Nitrendipine, L-type Ca2+ channel blocker

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Parkin also known as PRKN functions as an E3 ubiquitin-protein ligase involved in the ubiquitination and degradation of proteins. It has a mass of approximately 52 kDa and is expressed mainly in the brain heart and muscle tissues. The gene encoding for this protein is located on chromosome 6q25.2-q27. Interferon beta CACNA1C TDP1 and Androgen Receptor are integral to cellular processes with expressions in various tissues. CACNA1C constitutes a vital part of the voltage-gated calcium channel while the Androgen Receptor acts in signal transduction for hormones. These targets contribute to modulating cellular functions and responses.

Biological function summary

Parkin is essential in maintaining cellular homeostasis and stress response through its role in the ubiquitin-proteasome system. It forms a complex with PINK1 facilitating the clearance of damaged mitochondria. CACNA1C is part of the L-type calcium channel complex playing a role in cardiac and smooth muscle contraction. TDP1 assists in DNA repair processes. The Androgen Receptor modulates the expression of genes related to cellular proliferation. Other targets like PXR TRPA1 and GPCR GPR55 mediate cellular responses to various stimuli impacting metabolic and sensory pathways.

Pathways

Parkin integrates into the mitophagy pathway and is associated with PINK1 to regulate mitochondrial quality. CACNA1C participates in calcium signaling pathways influencing cardiac action potentials. Androgen Receptor links with the androgen signaling pathway impacting reproductive tissue function. PXR interacts with drug metabolism pathways affecting the detoxification of xenobiotics. Adenosine A3 Receptor and HLA B7 involve immune response modulation whereas SCN1a and Nav1.5/SCN5A influence the sodium channel pathways critical for neuronal and cardiac function.

Parkin mutations associate with Parkinson's disease linking it to dopaminergic neuron degradation. CACNA1C mutations correlate with Timothy syndrome affecting calcium signaling and cardiac rhythm. Androgen Receptor abnormalities connect to prostate cancer playing a role in tumor growth through hormone regulation. Mutations in SCN1a relate to epilepsy influencing neuronal excitability. H-ERG mutations lead to Long QT syndrome affecting cardiac rhythm. These proteins interact with various signaling molecules in disease pathogenesis highlighting their clinical relevance.