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Last update 08 May 2025

PPP6C

Last update 08 May 2025

Basic Info

Synonyms

PP6, PP6C, PPP6

+ [4]

Introduction

Catalytic subunit of protein phosphatase 6 (PP6) (PubMed:17079228, PubMed:29053956, PubMed:32474700). PP6 is a component of a signaling pathway regulating cell cycle progression in response to IL2 receptor stimulation (PubMed:10227379). N-terminal domain restricts G1 to S phase progression in cancer cells, in part through control of cyclin D1 (PubMed:17568194). During mitosis, regulates spindle positioning (PubMed:27335426). Down-regulates MAP3K7 kinase activation of the IL1 signaling pathway by dephosphorylation of MAP3K7 (PubMed:17079228). Participates also in the innate immune defense against viruses by desphosphorylating RIGI, an essential step that triggers RIGI-mediated signaling activation (PubMed:29053956). Also regulates innate immunity by acting as a negative regulator of the cGAS-STING pathway: mediates dephosphorylation and inactivation of CGAS and STING1 (PubMed:32474700, PubMed:32753499). CGAS dephosphorylation at 'Ser-435' impairs its ability to bind GTP, thereby inactivating it (PubMed:32474700).

Drugs associated with PPP6C

CN118063558

Patent Mining

Target

PPP6C

Mechanism-

Active Org.

Shenzhen People's Hospital [+1]

Originator Org.

Shenzhen People's Hospital [+1]

Active Indication

Respiratory Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PPP6C

100 Translational Medicine associated with PPP6C

0 Patents (Medical) associated with PPP6C

239

Literatures (Medical) associated with PPP6C

01 May 2025·Phytomedicine

10-Hydroxydec-2-enoic acid reduces vascular smooth muscle cell inflammation via interacting with Toll-like receptor 4

Article

Author: Wang, Yongqing ; Chen, Zhiqiang ; Jia, Feng ; Wang, Yanyan ; Zeng, Lei ; Jin, Jingxian ; Tang, Huaijian ; Zhang, Li ; Fan, Pei

BACKGROUND10-Hydroxydec-2-enoic acid (10-HDA), a unique and marker compound in royal jelly, has a wide range of bio-activities. However, its role in regulating inflammation of vascular smooth muscle cell (VSMC), which is essential to a set of vascular diseases, is still unknown.PURPOSEOur study aimed to investigate whether 10-HDA exerts effect on VSMC inflammation via interacting with toll-like receptor 4 (TLR4), a pivotal inflammatory initiator.METHODSA package of proteins, which might participate in TLR4-mediated signaling, influenced by 10-HDA were analyzed in mouse VSMCs with Angiotensin Ⅱ(Ang Ⅱ) or lipopolysaccharide (LPS) stimulation. Accordingly, pro- or anti-inflammatory cytokines, reactive oxygen species (ROS), and anti-oxidants that are closely relevant to inflammatory process were determined. The possible mode for 10-HDA interacting with TLR4 was also characterized. Moreover, involvement of a key miRNA in 10-HDA regulating VSMC inflammation was identified.RESULTSIn the presence of Ang Ⅱ, 10-HDA inhibited the TLR4 expression in a dose-dependent manner. In such occasion, 10-HDA hindered the up-regulation of specificity protein 1 (SP1) and serine/threonine-protein phosphatase 6 catalytic subunit (PPP6C), the phosphorylation of extracellular signal-regulated kinase 1/2, TGF-β-activated kinase 1, and nuclear factor-κB p56, as well as the enhancement of myeloid differentiation primary response gene 88. Apart from SP1 and PPP6C, the level change of these proteins by 10-HDA was similar with LPS stimulation. The effect might be resulted from 10-HDA blocking TLR4 through multiple atomic interactions. 10-HDA mitigated the increase of pro-inflammatory cytokines tumor necrosis factor-alpha, interleukin-2 (IL-2), and IL-6, as well as increased the anti-inflammatory cytokine IL-10, in the Ang Ⅱ- or LPS-induced VSMCs. Correspondingly, the level of ROS was attenuated and the anti-oxidants such as glutathione and superoxide dismutase were fortified. The data indicated the anti-inflammatory potential of 10-HDA in VSMCs, which was associated with 10-HDA's capability of relieving oxidative stress. Additionally, the expression of miR-17-5p was saved by 10-HDA from Ang Ⅱ- or LPS-treated VSMCs, which might be relevant to SP1 and PPP6C targeting.CONCLUSIONThe present work of 10-HDA, for the first time, revealed its ability to alleviate VSMC inflammation by targeting TLR4 and therefore modulate the downstream inflammatory participants. Our data will cast light on the utilization of 10-HDA in VSMC inflammation-related vascular disorders.

