| Expression pattern: |
DN |
| Associated gene: |
STAT3, QKI, FOXP1 pre-mRNA, ubiquitin, Bcl2, Bax, Caspase-3 |
| Associated microRNA: |
- |
| Biological function: |
Alleviates brain injury after cerebral ischemia, attenuates neurological deficits, improves functional recovery, inhibits apoptotic signaling and cell apoptosis, increases cell viability after OGD/R treatment, and acts as a favorable prognostic factor in AIS. |
| Molecular mechanism: |
Decreased QKI inhibits circFOXP1 biogenesis under hypoxia; reduced circFOXP1 binds STAT3 and increases STAT3 ubiquitination and proteasomal degradation, thereby enhancing apoptotic signaling after cerebral ischemia. |
| Biological pathway or process: |
apoptosis (inhibits); JAK/STAT (promotes); ubiquitination (inhibits); other pathway/process (promotes) |
| Detected method: |
Q
|
| Validation methods: |
Back-Splice Junction PCR / divergent primers PCR; RNase R Treatment; Sanger Sequencing; Actinomycin D / DRB Stability Assay; RT-qPCR; FISH / smFISH; Nuclear-Cytoplasmic Fractionation; Clinical Sample Validation; RIP (RNA Immunoprecipitation); CLIP; RNA Pull-Down; Co-IP; Transfection; CCK8; EdU Staining; Annexin V/PI Flow Cytometry; TUNEL; In Vivo Animal Model; Western Blot; Cohort Study; Survival Analysis; ROC Analysis; Bioinformatics Analysis |
| Clinical significance: |
circFOXP1 expression is associated with AIS severity and prognosis; high circFOXP1 expression is an independent protective factor for AIS prognosis and circFOXP1 may serve as a prognostic biomarker. |
| Description: |
circFOXP1 is down-regulated in peripheral blood from AIS patients and its higher expression is linked to milder disease and better prognosis. Functionally, circFOXP1 protects against ischemic/hypoxic injury by binding STAT3, reducing STAT3 ubiquitination and degradation, and suppressing apoptotic signaling; QKI promotes circFOXP1 biogenesis under these conditions. |
| Confidence score: |
0.8999 |