| 1994 |
NF90 (90-kDa subunit) and NF45 (45-kDa subunit) together constitute the NF-AT transcription factor complex that binds the antigen receptor response element in the IL-2 promoter; immunofluorescence demonstrated both proteins are nuclear in Jurkat T-cells, and the complex's DNA-binding activity is enhanced by T-cell stimulation but blocked by cyclosporin A or FK506. |
Protein purification, cDNA cloning, polyhistidine-tag affinity purification, immunofluorescence microscopy, electrophoretic mobility shift assay (EMSA) |
The Journal of biological chemistry |
High |
7519613
|
| 1998 |
NF90 and NF45 physically interact with DNA-PK (DNA-PKcs and Ku subunits), stabilize the DNA-PKcs–Ku–DNA complex, and are substrates for DNA-PK phosphorylation in vitro; recombinant NF90 promotes DNA-PKcs–Ku–DNA complex formation, and antibodies to NF90 or NF45 immunoprecipitate DNA-PKcs. |
EMSA, amino-terminal sequence analysis, immunoblotting, in vitro kinase assay, immunoprecipitation |
The Journal of biological chemistry |
High |
9442054
|
| 2000 |
TCP80/NF90 binds the coding region of glucocerebrosidase (GCase) mRNA and inhibits its translation by reducing polysome association, an activity reconstituted in insect Sf9 cells that lack endogenous NF90. |
Baculovirus/Sf9 insect cell reconstitution, in vitro translation assay, polysome sedimentation, RNA binding assay |
Molecular genetics and metabolism |
High |
10873392
|
| 2001 |
NFAR-1 (NF90, 90 kDa) and NFAR-2 (NF110, 110 kDa), derived from the same gene by alternative splicing, are phosphorylated by PKR, reciprocally co-immunoprecipitate with PKR, colocalize with PKR in the nucleus, associate with both pre-mRNAs and spliced mRNAs, and interact with RNA-processing factors FUS and SMN via their C-termini. |
Reciprocal co-immunoprecipitation, subcellular colocalization, in vitro phosphorylation assay, transfection-based gene expression assays |
The Journal of biological chemistry |
High |
11438536
|
| 2002 |
NF90 binds the AU-rich element-containing 3'UTR of IL-2 mRNA, slows its degradation, and nuclear export of NF90 to the cytoplasm upon T-cell activation is required for IL-2 mRNA stabilization. |
RNA–protein binding assay, mRNA half-life measurement, subcellular fractionation, T-cell stimulation assays |
Molecular cell |
High |
12504009
|
| 2003 |
ILF3 preferentially binds minihelix-motif RNAs (e.g., adenovirus VA1 RNA) and assembles a quaternary export complex with exportin-5, RanGTP, and the RNA; this complex mediates co-transport of VA1 RNA and ILF3 from nucleus to cytoplasm, identifying exportin-5 as the export receptor for ILF3. |
Gel retardation assay, GST pulldown, microinjection in HeLa cell nuclei, transfection experiments |
The Journal of biological chemistry |
High |
14570900
|
| 2003 |
NFAR proteins (NF90/NF110 group) are recruited by the BVDV replication machinery through specific binding to both 5' and 3' non-translated regions of the viral RNA; mutation of the NF90 interaction sites in the 3'NTR yields replication-deficient RNA, and RNAi depletion of RNA helicase A (an NFAR group member) inhibits replication. |
RNA–protein binding assay, viral RNA mutagenesis, RNAi knockdown, viral replication assay |
The EMBO journal |
High |
14592965
|
| 2003 |
Cell-cycle-dependent nucleocytoplasmic shuttling of TCP110/ILF3 is directed by a C-terminal nuclear localization signal; TCP80 (NF90) remains stable in the cytoplasm (t½ ~5 days), whereas TCP110/ILF3 translocates between cytoplasm and nucleus during the cell cycle. |
Subcellular fractionation, 5'RACE cDNA cloning, metabolic turnover assay, immunofluorescence |