06 Mar 2025·Current Medicinal Chemistry

Functional Role of Protein Phosphatase-6 (PPP6c): Regulation of Expression and Modulation of Activity

Article

Author: Tatiana, Ruksha ; Mariya, Aksenenko

Abstract:This review produces information about the role of protein phosphatase-6 (PPP6C) in various biological processes such as cell proliferation, cell cycle regulation, apoptosis, autophagy, cell migration and differentiation, and DNA damage repair. The issues of the participation of PPP6C in the formation of tumor progression and the role of PPP6C in the epigenetic regulation of the tumor process are covered. The article presents in detail the classification of mutations depending on the biological effects they have. It has been shown that various types of mutations in the PPP6C gene can change the composition of the heterotrimeric complex, favoring some regulatory subunits over others, which promotes selective dephosphorylation of substrates to maintain cell viability and change their biological behavior. In particular, their proliferative activity is disrupted, leading to mitosis arrest at various cell cycle stages. An increase in the activity of Aurora A or a decrease in the activity of DNA-dependent protein kinase is considered the main molecular mechanism of tumor development associated with the inactivation of the pp6c protein. The article also discusses the topic of pharmacological modulation of PPP6C activity. PP6 is a protein involved in many biological processes. In this regard, it is especially important to clarify the role of each PP6 holoenzyme and the molecular mechanisms that regulate the formation of the PP6 complex. Changes in the activity of this phosphatase can disrupt cell functioning.

01 Mar 2025·Phytomedicine

Exploring the therapeutic potential of Abelmoschi Corolla in psoriasis: Mechanisms of action and inflammatory pathway disruption

Article

Author: Qu, Baoquan ; Zhao, Ning ; Zhu, Haoyue ; Li, Ping ; Zhao, Jingxia ; Li, Ruonan ; Ma, Huike ; Li, Guanglu

BACKGROUNDPsoriasis is a prevalent chronic inflammatory skin condition for which existing treatments often fall short of fully addressing patient needs. Abelmoschi Corolla (AC), a traditional Chinese medicine, and its ethanol extract, huangkui capsule, are well established for the treatment of chronic kidney diseases. The therapeutic mechanisms of AC include anti-inflammatory effects and immune modulation, which align with psoriasis treatment strategies. Nevertheless, the potential of AC as a therapeutic agent for psoriasis remains unexplored.PURPOSEThis study aimed to evaluate the efficacy of AC in treating psoriasis and, if effective, to elucidate the underlying mechanisms by which AC exerts its therapeutic effects.METHODSTo assess the therapeutic potential of AC, an imiquimod-induced psoriasis-like mouse model was utilized. Bioinformatics and machine learning approaches were employed to predict the targets and mechanisms of AC in psoriasis. Further validation was performed using targeted metabolite quantification, immunohistochemistry, polymerase chain reaction, and western blotting.RESULTSAC treatment significantly improved psoriasis-like skin lesions, as indicated by enhancements in appearance, PASI scores, a reduction in epidermal hyperproliferation, and decreased immune cell infiltration. Bioinformatics and machine learning analyses identified arginase 1 (ARG1) as a key target of AC in psoriasis. Experimental validation demonstrated that AC reduced ARG1 expression, arginine metabolism, and polyamine production by upregulating PP6 expression and inhibiting C/EBP-β activation in psoriatic keratinocytes, resulting in the suppression of dendritic cell infiltration and a reduction in the expression of inflammatory cytokines, including IL-23, IL-6, IL-1β, IL-17A, and TNF-α.CONCLUSIONSAC disrupted the inflammatory pathways associated with psoriasis and alleviated imiquimod-induced psoriasis-like skin inflammation by inhibiting ARG1 overexpression and arginine metabolism in psoriatic keratinocytes. These findings suggest that AC has significant potential as a therapeutic agent for psoriasis and warrants further research and development.

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PPP6C

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