| Expression pattern: |
UP |
| Associated gene: |
TIPARP / 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly (ADP-ribose) polymerase |
| Associated microRNA: |
miR-335-3p |
| Biological function: |
circTLK1 aggravates ischemic stroke-associated neuronal injury, increases cerebral infarction and neurological deficits, and its knockdown decreases infarct volumes, attenuates neuronal injury, improves neurological deficits, reduces brain atrophy, and preserves neuronal plasticity. |
| Molecular mechanism: |
circTLK1 acts as an endogenous miR-335-3p sponge, inhibits miR-335-3p activity, and increases TIPARP expression, thereby exacerbating neuronal injury after ischemic stroke. |
| Biological pathway or process: |
apoptosis (promotes); ceRNA regulation (promotes); other pathway/process (promotes) |
| Detected method: |
Q
M
|
| Validation methods: |
Back-Splice Junction PCR / divergent primers PCR; RNase R Treatment; RT-qPCR; Microarray; FISH / smFISH; IF (Immunofluorescence); IHC (Immunohistochemistry); Clinical Sample Validation; RNA Pull-Down; Luciferase Reporter Assay; Transfection; CCK8; Western Blot; In Vivo Animal Model; ROC Analysis; Bioinformatics Analysis |
| Clinical significance: |
Plasma circTLK1 is increased in patients with AIS, shows diagnostic potential with ROC AUC of 0.868, and positively correlates with infarct volume. |
| Description: |
circTLK1 is up-regulated in ischemic stroke models and in plasma from patients with AIS. It aggravates neuronal injury and neurological deficits by sponging miR-335-3p and increasing TIPARP expression, while circTLK1 knockdown reduces infarct volume, apoptosis-related injury, brain atrophy, and functional deficits. Clinically, elevated plasma circTLK1 shows diagnostic potential and correlates with larger infarct volume. |
| Confidence score: |
0.8649 |