Molecular genetics and metabolism |
Medium |
14654356
|
| 2004 |
Ilf3 and NF90 directly bind the axonal targeting element (stem-loop in the 3'UTR) of Tau mRNA via their double-stranded RNA-binding motifs; both proteins are detected in neuronal nuclei, cell bodies, and proximal neuritic segments, consistent with a role in Tau mRNA translocation. |
Northwestern blotting, specific antibodies, immunolocalization |
FASEB journal |
Medium |
15364895
|
| 2005 |
NF90 knockout mice die perinatally from neuromuscular respiratory failure with skeletal muscle disorganization, decreased myofiber number, and severely reduced expression of MyoD, myogenin, and p21WAF1/CIP1; Northwestern blotting identified NF90 as the principal RNA-binding protein for the p21 and MyoD 3'UTRs in developing muscle, establishing a direct post-transcriptional role in muscle differentiation. |
Gene knockout (NF90−/− mice), Northwestern blotting, histology, immunohistochemistry |
The Journal of biological chemistry |
High |
15746098
|
| 2007 |
NF90 and NF45 together with Ku80 and Ku70 bind specifically to the IL-2 ARRE/NF-AT DNA sequence in vivo; T-cell activation induces binding of Ku80 and NF90 but decreases Ku70 binding at the IL-2 promoter, and these dynamic changes are blocked by cyclosporin A and triptolide. |
Chromatin immunoprecipitation (ChIP), EMSA with monoclonal antibody inhibition, purification from activated Jurkat nuclei |
Nucleic acids research |
High |
17389650
|
| 2007 |
NF90ctv (C-terminal variant of NF90) binds the HIV-1 TAR RNA with high affinity, competes with Tat for TAR binding in vitro, inhibits Tat-transactivation of the HIV-1 LTR in vivo, and is associated with histone H3K4/K9 methylation changes consistent with transcriptional repression. |
TAR RNA affinity fractionation, Northwestern blotting, EMSA, luciferase transactivation assay, chromatin histone methylation analysis |
Retrovirology |
Medium |
17565699
|
| 2008 |
AKT phosphorylates NF90 at Ser647 in response to CD28 costimulation; this phosphorylation is necessary and sufficient for nuclear export of NF90 and subsequent IL-2 mRNA stabilization, as a Ser647→Ala mutation abolishes both nuclear export and mRNA stabilization. |
In vitro kinase assay, phospho-specific antibody, site-directed mutagenesis, nuclear export assay, mRNA stability assay, T-cell stimulation |
Journal of immunology |
High |
18097023
|
| 2008 |
NF90 and NF45 form heterodimeric core complexes (NF90-NF45 and NF110-NF45); depletion of NF45 dramatically decreases NF90/NF110 protein levels (posttranscriptional destabilization), and depletion of NF90 (but not NF110) greatly reduces NF45; depletion of the NF90-NF45 complex retards cell growth by inhibiting DNA synthesis and causes giant multinucleated cells, revealing a specific role in cell division. |
RNA interference (RNAi) knockdown, flow cytometry, immunoblot, cell growth assay, time-lapse microscopy |
Molecular and cellular biology |
High |
18458058
|
| 2008 |
NF90 and HuR bind the AU-rich 3'UTR of MKP-1 mRNA; H2O2 treatment increases association of MKP-1 mRNA with HuR and NF90 and decreases association with translational repressors TIAR and TIA-1; silencing NF90 or HuR diminishes H2O2-stimulated MKP-1 mRNA stability, and HuR silencing also reduces MKP-1 translation. |
Ribonucleoprotein immunoprecipitation (RIP), biotinylated RNA pulldown, mRNA stability assay, siRNA knockdown |
Molecular and cellular biology |
High |
18490444
|
| 2008 |
