Research on the function of the Cend1 regulatory mechanism on p75NTR signaling in spinal cord injury.

How to use NSC repair mechanisms, minimize the loss of neurons, and recover the damaged spinal cord functions are hotspots and difficulties in spinal cord injury research. Studies have shown that Cend1 signaling is involved in regulating the NSC differentiation, that p75NTR signaling is involved in the regulation of mature neuronal apoptosis and that NSC differentiation decreases mature neuron apoptosis. Our research group found an interaction between Cend1 and p75NTR, and there was a correlation with spinal cord injury. Therefore, we speculate that Cend1 regulates p75NTR signals and promotes the differentiation of NSCs, and inhibits neuronal apoptosis. Therefore, this study first analyzed the expression of p75NTR and Cend1 in spinal cord injury and its relationship with NSCs and neurons and then analyzed the regulatory mechanism and the mechanism of survival on neuronal apoptosis and differentiation of NSCs. Finally, we analyzed the effect of p75NTR and the regulation of Cend1 damage on functional recovery of the spinal cord with overall intervention. The completion of the subject will minimize the loss of neurons, innovative use of NSC repair mechanisms, and open up a new perspective for the treatment of spinal cord injury.

Benzo[c][1,2,5]thiadiazole derivatives: A new class of potent Src homology-2 domain containing protein tyrosine phosphatase-2 (SHP2) inhibitors.

The Src homology-2 domain containing protein tyrosine phosphatase-2 (SHP2) is an oncogenic phosphatase linked to various kinds of cancers. Consequently, SHP2 has emerged as a promising target for novel anti-cancer agents. Using scaffold-hopping strategy, a series of benzo[c][1,2,5]thiadiazole derivatives was designed from PTP1B inhibitors with 1H-2,3-Dihydroperimidine motif, synthesized and evaluated their biological activities against PTP1B and SHP2. Among them, the representative compound 11g displayed SHP2 inhibitory activity with IC50 of 2.11 ±â€¯0.99 µM, exhibited 2.02-fold and 25-fold selectivity for SHP2 over SHP1 and PTP1B respectively and had no visible activity against TCPTP. These preliminary results could provide a possible opportunity for the development of novel SHP2 inhibitors with optimal potency and improved pharmacological properties.