Stress-Induced c-Jun-Dependent Vitamin D Receptor Activation Dissects the Non-Classical VDR Pathway from the Classical VDR Activity

The 2007 document reveals that the Vitamin D receptor (VDR) is involved in gene expression and cell death in response to stress, with c-Jun, a part of the AP-1 transcription factor, being essential for VDR expression. The study showed that c-Jun is necessary for the initiation of VDR protein expression and that the absence of c-Jun reduces VDR expression, which can be reversed by c-Jun restoration. Additionally, the research identified a non-classical VDR pathway that requires both c-Jun and VDR for stress-induced VDR activity, where VDR can also inhibit c-Jun-mediated cell death independently of its classical role in transcription and vitamin D3. This indicates that VDR can alter c-Jun activity during stress response through a non-transcriptional mechanism that enhances protein expression. The document does not mention the number of subjects as it focuses on cellular mechanisms, not clinical studies.