| 2011 |
STAU1-binding sites on target mRNAs can be formed by imperfect base-pairing between an Alu element in the 3' UTR of an SMD target mRNA and a complementary Alu element in a cytoplasmic polyadenylated lncRNA (named 1/2-sbsRNA), thereby transactivating STAU1-mediated mRNA decay (SMD) in trans. |
RNA co-immunoprecipitation, reporter assays, siRNA knockdown, identification of Alu-element base-pairing between lncRNAs and target 3' UTRs |
Nature |
High |
21307942
|
| 2013 |
STAU1 binding to inverted repeat Alu elements (IRAlus) in the 3' UTR of mRNAs inhibits nuclear retention, augmenting nuclear export of IRAlus-containing mRNAs, and also precludes PKR binding to those dsRNA structures, thereby preventing PKR-mediated eIF2α phosphorylation and global translational repression. |
siRNA knockdown, nuclear/cytoplasmic fractionation, reporter assays, co-immunoprecipitation, eIF2α phosphorylation assays |
Genes & development |
High |
23824540
|
| 2012 |
TDP-43 physically associates with FMRP and STAU1 to form a functional complex that binds the 3' UTR of SIRT1 mRNA (demonstrated by RIP and RNA pulldown), stabilizing SIRT1 mRNA; knockdown of any one of the three proteins reduces SIRT1 mRNA and protein and sensitizes cells to apoptosis. |
Co-immunoprecipitation, RNA immunoprecipitation (RIP), RNA pulldown, siRNA knockdown, microarray |
The Journal of biological chemistry |
Medium |
22584570
|
| 2008 |
Stau1 negatively regulates myogenic differentiation in C2C12 myoblasts; Stau1 knockdown increases myogenin mRNA and protein levels and promotes spontaneous myogenesis, through a mechanism independent of its co-factor Upf1 (Upf1 knockdown did not affect myogenesis). |
siRNA knockdown in C2C12 cells, RT-PCR, western blot, myogenin promoter reporter assay, immunofluorescence |
Genes to cells |
Medium |
18422603
|
| 2011 |
Stau1 binds the 3' UTR of Dvl2 mRNA and stabilizes it in undifferentiated C2C12 myoblasts; Stau1 knockdown shortens the half-life of Dvl2 3' UTR-containing reporter mRNA, and association of Stau1 with Dvl2 3' UTR decreases upon induction of myogenic differentiation, correlating with reduced Dvl2 mRNA levels. |
RNA immunoprecipitation, mRNA half-life assay (reporter with Dvl2 3' UTR), siRNA knockdown, RT-PCR, western blot |
Biochemical and biophysical research communications |
Medium |
22166206
|
| 2018 |
STAU1 directly binds IBDV genomic double-stranded RNA via its N-terminal moiety (residues 1–468); this binding decreases MDA5 association with viral dsRNA in vitro, attenuating MDA5-dependent IFN-β induction and promoting IBDV replication. A binding-deficient mutant (residues 469–702) failed to suppress IFN-β promoter activity. |
In vitro binding assay, co-immunoprecipitation, IFN-β promoter reporter assay, siRNA knockdown, overexpression of deletion mutants |
FASEB journal |
Medium |
29979632
|
| 2022 |
STAU1 protein levels are downregulated during mitosis by the E3 ubiquitin ligase APC/C; the degradation determinant was mapped to a short FPL-motif (F39PxPxxLxxxxL50) by alanine scanning, and mutation of this motif prevents APC/C-mediated STAU1 degradation. Additionally, TRIM25 (an E3 ubiquitin ligase) was identified by proximity labeling as responsible for degrading STAU1 and MAP4K1 in a FPL-motif-dependent manner. |
Alanine scanning mutagenesis, cycloheximide chase, proximity labeling (BioID), proteasome inhibitor assays, mass spectrometry |
International journal of molecular sciences |
Medium |
36232890
|
| 2022 |
Phosphomimicry at STAU1 serine 20 (S20D mutation) impairs STAU1-mediated translational regulation and mRNA decay, triggers apoptosis in cancer cells, and alters proliferation; even the isolated N-terminal 88-amino-acid fragment (RBD2S20D, lacking RNA-binding activity) induces apoptosis by acting in trans on endogenous STAU1 posttranscriptional functions. |
Site-directed mutagenesis (S20D phosphomimetic), overexpression in cancer cell lines, apoptosis assays, polysome profiling, mRNA stability assays |
International journal of molecular sciences |
Medium |
35806349
|
| 2024 |
Endogenous STAU1 forms dynamic cytoplasmic condensates; these condensates recruit MTOR mRNA at its 5' UTR and promote mTOR translation both in vitro and in vivo. Excessive STAU1 condensate formation leads to mTOR hyperactivation and autophagy-lysosome dysfunction, and interference with condensate formation normalizes mTOR levels and restores autophagic flux. |
Live-cell imaging of condensates, in vitro translation assay, in vivo mouse models, STAU1 overexpression/knockdown, autophagy flux assays, mTOR pathway western blot |
The Journal of cell biology |
High |
38913026
|
| 2023 |
STAU1 overexpression in HEK293 cells increases mTOR translation by directly interacting with the MTOR mRNA 5' UTR, activating downstream mTOR targets and impairing autophagic flux; reducing STAU1 in ALS mouse models normalizes mTOR activity and autophagy-related marker proteins. |
STAU1 overexpression/knockdown, mTOR 5' UTR binding assay, western blot for mTOR pathway components, mouse model intervention |
Autophagy |
Medium |
