PPP3CA: A Promising Drug Target and Biomarker for the Treatment of Chronic Pain

Target Name: PPP3CA

NCBI ID: G5530

PPP3CA: A Promising Drug Target and Biomarker for the Treatment of Chronic Pain

Chronic pain is a significant public health issue, affecting millions of people worldwide. The constant and severe pain can have a significant impact on an individual's quality of life, leading to reduced mobility, social isolation, and even depression. In addition, chronic pain can also lead to significant economic burden due to lost productivity and increased healthcare costs. Therefore, the development of new treatments for chronic pain is of great importance.

PPP3CA: A Potential Drug Target and Biomarker

The protein phosphatase 3 (PPP3CA) is a key enzyme involved in the regulation of cellular signaling pathways. PPP3CA has been identified as a potential drug target for the treatment of chronic pain due to its involvement in the regulation of pain signaling pathways. Several studies have suggested that inhibition of PPP3CA could provide relief from chronic pain.

PPP3CA is a transmembrane protein that contains two distinct catalytic subunits, alpha and beta. The alpha subunit is responsible for the catalytic activity, while the beta subunit plays a structural role. PPP3CA has been shown to regulate various cellular signaling pathways, including the production of pain signals.

Recent studies have suggested that PPP3CA is involved in the regulation of pain signaling pathways, including the production of neuropeptides. Neuropeptides are important signaling molecules that play a crucial role in pain modulation. The production of neuropeptides is regulated by various enzymes, including PPP3CA. Therefore, inhibition of PPP3CA could potentially lead to the decreased production of neuropeptides, which could provide relief from chronic pain.

Another study has shown that PPP3CA is involved in the regulation of pain modulation by the endogenous opioid system. The endogenous opioid system is a natural pain modulation system that involves the production and release of endogenous opioids, such as endorphins and opioid-derived neurotrophic factor (ODNF). PPP3CA has been shown to regulate the activity of the endogenous opioid system, which could potentially contribute to the decreased production of endogenous opioids and increased pain sensitivity.

In addition, PPP3CA has also been shown to be involved in the regulation of pain modulation by ion channels. Pain signals are transmitted through ion channels in the nervous system, and the activity of these channels can be regulated by various enzymes, including PPP3CA. Therefore, inhibition of PPP3CA could potentially lead to the modulation of ion channels, which could contribute to the decreased pain sensitivity.

Conclusion

In conclusion, PPP3CA is a protein that has been shown to be involved in the regulation of various cellular signaling pathways, including pain signaling pathways. The inhibition of PPP3CA has been shown to provide relief from chronic pain in various models. Therefore, PPP3CA is a promising drug target and biomarker for the treatment of chronic pain. Further studies are needed to fully understand the role of PPP3CA in pain modulation and to develop effective treatments for chronic pain.

Protein Name: Protein Phosphatase 3 Catalytic Subunit Alpha

Functions: Calcium-dependent, calmodulin-stimulated protein phosphatase which plays an essential role in the transduction of intracellular Ca(2+)-mediated signals (PubMed:15671020, PubMed:18838687, PubMed:19154138, PubMed:23468591, PubMed:30254215). Many of the substrates contain a PxIxIT motif and/or a LxVP motif (PubMed:17498738, PubMed:17502104, PubMed:22343722, PubMed:23468591, PubMed:27974827). In response to increased Ca(2+) levels, dephosphorylates and activates phosphatase SSH1 which results in cofilin dephosphorylation (PubMed:15671020). In response to increased Ca(2+) levels following mitochondrial depolarization, dephosphorylates DNM1L inducing DNM1L translocation to the mitochondrion (PubMed:18838687). Positively regulates the CACNA1B/CAV2.2-mediated Ca(2+) release probability at hippocampal neuronal soma and synaptic terminals (By similarity). Dephosphorylates heat shock protein HSPB1 (By similarity). Dephosphorylates and activates transcription factor NFATC1 (PubMed:19154138). In response to increased Ca(2+) levels, regulates NFAT-mediated transcription probably by dephosphorylating NFAT and promoting its nuclear translocation (PubMed:26248042). Dephosphorylates and inactivates transcription factor ELK1 (PubMed:19154138). Dephosphorylates DARPP32 (PubMed:19154138). May dephosphorylate CRTC2 at 'Ser-171' resulting in CRTC2 dissociation from 14-3-3 proteins (PubMed:30611118). Dephosphorylates transcription factor TFEB at 'Ser-211' following Coxsackievirus B3 infection, promoting nuclear translocation (PubMed:33691586). Required for postnatal development of the nephrogenic zone and superficial glomeruli in the kidneys, cell cycle homeostasis in the nephrogenic zone, and ultimately normal kidney function (By similarity). Plays a role in intracellular AQP2 processing and localization to the apical membrane in the kidney, may thereby be required for efficient kidney filtration (By similarity). Required for secretion of salivary enzymes amylase, peroxidase, lysozyme and sialic acid via formation of secretory vesicles in the submandibular glands (By similarity). Required for calcineurin activity and homosynaptic depotentiation in the hippocampus (By similarity). Required for normal differentiation and survival of keratinocytes and therefore required for epidermis superstructure formation (By similarity). Positively regulates osteoblastic bone formation, via promotion of osteoblast differentiation (By similarity). Positively regulates osteoclast differentiation, potentially via NFATC1 signaling (By similarity). May play a role in skeletal muscle fiber type specification, potentially via NFATC1 signaling (By similarity). Negatively regulates MAP3K14/NIK signaling via inhibition of nuclear translocation of the transcription factors RELA and RELB (By similarity). Required for antigen-specific T-cell proliferation response (By similarity)

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