Mouse Chordin Like Protein 1 (CHRDL1) ELISA Kit-Sandwich

Chordin-like protein 1 appears to counteract the function of BMP4 by binding to it and preventing its receptor interaction. It shifts the fate commitment of neural stem cells from gliogenesis to neurogenesis, aiding in their neuronal differentiation by inhibiting glial fate adoption. Chordin-like protein 1 may play a vital role in dorsoventral axis formation. In ischemic stroke models, such as cerebral ischemia, Chrdl1 is significantly upregulated during the acute phase, particularly in the peri-infarct area. Research indicates that Chrdl1 reduces neuronal apoptosis and dendritic spine loss by stabilizing the distribution of AMPA receptors (GluA2-AMPA-Rs) and moderating synaptic plasticity. A deficiency in Chrdl1 enhances synaptic plasticity, resulting in increased dendritic spine density and improved motor recovery. Furthermore, while Chrdl1 deficiency does not significantly impact infarct volume or inflammatory response, it reduces apoptosis in the acute phase.