| 2023 |
FUBP1 is a general splicing factor that binds a novel cis-regulatory motif and stabilizes U2AF2 and SF1 (key 3' splice site components) through multivalent binding interfaces in its disordered regions; it is required for efficient splicing of long introns (representing ~80% of human introns) and interacts with U1 snRNP-associated proteins, suggesting a role in splice site bridging. NMR, structural, and in vivo interaction data, plus transcriptional profiling and kinetic modeling, support this model. |
NMR, crystal structures, in vivo CLIP/interaction data, transcriptional profiling, kinetic modeling, mutagenesis |
Molecular cell |
High |
37506698
|
| 2020 |
Crystal structures of all four KH domains (KH1–4) of FUBP1 show they are highly conserved topologically and each can independently bind the FUSE ssDNA sequence; KH3 shows higher nucleotide-binding potency; differences in amino acid composition at the binding cleft account for diverse nucleotide-sequence preferences among KH1–4; cooperativity of all four KH modules is required for nanomolar-affinity FUSE binding. |
X-ray crystallography, ssDNA-binding characterization (biophysical assays) |
Scientific reports |
High |
32778776
|
| 2014 |
FUBP1 binds discrete cis-regulatory elements within intron 11 of MDM2 pre-mRNA and acts as a positive splicing regulator; blocking FUBP1 function in in vitro splicing reactions decreased splicing efficiency, and FUBP1 knockdown in cells induced formation of the stress-induced MDM2-ALT1 splice variant under normal conditions. |
In vitro splicing assays, RNA binding assays, siRNA knockdown, minigene splicing reporter |
The Journal of biological chemistry |
High |
24798327
|
| 2015 |
FUBP1 promotes constitutive inclusion of DMD exon 39 by binding a functional intronic splicing enhancer (ISE) in intron 38; binding was established by RNA pulldown, RNA EMSA, and RNA-ChIP on endogenous DMD pre-mRNA; serial deletion and mutagenesis of minigenes delineated the functional ISE. |
RNA pulldown, RNA EMSA, RNA-ChIP, minigene deletion/mutagenesis analysis |
Nucleic acids research |
High |
25662218
|
| 2019 |
FUBP1 participates in regulating N6-methyladenosine (m6A) RNA methylation; its loss leads to global changes in RNA splicing and widespread expression of aberrant driver isoforms, as demonstrated by an in vivo CRISPR screen identifying FUBP1 as a long-tail tumor suppressor that cooperates with other tumor suppressor genes to transform mammary epithelial cells. |
In vivo CRISPR screen, RNA splicing profiling, m6A methylation analysis |
Cell reports |
Medium |
31553912
|
| 2025 |
FUBP1 is an Nm (2'-O-methylation) RNA-binding protein: EMSA validated preference of FUBP1 for Nm-modified RNA; FUBP1 predominantly binds intronic regions; Nm sites in chromatin-associated RNA (caRNA) overlap with FUBP1-binding sites; Nm depletion reduced FUBP1 occupancy on modified regions; FUBP1 depletion induced exon skipping in Nm-modified genes, establishing FUBP1 as a mediator of Nm-dependent splicing regulation. |
RNA affinity purification/mass spectrometry, EMSA, caRNA Nm profiling, ChIP-seq/CLIP, siRNA depletion with splicing analysis |
Science advances |
High |
41105785
|
| 2015 |
FUBP1 is essential for fetal and adult hematopoietic stem cell (HSC) self-renewal; conditional functional inactivation in two mouse models caused embryonic lethal anemia (~E15.5) with severely diminished HSCs; FUBP1-deficient HSCs showed intrinsic defects in maintenance and long-term reconstitution, with upregulation of cell-cycle inhibitor p21 and pro-apoptotic Noxa, leading to increased generation time and HSC death tracked by video-microscopy. |
Conditional knockout mouse models (two independent models), transplantation assays, video-microscopy cell tracking, transcriptional analysis |
Cell reports |
High |
26095368
|
| 2018 |
RUNX1 and FUBP1 interact in the same transcriptional regulatory complex in human B-cell precursor lymphoblasts and co-occupy active chromatin at the c-KIT locus, including a novel FUBP1 FUSE-like binding sequence at +30 kb enhancer; FUBP1 and RUNX1 cooperate to upregulate c-KIT expression, promoting cell proliferation and resistance to imatinib. |
