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Last update 08 May 2025

PPM1A

Last update 08 May 2025

Basic Info

Synonyms

MGC9201, PP2C-alpha, PP2CA

+ [7]

Introduction

Enzyme with a broad specificity. Negatively regulates TGF-beta signaling through dephosphorylating SMAD2 and SMAD3, resulting in their dissociation from SMAD4, nuclear export of the SMADs and termination of the TGF-beta-mediated signaling. Dephosphorylates PRKAA1 and PRKAA2. Plays an important role in the termination of TNF-alpha-mediated NF-kappa-B activation through dephosphorylating and inactivating IKBKB/IKKB.

Drugs associated with PPM1A

SMIP-30

Target

PPM1A

Mechanism

PPM1A inhibitors

Active Org.

University of Ottawa

Originator Org.

University of Ottawa

Active Indication

Tuberculosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NPLC0393

Target

PPM1A

Mechanism

PPM1A activators

Active Org.

Shanghai Institute of Materia Medica Chinese Academy of Sci

Originator Org.

Shanghai Institute of Materia Medica Chinese Academy of Sci

Active Indication

Fibrosis, Liver

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

SMIP-031

Target

PPM1A

Mechanism

PPM1A activators

Active Org.

Nanjing University of Chinese Medicine

Originator Org.

Nanjing University of Chinese Medicine

Active Indication

Tuberculosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PPM1A

100 Translational Medicine associated with PPM1A

0 Patents (Medical) associated with PPM1A

216

Literatures (Medical) associated with PPM1A

01 Jul 2025·Plant Physiology and Biochemistry

Identification of PP2C gene family in moso bamboo (Phyllostachys edulis) and function analysis of PhePP2CA13

Article

Author: Lin, Qihan ; Si, Qin ; Liu, Yidong ; Wu, Min ; Shan, Xin

The protein phosphatase 2C (PP2C) gene family plays an important role in plant growth and development and resistance to abiotic stresses. In our research, the PP2C family containing 103 genes was comprised eleven distinct subfamilies in moso bamboo (Phyllostachys edulis). PP2C gene family mainly expand through segmental duplications and basically underwent purifying selection in moso bamboo. PP2CA subfamily, the most extensively studied subfamily, carried 19 members in moso bamboo PP2CA subfamily. The cis-acting elements analysis and expression patterns of PhePP2CA genes indicated their potential functions in response to abiotic stress. Next, we gained the lines of transgenic PhePP2CA13-overexpressing plants. Overexpression of PhePP2CA13 significantly decreased tolerance to drought stress, along with a lower germination rate and suppressed root length under drought treatment. Moreover, OE lines also reduced the sensitivity to exogenous ABA in OE lines. More importantly, yeast one-hybrid assays demonstrated that PhePP2CA13 acted downstream of PhebZIP47, and Dual-luciferase assays further showed that the expression of PhePP2CA13 was inhibited by PhebZIP47. This study enriched the knowledge of PP2CA genes and provided genetic resources for stress resistant breeding in moso bamboo.

01 Mar 2025·Toxicology in Vitro

Tripartite motif 22 interacts with protein phosphatase magnesium-dependent 1 A to aggravate radiation-induced epithelial-mesenchymal transition and fibrogenesis in lung epithelial cells

Article

Author: Wang, Menglei ; Lu, Jinhua ; Zhong, Yazhen ; Lin, Shengyou ; Zhou, Yeyue

Radiation-induced lung injury (RILI) is the damage to lung tissue caused by radiation. Epithelial-mesenchymal transition (EMT) and fibrogenesis in radiated lung epithelial cells play critical roles in RILI. Tripartite motif-containing (TRIM) family proteins have been shown to be involved in fibrotic diseases, but whether TRIM22 plays a role in RILI and relative underlying mechanism remain unexplored. Here, we reported a unique comprehensive analysis of the impact of TRIM22 on radiation-induced EMT and fibrogenesis in A549 and BEAS-2B cells. Cell viability and proliferation were measured by Cell-Counting Kit (CCK)-8 and colony formation assays. The interaction between TRIM22 and protein phosphatase magnesium-dependent 1 A (PPM1A) was validated using co-immunoprecipitation. A chromatin immunoprecipitation assay was used to verify the interaction between SMAD3 and TRIM22 promoter. Cell viability and proliferation were decreased by 8 Gy raddition. TRIM22 was elevated in a dose- and time-dependent manner after radiation, and its knockdown reduced EMT and fibrogenesis. TRIM22 could interact with PPM1A and promote its ubiquitination to activate the TGF-β1/Smad pathway. The overexpression of PPM1A abolished TRIM22-mediated EMT and fibrogenesis. Meanwhile, SMAD3 could bind to the TRIM22 promoter to elevate its expression. This study revealed a novel TRIM22/PPM1A/Smad3 signaling pathway that contributes to the raddition-induced EMT and fibrogenesis, which would provide novel targets and strategies for treating RILI.

01 Jan 2025·Acta Pharmacologica Sinica

Otilonium bromide ameliorates pulmonary fibrosis in mice through activating phosphatase PPM1A

Article

Author: Zhao, Shi-Mei ; Li, Hong-Lin ; Li, Wei ; Wan, Hui-Qi ; Shen, Xu ; Lu, Da-Yun ; Feng, Tian ; Li, Xiao-Qian ; Qian, Min-Yi ; Zhou, Zhi-Ruo ; Hou, Ji-Wei ; Hu, Xu-Hui ; Zhao, Tong

Pulmonary fibrosis (PF) is a chronic, progressive and irreversible interstitial lung disease characterized by unremitting pulmonary myofibroblasts activation, extracellular matrix (ECM) deposition and inflammatory recruitment. PF has no curable medication yet. In this study we investigated the molecular pathogenesis and potential therapeutic targets of PF and discovered drug lead compounds for PF therapy. A murine PF model was established in mice by intratracheal instillation of bleomycin (BLM, 5 mg/kg). We showed that the protein level of pulmonary protein phosphatase magnesium-dependent 1A (PPM1A, also known as PP2Cα) was significantly downregulated in PF patients and BLM-induced PF mice. We demonstrated that TRIM47 promoted ubiquitination and decreased PPM1A protein in PF progression. By screening the lab in-house compound library, we discovered otilonium bromide (OB, clinically used for treating irritable bowel syndrome) as a PPM1A enzymatic activator with an EC₅₀ value of 4.23 μM. Treatment with OB (2.5, 5 mg·kg^-1·d^-1, i.p., for 20 days) significantly ameliorated PF-like pathology in mice. We constructed PF mice with PPM1A-specific knockdown in the lung tissues, and determined that by targeting PPM1A, OB treatment suppressed ECM deposition through TGF-β/SMAD3 pathway in fibroblasts, repressed inflammatory responses through NF-κB/NLRP3 pathway in alveolar epithelial cells, and blunted the crosstalk between inflammation in alveolar epithelial cells and ECM deposition in fibroblasts. Together, our results demonstrate that pulmonary PPM1A activation is a promising therapeutic strategy for PF and highlighted the potential of OB in the treatment of the disease.

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PPM1A

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