoprecipitation, deletion mutagenesis, subcellular localization imaging (co-transfection/co-localization) FEBS letters High 19059247
2006 THOC5/FMIP overexpression in C2C12 cells prevents adipocyte differentiation and promotes granulocyte/muscle phenotype, while FMIP knockdown promotes adipocyte lineage commitment and impairs muscle differentiation. Mechanistically, FMIP-overexpressing cells lack polyadenylated C/EBPα mRNA but retain C/EBPα pre-mRNA (detected by Northern blot and RT-PCR), implicating FMIP in RNA processing/export of C/EBPα. THOC1 co-precipitates with FMIP, placing it in the THO complex in this context. Ectopic expression and siRNA knockdown, Northern blot, RT-PCR, co-immunoprecipitation Oncogene Medium 16909111
2010 Conditional knockout of THOC5 in mice leads to rapid apoptosis of hematopoietic progenitor cells (committed myeloid progenitors and long-term reconstituting cells) within days, demonstrating THOC5 is essential for hematopoietic primitive cell survival in vivo. Mechanistically, THOC5 depletion causes down-regulation of its direct interacting partner THOC1, potentially disrupting THO complex function. Interferon-inducible conditional knockout mouse, bone marrow transplantation rescue, flow cytometry, histology BMC biology High 20051105
2011 THOC5 is required for export of a specific subset (~10 identified) of mRNAs (including HoxB3, CBX2); these mRNAs are spliced but not exported to the cytoplasm in THOC5-depleted MEF cells and co-purify with THOC5. Hsp70 mRNA export is specifically dependent on THOC5 under heat shock (42°C) but not under normal conditions (37°C), indicating THOC5 is required for stress-induced mRNA export rather than basal export. Conditional knockout (Cre-lox MEF cells), transcriptome analysis of cytoplasmic RNA, RNA co-immunoprecipitation (RIP) RNA (New York, N.Y.) High 21525145
2013 THOC5 physically interacts with CFIm68 (large subunit of mammalian cleavage factor I involved in polyadenylation site choice). Most likely via direct Thoc5–CFIm68 interaction. THOC5 depletion selectively attenuates expression of mRNAs polyadenylated at distal polyadenylation sites (phenocopying CFIm68 depletion) and globally reduces CFIm68 association with the 5' regions of genes (by ChIP-seq), indicating THOC5 controls polyadenylation site choice by co-transcriptional loading of CFIm68. Co-immunoprecipitation (antibodies against different TREX components), microarray, ChIP-seq, siRNA knockdown Nucleic acids research High 23685434
2013 THOC5 is localized in nuclear speckles and translocates from nucleus to cytoplasm during M-CSF-induced macrophage differentiation. THOC5 is required for processing/export of a subset of M-CSF-inducible mRNAs (including Ets1); depletion causes accumulation of unspliced Ets1 mRNA in the nucleus. THOC5 is recruited to chromatin at the Ets1 gene locus and binds both unspliced and spliced Ets1 transcripts. Immunofluorescence/subcellular localization, tamoxifen-inducible conditional KO, transcriptome analysis, chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP) Cell death & disease High 24157873
2013 THOC5 is required for processing and export of a subset of Wnt target mRNAs (Sox9 and Ascl2, but not Fn1) in intestinal epithelium; these mRNAs co-purify with THOC5 by RIP. THOC5 is also required for expression of the Toll-like receptor-inducible gene COX2/Ptgs2, whose transcript is a THOC5 target mRNA. THOC5 deficiency disrupts gut epithelial differentiation and self-renewal, causing bacterial translocation and sepsis in mice. Tamoxifen-inducible conditional knockout mouse, RNA co-immunoprecipitation (RIP), transcriptome analysis, histopathology BMC cell biology High 24267292
2014 THOC5 forms a complex with polyadenylation-specific factor 100 (CPSF100) upon serum stimulation. THOC5 is required for recruitment of CPSF100 to the 3'UTR of THOC5 target genes (including Id1, Id3, Wnt11, Myc, Smad7). Without THOC5, a subset of IEG transcripts fail to be released from chromatin or are released with shortened 3'UTRs and impaired nuclear export. Over 90% of immediate-early genes fail to be induced by serum in THOC5-depleted cells. Interactome analysis (THOC5 as bait/MS), chromatin association assays, transcriptome analysis, serum stimulation experiments with siRNA knockdown Nucleic acids research High 25274738
2011 ATM kinase pathway regulates THOC5 mRNA-binding activity in response to DNA damage. DNA damage decreases cytoplasmic levels of THOC5-dependent mRNAs and impairs THOC5/mRNA complex formation. The C-terminal domain of THOC5 (not phosphorylation at S307/312/314 in the PEST domain) is required for this regulatory response. ATM kinase inhibitor (KU55933) or siRNA against ATM or p53 restores THOC5-dependent mRNA export after DNA damage, indicating the ATM-p53 pathway suppresses THOC5 mRNA-binding ability. Site-directed mutagenesis (S307/312/314A and C-terminal deletion mutants), RNA immunoprecipitation (RIP), ATM kinase inhibitor treatment, siRNA knockdown of ATM and p53 RNA (New York, N.Y.) High 21937706