NFAR-1 and NFAR-2 retain cellular transcripts in intranuclear foci and regulate mRNA export; loss of NFAR function (embryonic lethal) increases protein synthesis rates; NFAR-depleted murine fibroblasts are dramatically susceptible to VSV replication, demonstrating an innate immune translational surveillance function. |
NFAR knockout (embryonic lethal), RNA export assay, polysome/translation rate measurement, VSV infection assay in NFAR-depleted cells |
Proceedings of the National Academy of Sciences |
High |
18337511
|
| 2009 |
The NF90-NF45 complex functions as a negative regulator of miRNA biogenesis: overexpression inhibits pri-miRNA processing to pre-miRNA, causing pri-miRNA accumulation; the complex binds pri-miRNAs (e.g., pri-let-7a) but does not interact with the Microprocessor, suggesting it blocks Microprocessor access; depletion of NF90 reduces pri-let-7a and increases mature let-7a. |
Overexpression and RNAi knockdown, pri-miRNA/pre-miRNA/mature miRNA quantification, RNA polymerase II inhibitor experiments, RNA immunoprecipitation |
Molecular and cellular biology |
High |
19398578
|
| 2009 |
NF90 binds an AU-rich 25–30 nucleotide RNA motif in the 3'UTR of target mRNAs and represses their translation without significantly affecting mRNA stability; insertion of this NF90 motif into an EGFP reporter 3'UTR specifically confers NF90-dependent translational repression as shown by polysome gradient analysis. |
RIP-seq, biotinylated transcript pulldown, polysome gradient analysis, EGFP reporter assay, siRNA knockdown |
Nucleic acids research |
High |
19850717
|
| 2010 |
PKCβI phosphorylates NF90 at Ser647 in response to PMA stimulation, triggering nuclear export of NF90 and stabilization of IL-2 mRNA; Ser647→Ala mutation abolishes PMA-induced nuclear export and IL-2 mRNA stabilization. |
In vitro kinase assay with PKCβI, phospho-specific antibody, site-directed mutagenesis, nuclear export assay, mRNA stability assay |
Journal of immunology |
High |
20870937
|
| 2010 |
NF45 and NF90 bind the HS4 element of the IL-13 promoter in T cells and are required for HS4-dependent IL-13 transcriptional activation; the CTGTT binding motif within HS4-3' is critical, and HS4 activity is abrogated in NF45+/− primary Th2 cells and reduced in NF90+/− cells. |
DNA affinity chromatography coupled with tandem mass spectrometry, ChIP, EMSA, reporter transfection in primary Th2 cells from NF45+/− and NF90+/− mice |
The Journal of biological chemistry |
High |
20051514
|
| 2011 |
The NF90-NF45 complex is required for DNA double-strand break repair by nonhomologous end joining (NHEJ): immunodepletion of NF90/NF45 reduces in vitro NHEJ activity comparably to DNA-PKcs depletion; NF90/NF45-depleted cells accumulate γ-H2A.X foci and are hypersensitive to ionizing radiation. |
In vitro NHEJ assay with immunodepletion, γ-H2A.X foci quantification, ionizing radiation sensitivity assay, time-lapse microscopy, RNAi knockdown |
Molecular and cellular biology |
High |
21969602
|
| 2011 |
NF90 binds the dengue virus 3' stem-loop RNA via affinity chromatography; NF90 depletion by siRNA reduces dengue RNA levels and infectious virus production by 50–70%; cytoplasmic relocalization of NF90 occurs in dengue-infected cells. |
RNA affinity column chromatography, siRNA knockdown, viral RNA quantification, infectious virus titration, immunofluorescence |
PloS one |
High |
21386893
|
| 2012 |
NF45 dimerizes with NF90 (and related proteins SPNR and Zfr) through the DZF domain, which has structural similarity to the template-free nucleotidyltransferase family but lacks catalytic residues; crystal structure at 1.9-Å resolution reveals the dimerization interface, confirmed by co-immunoprecipitation with site-specific mutants. |