Co-immunoprecipitation, ChIP-seq, enhancer characterization, luciferase reporter, functional proliferation assays |
Nucleic acids research |
High |
30500954
|
| 2018 |
FUBP1 is a novel binding partner of adenovirus 5 E1A; FUBP1 binds directly to E1A via its N-terminus (residues 1–82) and conserved region 3 (residues 139–204); FUBP1 depletion reduces virus growth and activates p53-regulated genes; during infection FUBP1 is relocalized within the nucleus, recruited to viral promoters with E1A while lost from the FUSE upstream of c-Myc; FUBP1 suppresses p53 DNA binding, and E1A stabilizes the FUBP1-p53 complex to prevent p53 promoter binding. |
Co-immunoprecipitation, siRNA depletion, ChIP, gene expression analysis, domain mapping |
Journal of virology |
Medium |
29743362
|
| 2017 |
Camptothecin (CPT) and its derivative SN-38 (active irinotecan metabolite) inhibit FUBP1 activity by preventing FUBP1 binding to its single-stranded DNA target FUSE in vitro, and induce deregulation of FUBP1 target genes in HCC cells. |
In vitro DNA binding assay (FUBP1/FUSE interaction), gene expression analysis in HCC cells, drug library screen |
Biochemical pharmacology |
Medium |
29031818
|
| 2016 |
Pyrazolo[1,5a]pyrimidine-based compounds (e.g., compound 6) inhibit FUBP1 binding to its single-stranded DNA target FUSE with IC50 of 11.0 μM in biophysical assays, and reduce expansion and induce death in hepatocellular carcinoma cells. |
Biophysical binding assay (FUBP1-FUSE interaction), cell viability assay, medium-throughput screening |
Bioorganic & medicinal chemistry |
Medium |
27729195
|
| 2021 |
FUBP1 binds the Nrf2 5'UTR in response to H2O2 (identified by LC-MS/MS, Far Western blot, and RNP-IP); FUBP1 undergoes cytosolic redistribution to ribosomal fractions under oxidative stress; FUBP1 gains physical interaction with eIF3η (but not eIF4E, eIF2α, or eIF1) upon H2O2 treatment; FUBP1 promotes 40S ribosomal subunit attachment to Nrf2 mRNA and 43S pre-initiation complex formation, facilitating de novo Nrf2 protein translation under oxidative stress. |
LC-MS/MS, Far Western blot, RNP-immunoprecipitation, ribosome fractionation, siRNA knockdown, co-immunoprecipitation with translation initiation factors |
Redox biology |
Medium |
33676361
|
| 2021 |
FUBP1 promotes colorectal cancer stemness and metastasis by directly binding to the DVL1 promoter to activate DVL1 transcription, thereby activating Wnt/β-catenin signaling and increasing pluripotent transcription factors (c-Myc, NANOG, SOX2); FUBP1 protein stability is regulated by Smurf2-mediated ubiquitin degradation (reduced in KRAS-wild-type CRC) and by caspase-3-dependent cleavage (reduced in KRAS-mutant CRC). |
ChIP, luciferase reporter, co-immunoprecipitation, overexpression/knockdown, in vitro and in vivo tumor assays |
Molecular oncology |
Medium |
34288405
|
| 2019 |
FUBP1 inhibits HIF1α degradation by downregulating VHL (the E3 ligase for HIF1α), resulting in upregulation of LDHB and enhanced glycolysis in neuroblastoma cells; this pro-glycolytic mechanism is independent of N-Myc regulation. |
Luciferase assay, Western blot, ChIP, ELISA for glycolytic metabolites, siRNA knockdown |
Journal of experimental & clinical cancer research : CR |
Medium |
31511046
|
| 2019 |
Fubp1 upregulates mRNA levels of hexokinase genes Hk1 and Hk2, supporting aerobic glycolysis and the lactate-Akt-mTOR survival axis in cells; Fubp1 deficiency reduces Hk1/Hk2 expression. |
qRT-PCR, Western blot, cell survival assays, metabolic assays |
Biochemical and biophysical research communications |
Low |
30871777
|
| 2020 |
FUBP1 protein level is enriched in S phase; FUBP1 deficiency alters cell cycle progression in S phase by downregulating Ccna (cyclin A) mRNA expression; FUBP1 deficiency also confers survival advantages against metabolic stress and anti-cancer drugs. |
Cell cycle synchronization, flow cytometry, qRT-PCR, Western blot, CRISPR/Cas9 KO cells |
Cells |
Low |
32481602
|
| 2019 |
CRISPR/Cas9-mediated Fubp1 silencing disrupts circadian oscillation of Per1 protein; Fubp1 upregulates Syncrip (main post-transcriptional regulator of Per1 protein oscillation) at mRNA and protein levels, establishing a Fubp1-Syncrip-Per1 regulatory axis for circadian clock maintenance. |
