TRIM67 alleviates cerebral ischemia‒reperfusion injury by protecting neurons and inhibiting neuroinflammation via targeting IκBα for K63-linked polyubiquitination.
Yongbo YuQian XiaGaofeng ZhanShuai GaoTangrui HanMeng MaoXing LiYonghong WangPublished in: Cell & bioscience (2023)
Taken together, this study demonstrated a previously unidentified mechanism whereby TRIM67 regulates neuroinflammation and neuronal apoptosis and strongly indicates that upregulation of TRIM67 may provide therapeutic benefits for ischemic stroke.
Keyphrases
- cerebral ischemia
- ischemia reperfusion injury
- oxidative stress
- traumatic brain injury
- lipopolysaccharide induced
- signaling pathway
- lps induced
- subarachnoid hemorrhage
- cognitive impairment
- spinal cord
- poor prognosis
- endoplasmic reticulum stress
- cell death
- atrial fibrillation
- cell proliferation
- inflammatory response
- cancer therapy
- cell cycle arrest
- spinal cord injury
- long non coding rna