X-ray crystallography (1.9 Å), co-immunoprecipitation with site-directed mutants |
Nucleic acids research |
High |
22833610
|
| 2012 |
YM155 directly binds ILF3 and disrupts the ILF3/p54(nrb) complex, causing different subcellular localization of ILF3 and p54(nrb), which results in suppression of survivin promoter activity. |
Small-molecule binding assay, co-immunoprecipitation, subcellular localization analysis, survivin promoter activity assay |
Biochemical and biophysical research communications |
Medium |
22842455
|
| 2012 |
NF90 coordinately represses translation (not stability) of multiple SASP factor mRNAs (MCP-1, GROα, IL-6, IL-8) in proliferating fibroblasts; NF90 levels decline in senescent cells, allowing SASP factor expression to rise. |
RIP, siRNA knockdown, ELISA for secreted proteins, mRNA stability assay, immunoblot |
Aging |
Medium |
23117626
|
| 2012 |
Depletion of NF90/NF45 in HPV-transformed cervical carcinoma cells restores p53 protein (post-transcriptionally, not at mRNA level) and p21 (via p53-dependent transcription); NF90 knockdown attenuates HPV E6 RNA levels and inhibits transcription from the HPV early promoter, revealing that NF90/NF45 supports viral E6 expression. |
siRNA knockdown, RT-PCR, immunoblot, PARP cleavage assay, camptothecin sensitivity assay |
Oncogene |
High |
23208500
|
| 2014 |
NF90 binds the 5'-terminal double-stranded region of the HCV genome; siRNA depletion of NF90 significantly impairs HCV RNA replication and reduces infectious virus yields; NF90 co-immunoprecipitates with NS5A in an RNA-dependent manner and co-fractionates with detergent-resistant membranes containing viral replication complexes. |
Biotinylated RNA pulldown with mass spectrometry, siRNA knockdown, viral RNA quantification, co-immunoprecipitation, detergent-resistant membrane fractionation |
Journal of virology |
High |
24719423
|
| 2014 |
NF90 interacts with PKR through its C-terminal domain independently of NF90 RNA-binding properties; NF90 knockdown reduces PKR phosphorylation in response to dsRNA/influenza infection; NF90 is a component of stress granules, and NF90 depletion reduces dsRNA-induced stress granule formation; an NS1 mutant influenza virus specifically attenuated in PKR inhibition replicates indistinguishably from WT in NF90-depleted cells, placing NF90 in the PKR–stress granule antiviral pathway. |
Co-immunoprecipitation, C-terminal domain mapping, siRNA knockdown, PKR phosphorylation assay, stress granule immunofluorescence, viral replication assay with NS1 mutant |
Journal of immunology |
High |
24623135
|
| 2014 |
NF90 binds the 3'UTR of cyclin E1 mRNA in vitro and in vivo (RIP), stabilizing it; NF90 knockdown decreases cyclin E1 mRNA half-life, delays G1/S transition, and inhibits HCC tumor growth in xenografts; ectopic NF90 expression rescues cyclin E1 mRNA stability. |
RIP, 3'UTR binding assay, mRNA half-life measurement (actinomycin D chase), siRNA knockdown, xenograft tumor assay, flow cytometry |
Oncogene |
High |
25399696
|
| 2015 |
The NF45/NF90 heterodimer associates with pre-60S ribosomal particles via NF90's double-stranded RNA-binding domains (identified by tandem affinity purification); depletion of NF45 and NF90 causes a 60S biogenesis defect, altered nucleolar morphology (spherical nucleoli), and a p53/p21 stress response suppressible by RPL11 depletion. |
Tandem affinity purification, density gradient sedimentation, RNAi knockdown, nucleolar morphology imaging, immunoblot, rRNA processing analysis |