2012 THOC5 phosphorylation on tyrosine 225 is mediated by Src PTK and reversed by CD45 protein tyrosine phosphatase, and is elevated in CML stem cells. This Y225 phosphorylation specifically governs THOC5 mRNA-binding activity (site-directed mutagenesis of Y225 modulates motile response to CXCL12). CXCL12 chemokine stimulation also induces THOC5 Y225 phosphorylation. THOC5 Y225 phosphorylation is sensitive to frontline CML drugs (imatinib). Site-directed mutagenesis (Y225), mass spectrometry (phosphorylation site identification), in vitro kinase/phosphatase assays, RNA-binding assay, chemokinesis assay, primary CML patient cells Leukemia High 23032722
2008 TEL/PDGFRB leukemogenic tyrosine kinase increases THOC5 expression and phosphorylation; elevated THOC5 expression increases PIP3 (phosphatidylinositol 3,4,5-trisphosphate) levels and decreases apoptosis. Mass spectrometry identified the TEL/PDGFRB phosphorylation site on THOC5, which is also a target for multiple other leukemogenic tyrosine kinases. Mass spectrometry (phosphosite identification), PIP3 measurement, apoptosis assay, ectopic expression British journal of haematology Medium 18373705
2008 THOC5 forms a complex with the transcription factor C/EBPβ (detected by co-immunoprecipitation). Ectopic THOC5 expression mimics M-CSF-stimulated monocytic maturation and enhances protein expression of C/EBPβ, C/EBPα, PU.1, and GAB2. THOC5-induced increases in PtdInsP3 are required for elevated C/EBPβ, as PI3K inhibition abrogates this effect. Co-immunoprecipitation, ectopic expression, PI3K inhibition, PtdInsP3 measurement Cellular signalling Medium 19015024
2021 THOC2 promotes stem-like properties and radioresistance of triple-negative breast cancer cells in a THOC5-dependent manner by facilitating nuclear export of SOX2 and NANOG mRNA transcripts. Silencing THOC5 decreases SOX2 and NANOG protein expression and depletes stem-like properties. siRNA knockdown of THOC2 and THOC5, xenograft tumor assays, protein expression analysis Advanced science Medium 34708581
2022 THOC5 depletion results in altered 3' cleavage of >50% of mRNAs and decreases RNA polymerase II elongation rates in vivo. THOC5 is recruited to chromatin preferentially near high-density polymerase II sites. In slow polymerase II cells, chromatin-associated THOC5 interacts with CDK12 (a transcription elongation modulator), RNA helicases DDX5, DDX17, and THOC6. The CDK12-THOC5 interaction promotes CDK12 recruitment to R-loops in a THOC6-dependent manner. THOC5 depletion (siRNA/KO), in vivo transcription elongation rate measurement, ChIP-seq, co-immunoprecipitation of chromatin-associated proteins, R-loop analysis iScience High 36590164
2024 The cancer-associated SF3B1 K700E mutation attenuates SF3B1 interaction with THOC5, reduces THOC5 binding to a subset of mRNAs, and inhibits nuclear export of those mRNAs. Overexpression of THOC5 restores nuclear export of these mRNAs in SF3B1 K700E cells. Other cancer-associated SF3B1 mutations similarly inhibit mRNA nuclear export via this mechanism. Co-immunoprecipitation (SF3B1 K700E vs. wild-type), RNA immunoprecipitation (RIP), mRNA nuclear export assays, THOC5 overexpression rescue Journal of biochemistry Medium 39259498
2022 THOC5 shuttles between nucleus and cytoplasm in an M-CSF signaling-dependent manner in osteoclast precursors. THOC5 binds to FICD (a proteolytic cleavage product of c-FMS receptor) and facilitates nuclear translocation of FICD. THOC5 knockdown suppresses osteoclast differentiation partly by reducing RANKL-induced FOS and NFATc1 expression. siRNA knockdown, co-immunoprecipitation (THOC5-FICD interaction), subcellular fractionation/localization, osteoclast differentiation assay European journal of cell biology Medium 35688054
2016 MPL W515L mutant receptor induces phosphorylation of THOC5 on tyrosine 225, which mediates dysregulation of MYC mRNA expression (RNA transport) and increased chemokinesis. This was demonstrated by site-directed mutagenesis showing that THOC5 Y225 phosphorylation is required for MPL W515L-mediated effects on chemokinesis and MYC expression. Proteomics (relative quantification mass spectrometry), site-directed mutagenesis (Y225), chemokinesis assay, primary CD34+ patient cells Oncotarget Medium 26919114

Source papers

Stage 0 corpus · 31 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Adaptor Aly and co-adaptor Thoc5 function in the Tap-p15-mediated nuclear export of HSP70 mRNA. The EMBO journal 118 19165146