CRISPR/Cas9 knockout, qRT-PCR, Western blot, circadian oscillation profiling |
Cell biology international |
Low |
31535751
|
| 2019 |
TAL1 directly activates the FUBP1 promoter in erythroid progenitor cells, requiring an intact GATA sequence in a combined E-box/GATA motif; this TAL1-driven FUBP1 expression is required for efficient erythroid differentiation, as FUBP1-deficient progenitors show limited erythroid differentiation capacity. |
ChIP, promoter reporter assays, FUBP1 knockdown, erythroid differentiation assays |
PloS one |
Medium |
30653565
|
| 2023 |
FUBP1 is required for NR_109 lncRNA-mediated M2-like macrophage polarization; NR_109 competes with JVT-1 (JTV-1) to bind the C-terminus domain of FUBP1, preventing ubiquitin-mediated degradation of FUBP1, thereby stabilizing FUBP1 and enabling c-Myc transcription activation. |
Co-immunoprecipitation, RNA immunoprecipitation, ubiquitination assay, knockdown/overexpression, in vivo tumor models |
Journal for immunotherapy of cancer |
Medium |
37217247
|
| 2021 |
TNPO1 (Transportin-1) mediates nuclear import of FUBP1 through direct interaction; nuclear FUBP1 regulates transcription of the immune checkpoint gene NRP1; knockdown of FUBP1 inhibits cervical cancer cell proliferation and migration. |
Co-immunoprecipitation, nuclear/cytoplasmic fractionation, siRNA knockdown, functional assays |
Journal of immunology research |
Low |
33987449
|
| 2020 |
NORAD lncRNA binds the central domain of FUBP1 through multiple regions and attenuates FUBP1 nuclear localization, impairing FUBP1 occupancy on pro-apoptotic gene promoters and thereby inducing apoptosis in endometrial cancer cells; the NORAD-4 fragment sufficient for FUBP1 binding recapitulated the anti-tumor effects in vivo. |
RNA pulldown, co-immunoprecipitation, subcellular fractionation/localization, ChIP, xenograft model |
Cell death & disease |
Medium |
32555178
|
| 2024 |
FUBP1 directly activates USP29 gene transcription (demonstrated by ChIP and luciferase assay); USP29 in turn interacts with and stabilizes aurora kinase B (AURKB) by suppressing K48-linked polyubiquitination, constituting a FUBP1-USP29-AURKB regulatory axis promoting gastric cancer. |
ChIP, luciferase reporter, Co-IP, ubiquitination assay, mass spectrometry, qRT-PCR, xenograft model |
Cancer cell international |
Medium |
38233848
|
| 2011 |
FUBP1 protein binds the EV71 5'-UTR (an IRES element) as shown by RNA affinity pulldown coupled with LC-MS/MS; kaempferol treatment changes the composition of IRES-associated trans-acting factors including FUBP1, affecting IRES function and EV71 replication. |
RNA affinity pull-down, LC-MS/MS |
Food chemistry |
Low |
25212137
|
| 2025 |
FUBP1 promotes SPA lncRNA expression via two distinct mechanisms: (1) enhancing transcription of SPA-embedded polycistronic transcripts by targeting a FUSE-like sequence upstream of the promoter, and (2) facilitating SPA1 splicing and maturation by binding U-rich intronic sequences; both FUBP1 and MYEF2 are enriched in Prader-Willi syndrome (PWS) bodies. |
ChIP, RNA immunoprecipitation, minigene splicing assays, knockdown with expression analysis, FUSE-like sequence identification |
RNA (New York, N.Y.) |
Medium |
40147944
|
| 2020 |
FUBPs enforce epigenetic setpoints that restrict MYC expression; FUBP1/FUBP2-lacking murine embryonic fibroblasts express MYC at levels otherwise attained only after stimulation and show MYC chromatin changes (altered histone marks), establishing that FUBPs constrain MYC expression through chromatin-level regulation in single primary cells. |
Single-cell MYC expression tracking, chromatin mark profiling (ChIP for histone modifications), FUBP knockout MEFs and B-cells |
Communications biology |
Medium |
33005010
|
| 2025 |
FUBP1 contributes to miR-155-3p expression/maturation from pre-miR-155 in macrophages; FUBP1 may support miR-155-3p for specific subcellular functions, while KSRP inhibits both miR-155-5p and miR-155-3p maturation without altering relative strand expression. |
RNA-binding protein knockdown, miRNA quantification, strand-selective miRNA analysis |
Scientific reports |
Low |
40825800
|