Molecular and cellular biology |
High |
26240280
|
| 2015 |
Cold-inducible RBM3 inhibits PERK phosphorylation through cooperation with NF90; NF90 is a novel interacting protein of PERK (identified by affinity purification coupled with mass spectrometry, confirmed by co-IP and proximity ligation assay), and this NF90–PERK interaction is RNA-dependent and required for RBM3-mediated inhibition of the PERK–eIF2α–CHOP ER stress pathway. |
Affinity purification with mass spectrometry, co-immunoprecipitation, proximity ligation assay, RBM3 knockout mouse organotypic cultures, siRNA knockdown, PERK phosphorylation assay |
FASEB journal |
High |
26472337
|
| 2011 |
Alternatively spliced exon 3 of Ilf3/NF90 encodes a 13-amino-acid N-terminal motif that acts as a nucleolar localization signal; four arginines are essential for nucleolar targeting and three histidines stabilize proteins in the nucleolus; the long isoforms (L-Ilf3 and L-NF90) localize to the granular component of the nucleolus and exchange rapidly between nucleoli (FRAP); posttranslational modifications abrogate nucleolar targeting of L-Ilf3. |
Subcellular fractionation, confocal microscopy, FRAP, deletion and substitution mutagenesis, recombinant protein expression |
PloS one |
High |
21811582
|
| 2015 |
The NF45-NF90 and NF45-NF110 complexes act as direct transcriptional coactivators of the c-fos gene in a defined in vitro transcription system; their coactivator activity requires both the upstream enhancer and core promoter regions but not their dsRNA-binding activities; they cooperate with PC4 and Mediator and interact with activators and general transcription machinery; ChIP shows dynamic occupancy on the c-fos gene. |
In vitro transcription reconstitution, ChIP, RNAi knockdown, domain mutagenesis (dsRBM-inactive mutant), protein–protein interaction assays |
The Journal of biological chemistry |
High |
26381409
|
| 2016 |
NF90/NF110 occupies ~9,081 genomic sites in K562 cells, predominantly at active promoters and strong enhancers co-localizing with POLR2A, MYC, and YY1; NF90/NF110 knockdown activates proliferative transcription factors (EGR1, MYC) and suppresses erythroid differentiation (KLF1), establishing NF90/NF110 as a chromatin-associated transcriptional regulator. |
ChIP-seq, RNA-seq after shRNA knockdown, comparison with 150 ENCODE ChIP-seq datasets |
PloS one |
High |
29590119
|
| 2016 |
NF90-NF45 complex binds pri-miR-7-1 in vitro and inhibits its processing to mature miR-7; NF90/NF45 depletion elevates mature miR-7, reducing EGFR levels and AKT phosphorylation in HCC cells. |
miRNA microarray, qRT-PCR, in vitro RNA binding assay, overexpression and siRNA knockdown, immunoblot |
The Journal of biological chemistry |
High |
27519414
|
| 2016 |
NF90 is a novel interacting protein of IAV nonstructural protein NS1 (interaction dependent on NS1 RNA-binding properties); NS1 simultaneously associates with NF90 and PKR but restricts NF90–PKR interaction; NF90 coexpression antagonizes NS1-mediated inhibition of PKR phosphorylation and stress granule formation. |
Co-immunoprecipitation, domain mapping, PKR phosphorylation assay, stress granule immunofluorescence, siRNA knockdown |
FEBS letters |
Medium |
27423063
|
| 2016 |
Formation of the NF90–NF45 heterodimer substantially improves NF90's RNA-binding capacity, affinity for both single- and double-stranded RNA, and alters its binding mode; NF45 acts as a conformational scaffold that enables cooperative interplay between NF90's RNA-binding motifs. |