36652469
|
| 2022 |
STAU1 indirectly binds the HBV core promoter (CP) via TARDBP (TDP-43) and recruits the SAGA transcriptional coactivator complex to upregulate CP activity; STAU1 also binds HBx protein and stabilizes it in a ubiquitin-independent manner. |
TurboID-based proximity labeling, co-immunoprecipitation, ChIP, reporter assays, siRNA knockdown |
iScience |
Medium |
35663023
|
| 2021 |
STAU1 silencing in alveolar rhabdomyosarcoma (ARMS) cells reduces autophagy by destabilizing BECN1 and ATG16L1 mRNAs, and indirectly inhibits JNK signaling via increased DUSP8 expression; pharmacological JNK activation or DUSP8 silencing restores autophagy in STAU1-depleted ARMS cells. In contrast, in non-transformed skeletal muscle cells, STAU1 downregulation activates autophagy in an mTOR-dependent manner. |
siRNA knockdown, mRNA stability assay, western blot, JNK pathway pharmacological rescue, STAU1-transgenic mouse skeletal muscle analysis |
Cellular oncology |
Medium |
33899158
|
| 2024 |
STAU1 stabilizes BACE1 mRNA by binding to its 3' UTR, extending BACE1 mRNA half-life; STAU1 also enhances GADD45B expression, activating P38 MAPK signaling to promote Tau phosphorylation at Ser396 and Thr181, thereby promoting both amyloidogenesis and tauopathy. |
STAU1 knockdown/overexpression, mRNA half-life assay, RIP for 3' UTR binding, transcriptome analysis, western blot for P38 MAPK pathway |
Experimental neurology |
Medium |
38729552
|
| 2024 |
GIGYF2 upregulates STAU1, which then stabilizes PTEN mRNA by binding to its 3' UTR, leading to PI3K/AKT pathway inactivation and hepatic insulin resistance; STAU1 silencing prevents GIGYF2-induced PTEN upregulation and restores AKT signaling. |
RNA immunoprecipitation (RIP), siRNA knockdown, overexpression, western blot, in vivo high-fat diet mouse model |
Molecular medicine |
Medium |
39138413
|
| 2023 |
STAU1 regulates alternative splicing of Pparγ2 pre-mRNA in 3T3-L1 adipocytes, specifically affecting the splicing of exon E1, as demonstrated by RIP and PAR-CLIP showing STAU1 binding to Pparγ2 pre-mRNA; knockdown/overexpression of STAU1 alters adipocyte differentiation and lipid metabolism gene splicing patterns. |
RNA immunoprecipitation (RIP), PAR-CLIP, sucrose density gradient centrifugation, RNA-seq for alternative splicing, siRNA knockdown |
Biochimica et biophysica acta. Molecular and cell biology of lipids |
Medium |
36871938
|
| 2025 |
DDX50 monomers (formed upon glucose binding) bind STAU1 and redirect it from an RNA-decay-promoting complex with UPF1 to a DDX50-STAU1 ribonucleoprotein complex that stabilizes pro-differentiation mRNAs including JUN, OVOL1, CEBPB, PRDM1, and TINCR, reversing STAU1's canonical SMD role. |
Co-immunoprecipitation, RNA pulldown, CLIP-seq, mRNA stability assays, genetic knockdown, in vitro reconstitution of DDX50-STAU1 complex |
Cell reports |
Medium |
39764852
|
| 2025 |
tRF-3019A competitively binds STAU1 protein, displacing BECN1 mRNA from STAU1, thereby enhancing BECN1 mRNA stability and expression, which promotes autophagy and malignant progression in colon cancer. |
RNA pulldown, RNA immunoprecipitation (RIP), western blot, GFP-LC3B autophagy assay, xenograft tumor model |
Cellular signalling |
Low |
40268078
|
| 2025 |
STAU1 reduction inhibits p53-mediated apoptosis and DNA damage responses in multiple cell types (iPSC-derived neurons, mouse cortical neurons, SH-SY5Y cells, fibroblasts); in C9orf72-expanded patient fibroblasts and mouse ALS models with baseline STAU1 overabundance, STAU1 reduction prevents p53-driven pro-apoptotic signaling. |
RNAi knockdown, transcriptomic analysis, apoptosis assays (Nutlin-3 and etoposide treatment), p53 pathway western blot, patient-derived fibroblasts, C9orf72 mouse model |
Cell death & disease |
Medium |
41145462
|
| 2026 |
STAU1 directly binds the 3' UTR of ITGB5 mRNA to stabilize it; ITGB5 upregulation increases FOXP3 phosphorylation at serine 418, which activates FOXP3 binding to the STAU1 promoter, creating a STAU1-ITGB5-FOXP3 positive feedback loop driving CRC metastasis. |
RIP, RNA stability assay, ChIP, siRNA knockdown, overexpression, in vitro and in vivo metastasis assays |
Cancer letters |
Low |
41796846
|
| 2026 |
STAU1 binds the 3' UTR of Ucp1 mRNA and promotes its degradation via SMD; adipose-specific STAU1 deletion upregulates UCP1 protein and enhances thermogenesis in mice. The β3 adrenergic receptor/cAMP-PKA pathway modulates STAU1 activity, with cAMP-PKA inhibition downregulating STAU1. |
RIP for 3' UTR binding, adipose-specific Stau1 knockout mice, metabolic phenotyping, western blot, pharmacological pathway manipulation |
Metabolism: clinical and experimental |
Medium |
42242623
|
| 2026 |
An Alu element in lnc-APUE base-pairs with the Alu element in the 3' UTR of CDH1 mRNA, triggering CDH1 mRNA decay via the STAU1-UPF1 (SMD) pathway; silencing STAU1 or UPF1 abrogates lnc-APUE-mediated CDH1 decay and tumor metastasis promotion. |
siRNA knockdown of STAU1/UPF1, Alu element deletion/mutation reporter assays, xenograft mouse model, RIP |
Advanced science |
Medium |
41632098
|