2010 THOC5/FMIP, an mRNA export TREX complex protein, is essential for hematopoietic primitive cell survival in vivo. BMC biology 99 20051105
2011 Identification of mRNAs that are spliced but not exported to the cytoplasm in the absence of THOC5 in mouse embryo fibroblasts. RNA (New York, N.Y.) 56 21525145
2013 Human TREX component Thoc5 affects alternative polyadenylation site choice by recruiting mammalian cleavage factor I. Nucleic acids research 49 23685434
2021 THOC2 and THOC5 Regulate Stemness and Radioresistance in Triple-Negative Breast Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 48 34708581
1999 FMIP, a novel Fms-interacting protein, affects granulocyte/macrophage differentiation. Oncogene 42 10597251
2014 THOC5 controls 3'end-processing of immediate early genes via interaction with polyadenylation specific factor 100 (CPSF100). Nucleic acids research 33 25274738
2004 The M-CSF receptor substrate and interacting protein FMIP is governed in its subcellular localization by protein kinase C-mediated phosphorylation, and thereby potentiates M-CSF-mediated differentiation. Oncogene 33 15221008
2014 THOC5, a member of the mRNA export complex: a novel link between mRNA export machinery and signal transduction pathways in cell proliferation and differentiation. Cell communication and signaling : CCS 30 24410813
2013 Transcriptional regulation of immediate-early gene response by THOC5, a member of mRNA export complex, contributes to the M-CSF-induced macrophage differentiation. Cell death & disease 30 24157873
2006 FMIP controls the adipocyte lineage commitment of C2C12 cells by downmodulation of C/EBP alpha. Oncogene 28 16909111
2015 Depletion of three combined THOC5 mRNA export protein target genes synergistically induces human hepatocellular carcinoma cell death. Oncogene 23 26549021
2013 THOC5, a member of the mRNA export complex, contributes to processing of a subset of wingless/integrated (Wnt) target mRNAs and integrity of the gut epithelial barrier. BMC cell biology 23 24267292
2012 A pathway from leukemogenic oncogenes and stem cell chemokines to RNA processing via THOC5. Leukemia 19 23032722
2008 Nuclear localization of the pre-mRNA associating protein THOC7 depends upon its direct interaction with Fms tyrosine kinase interacting protein (FMIP). FEBS letters 17 19059247
2011 An ataxia-telangiectasia-mutated (ATM) kinase mediated response to DNA damage down-regulates the mRNA-binding potential of THOC5. RNA (New York, N.Y.) 16 21937706
2008 THOC5 spliceosome protein: a target for leukaemogenic tyrosine kinases that affects inositol lipid turnover. British journal of haematology 16 18373705
2008 THOC5 couples M-CSF receptor signaling to transcription factor expression. Cellular signalling 15 19015024
2022 THOC5 complexes with DDX5, DDX17, and CDK12 to regulate R loop structures and transcription elongation rate. iScience 14 36590164
2016 mRNA export protein THOC5 as a tool for identification of target genes for cancer therapy. Cancer letters 14 26828015
2013 THOC5: a novel gene involved in HDL-cholesterol metabolism. Journal of lipid research 12 24023261
2024 Acylcarnitines promote gallbladder cancer metastasis through lncBCL2L11-THOC5-JNK axis. Journal of translational medicine 10 38519939
2016 MPL W515L expression induces TGFβ secretion and leads to an increase in chemokinesis via phosphorylation of THOC5. Oncotarget 7 26919114
2024 Resveratrol regulates Thoc5 to improve maternal immune activation-induced autism-like behaviors in adult mouse offspring. The Journal of nutritional biochemistry 5 38583499
2019 Colla corii asini might upregulate ZNF471 and THOC5 by KRAB domain-containing zinc-finger protein pathway and THO complex subunit 5 pathway to improve anemia of pregnant women with β-thalassemia. Annals of hematology 5 31098739
2024 Cancer-associated SF3B1 mutations inhibit mRNA nuclear export by disrupting SF3B1-THOC5 interactions. Journal of biochemistry 2 39259498
2019 Polymorphism of the THOC5 of the transcription/export multiprotein complex and its correlation with the lipid and metabolic profile in middle-aged women. Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology 2 31402763
2025 Elevated THOC5 expression in liver cancer and its implications for tumor progression and therapeutic response. Frontiers in medicine 1 40901498
2025 Long non-coding RNA HMGCR suppresses vascular remodeling in streptozotocin-induced type 1 diabetic rats via interaction with THOC5. European journal of medical research 1 41024185
2022 THOC5 regulates human osteoclastogenesis. European journal of cell biology 1 35688054
2025 Targeting mRNA export complex macromolecules THO subunits (Thoc2 and Thoc5) for somatic cell reprograming. International journal of biological macromolecules 0 40107550

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