Biophysical binding assays (ITC/SPR), biochemical RNA-binding assays with purified recombinant proteins, thermodynamic stability measurements |
The Biochemical journal |
High |
28062840
|
| 2017 |
NF90/NF110 promote circRNA biogenesis in the nucleus by associating with intronic RNA pairs flanking circRNA-forming exons; NF90/NF110 also interact with mature circRNAs in the cytoplasm; upon viral infection, NF90/NF110 translocate to the cytoplasm, reducing circRNA production and becoming available to bind viral mRNAs as part of antiviral response. |
Genome-wide siRNA screen, circRNA expression reporter, RIP, subcellular fractionation, viral infection assay, fluorescence imaging |
Molecular cell |
High |
28625552
|
| 2017 |
NF90-NF45 acts as a selective RNA chaperone: NF90 alone has RNA annealing and strand displacement activity via a 'matchmaking' plus charge-compensation mechanism; NF45 binding enhances matchmaking efficiency and substantially increases RNA chaperone activity; this activity stimulates the first step of HCV RNA replication in vitro and stabilizes regulatory structures in VEGF mRNA. |
In vitro RNA annealing and strand displacement assays, HCV RNA replication in vitro assay, RNA structure probing, biochemical binding assays with purified recombinant NF90 and NF90-NF45 |
Nucleic acids research |
High |
29040738
|
| 2018 |
NF90/NF110 controls DICER expression by inhibiting processing of miR-3173 embedded in DICER pre-mRNA; miR-3173 in turn targets NF90, establishing a feedback amplification loop; NF90 overexpression in a nude mouse model reduces ovarian cancer proliferation, tumor size, and metastasis. |
miRNA processing assay, NF90 overexpression/knockdown, xenograft mouse model, miR-3173 reporter and functional assays |
Cell research |
High |
29563539
|
| 2018 |
NF90 (ILF3) selectively suppresses translation of wild-type BAFF mRNA (but not the disease-associated BAFF-var mRNA lacking the NF90-binding 3'UTR region) by recruiting miR-15a to the BAFF-WT 3'UTR; this reveals a paradigm in which a UTR polymorphism prevents NF90-mediated miRNA recruitment and raises BAFF protein levels. |
RNA immunoprecipitation, reporter assays, miRNA pulldown/recruitment assay, translation measurement |
Nucleic acids research |
Medium |
30272251
|
| 2019 |
ILF3 is a substrate of the E3 ligase SPOP: EGF-MEK-ERK signaling phosphorylates ILF3, which prevents SPOP-mediated poly-ubiquitination and proteasomal degradation of ILF3; stabilized ILF3 then directly binds and stabilizes SGOC pathway gene mRNAs, promoting serine biosynthesis and colorectal cancer growth. |
Co-immunoprecipitation, ubiquitination assay, phosphorylation assay, mRNA stability assay, RIP, patient-derived xenograft tumor model |
Cell research |
High |
31772275
|
| 2019 |
SRSF3 regulates alternative splicing of ILF3 by binding RNA sequence motifs to control exon 18 inclusion/exclusion or alternative 3' splice site selection, generating ILF3 isoforms 1 and 2 (pro-proliferative) versus isoforms 5 and 7 (anti-proliferative); isoform-7 induces apoptosis. |
Alternative splicing reporter assay, minigene splicing assay, siRNA knockdown of SRSF3, cancer cell proliferation and transformation assays |
RNA |
High |
30796096
|
| 2019 |
ILF3 binds the SINEUP lncRNA AS Uchl1 through its RNA-binding motif 2 (RBM2) interacting with the embedded inverted SINE B2 (invSINEB2) element; ILF3 also binds a free Alu monomer sequence and transcriptome-wide SINE sequences; the invSINEB2 element moderately influences AS Uchl1 nuclear localization in an ILF3-dependent manner. |
