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

January 2007 in “ Journal of biological chemistry/The Journal of biological chemistry ”

Qingping Li, Xiaomei Qi, Rocky Pramanik, Nicole M. Pohl, Mathew Loesch, Guan Chen

Vitamin D receptor VDR c-Jun AP-1 transcription factor gene expression cell death non-classical VDR pathway classical VDR activity stress response protein expression vitamin D3 AP-1

Studysummary This study found that c-Jun is essential for vitamin D receptor expression, and the vitamin D receptor inhibits c-Jun-dependent cell death through non-classical mechanisms independent of vitamin D3. Our plain-language summary of this paper — not a Tressless recommendation.

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.

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