C/EBPB: A transcription factor associated with the irreversible progression of Alzheimer's disease

C/EBPβ‐TRPC1‐SOCE signaling causes ER stress and dysregulation of protein enzymes and phosphatases. After G protein‐coupled receptors and tyrosine receptors were activated, PLC was subsequently activated to generate IP3 from PIP2. As a calcium channel, IP3R binds to IP3 and is activated, resulting in calcium ion outflow. When Ca2+ storage in the ER is depleted, STIM1/2 senses a reduction in Ca2+ in the ER, which leads to oligomerization and subsequent transfer from ER‐like sites to the plasma membrane, where it interacts with calcium conduction channels (ORAIs and TRPCs) to induce Ca2+ influx and storage regeneration. In the context of hTau overexpression, activated C/EBPβ binds to the TRPC1 promoter sequence, promoting TRPC1 transcription, then increases neuronal steady‐state [Ca2+] I, enhances endoplasmic reticulum (ER) stress, imbalances protein kinases, and phosphatases, and exacerbates tauopathy. The C/EBPβ‐Trpc1‐soce‐signaling pathway in turn increases hTau, thus accelerating the progression of AD.

Publication

C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease. (2024) Qing Yao, et al. CNS Neurosci Ther. 2024 Apr;30(4):e14721. Figure: F4. Homo sapiens

Disease mentions