RNA-interacting domainome technology, RNA pulldown, CLIP/eCLIP bioinformatic analysis, domain mutagenesis (RBM2), subcellular localization assay |
FASEB journal |
Medium |
31570000
|
| 2019 |
NF90 stabilizes PARP1 mRNA through binding to its 3'UTR (identified by RIP-seq and confirmed by 3'UTR assay); NF90 depletion decreases PARP1 mRNA and protein levels and sensitizes cells to PARP inhibitor Olaparib. |
RIP-seq, mRNA stability assay with 3'UTR reporter, siRNA knockdown, drug sensitivity assay |
Biochemical and biophysical research communications |
Medium |
28487110
|
| 2020 |
ILF3 is an essential host factor for efficient translation of IFNB1 and a subset of interferon-stimulated genes under conditions where cap-dependent translation is compromised; polysome profiling combined with next-generation sequencing showed ILF3 is required to establish both dsRNA-induced transcriptional and translational antiviral programs. |
Polysome profiling with next-generation sequencing, siRNA knockdown, IFNB1 reporter and protein assay, dsRNA stimulation |
Nucleic acids research |
High |
31701124
|
| 2020 |
NF90 modulates the processing of a subset (~38) of highly stable, intronic pri-miRNAs: NF90 associates with the stem region of these pri-miRNAs in a manner largely exclusive of Microprocessor; loss of NF90 increases mature miRNA from 22 bound targets; mutations that destabilize pri-miRNA structure reduce NF90 binding as shown by EMSA. |
CLIP-seq/RIP-seq, miRNA microarray, EMSA with RNA structure mutants, NF90 knockdown |
Nucleic acids research |
High |
32427329
|
| 2020 |
ILF3 stabilizes NEAT1 lncRNA through direct interaction; ATF3 transcriptionally represses ILF3 (ChIP assay shows ATF3 binding to ILF3 promoter); the ATF3/ILF3/NEAT1 axis regulates macrophage M2 polarization. |
RIP assay, RNA pulldown, RNA stability assay, ChIP assay, luciferase reporter, siRNA knockdown |
Molecular medicine |
Medium |
38395749
|
| 2021 |
ILF3 is required for mTORC1-dependent amino acid sensing: ILF3 tethers the GATOR complexes to lysosomes; artificially targeting GATOR2 component WDR24 to lysosomes bypasses the requirement for ILF3; ILF3's role is evolutionarily conserved in human cells, mouse cells, and C. elegans. |
Genome-wide CRISPR/Cas9 screen (FACS-based pS6 assay), lysosome-targeting rescue experiment, epistasis analysis with GATOR complexes, cross-species conservation studies |
Nature cell biology |
High |
37037994
|
| 2021 |
Tim-3 promotes ubiquitination and proteasomal degradation of NF90 via recruitment of E3 ubiquitin ligase TRIM47, which targets the zinc finger domain of NF90 at Lys297 via K48-linked ubiquitination; Tim-3 inactivation enhances NF90-dependent stress granule formation (increased PKR phosphorylation, eIF2α phosphorylation, G3BP1, and TIA-1) and protects mice from VSV challenge. |
Co-immunoprecipitation, ubiquitination assay (K48-linked), site-specific mutagenesis (Lys297), Tim-3 genetic inactivation, VSV infection mouse model, stress granule immunofluorescence |
eLife |
High |
34110282
|
| 2021 |
Macrophage ILF3 increases NF-κB activity by hastening p105 mRNA decay and represses anti-inflammatory Nrf2 signaling by facilitating ILF3/eIF4A1 complex-mediated enhancement of Keap1 translational efficiency, promoting abdominal aortic aneurysm progression. |
Multi-omics analysis, macrophage-specific transgenic and KO mice, mRNA stability assay (p105), translation efficiency assay (Keap1), co-immunoprecipitation (ILF3/eIF4A1), multiplex immunohistochemistry |
Nature communications |
High |
39179537
|
| 2021 |
ILF3 regulates ILF3 mRNA stability: ILF3 directly binds ILF3-AS1 and increases its transcript stability; HNRNPA2B1 recognizes m6A sites on ILF3 mRNA and enhances its stability, which in turn promotes AKT3 expression. |
m6A site mapping, RIP, mRNA stability assay, siRNA knockdown, immunohistochemistry |
Journal of hematology & oncology |
Medium |
33794982
|
| 2021 |
ILF3 (NF90/NF110) suppresses dendritic cell maturation and innate immune responses through a nuclear localization sequence-dependent mechanism, not through its dsRNA-binding domains; the DZF domain of NF110 isoform is additionally required; ILF3 regulates genes associated with cholesterol homeostasis alongside DC maturation genes. |
SiRNA depletion and overexpression in human monocyte-derived DCs, NLS and DZF domain mutagenesis, flow cytometry for DC maturation markers, RNA-seq |
Journal of immunology |
High |
34031149
|
| 2021 |
circACTA2 competes with CDK4 mRNA for binding to ILF3 (both shown by oligo pulldown and RIP); Ang II increases circACTA2 expression, facilitating its association with ILF3, thereby reducing ILF3-CDK4 mRNA interaction, decreasing CDK4 mRNA stability and protein levels, and promoting VSMC senescence. |
Oligo pulldown, RNA immunoprecipitation (RIP), mRNA stability assay, siRNA knockdown of circACTA2, cellular senescence assay (SA β-gal, p21/CDK4 levels) |
Aging |
Medium |
33885378
|
| 2023 |
circSLC38A1 interacts with ILF3 (RNA pulldown, mass spectrometry, RIP) and stabilizes ILF3 protein by modulating its ubiquitination; the circSLC38A1–ILF3 complex drives transcription of TGF-β2, promoting bladder cancer invasion and metastasis. |
RNA pulldown with mass spectrometry, RIP, ubiquitination assay, CUT&Tag-seq, RNA-seq, in vivo mouse metastasis model |
Cell death & disease |
Medium |
36697384
|
| 2023 |
PRMT1 mediates arginine methylation of ILF3, stabilizing the ILF3 protein; stabilized ILF3 in turn binds and stabilizes IL-8 mRNA, promoting M2 polarization of macrophages and prostate cancer progression. |
Co-immunoprecipitation, GST pulldown, mass spectrometry, RNA pulldown, RIP, in vivo mouse model |
Carcinogenesis |
Medium |
36394342
|
| 2024 |
Lefamulin directly binds the Ala99 site of ILF3 protein and interferes with GCN5/CBP-mediated acetylation of Lys100, disrupting ILF3-mediated transcription of MRPL12 and impairing mitochondrial biogenesis/function; this mechanism underlies lefamulin's ability to overcome sorafenib resistance in HCC. |
Drug–protein binding assay (direct binding to Ala99), site-directed mutagenesis (Lys100), acetylation assay (GCN5/CBP), ChIP/CUT&Tag for MRPL12 transcription, CDX and hydrodynamic mouse models |
Advanced science |
Medium |
38874478
|
| 2020 |
USP11 interacts with NF90 and promotes its deubiquitination, thereby stabilizing NF90 protein levels in HCC cells; the effect of USP11 on HCC cell proliferation and metastasis is dependent on NF90. |
Mass spectrometry, co-immunoprecipitation, ubiquitination assay, siRNA knockdown epistasis, in vivo mouse model |
American journal of cancer research |
Medium |
32509388
|
| 2024 |
Hyperglycemia/AGEs increase vascular smooth muscle cell NF90 activity; NF90 then stabilizes FBXW7 mRNA, and increased FBXW7 promotes ubiquitination and degradation of AGE receptor 1 (AGER1), causing accumulation of AGEs and atherosclerotic calcification; VSMC-specific NF90/110 knockout in male mice decreases AGEs-induced calcification. |
VSMC-specific NF90/110 KO mice, mRNA stability assay (FBXW7), ubiquitination assay (AGER1), multi-omics, immunohistochemistry |
Nature communications |
High |
38862515
|