PPP1R3C

Last update 08 May 2025

Basic Info

Synonyms

PP1 subunit R5, PPP1R3C, PPP1R5

+ [4]

Introduction

Acts as a glycogen-targeting subunit for PP1 and regulates its activity. Activates glycogen synthase, reduces glycogen phosphorylase activity and limits glycogen breakdown. Dramatically increases basal and insulin-stimulated glycogen synthesis upon overexpression in a variety of cell types.

100 Clinical Results associated with PPP1R3C

100 Translational Medicine associated with PPP1R3C

0 Patents (Medical) associated with PPP1R3C

Literatures (Medical) associated with PPP1R3C

22 Apr 2025·Proceedings of the National Academy of Sciences

Protein Phosphatase 1 Regulatory Subunit 3C integrates cholesterol metabolism and isocitrate dehydrogenase in chondrocytes and neoplasia

Article

Author: Browne, Makenna ; Miyamoto, Ryo ; Marius, Choiselle ; Hirata, Makoto ; Nadesan, Puviindran ; Peairs, Emily ; Guardino, Nicholas ; Ishikawa, Koji ; Nakagawa, Makoto ; Alman, Benjamin A. ; Puviindran, Vijitha ; Matarangas, Ariana ; Shimada, Eijiro ; Wallace, Asjah ; Nguyen, Tuyet

Enchondromas are common bone tumors composed of chondrocytes originating from growth plate cells which can progress to malignant chondrosarcoma. Mutations in the genes encoding isocitrate dehydrogenase (IDH1 and IDH2) are identified in a large proportion of these tumors. IDH enzymes convert isocitrate to alpha-ketoglutarate (α-KG), an essential component of the citric acid cycle. While mutant IDH enzymes produce 2-hydroxyglutarate, which has epigenetic effects important in tumor initiation, cell maintenance and growth rely on additional factors. Prior work shows that intracellular cholesterol and glycogen are upregulated in mutant IDH chondrocytes. Here, we show that Protein Phosphatase 1 Regulatory Subunit 3C (PPP1R3C, previously termed Protein Targeting to Glycogen or PTG) is highly expressed in chondrocytes harboring a mutant IDH. Furthermore, Sterol Regulatory Element-Binding Proteins (SREBPs), transcriptional regulators of sterol biosynthesis, regulate PPP1R3C expression. We found that PPP1R3C regulates glycolysis and glycolytic capacity in chondrocytes. Depletion of PPP1R3C in mouse chondrocytes in vivo suppresses the neoplastic phenotype. The growth plate phenotype associated with the genetic inhibition of cholesterol biosynthesis is partially rescued by PPP1R3C overexpression. Taken together, our data show that PPP1R3C integrates cholesterol metabolism and isocitrate dehydrogenase in growth plate and neoplastic chondrocyte metabolism by regulating intracellular glycogen levels.

01 Feb 2025·Biochemical Genetics

Comprehensive Analysis Based on the TCGA Database Identified SCIN as a Key DNA Methylation-Driver Gene in Epstein-Barr Virus-Associated Gastric Cancer

Article

Author: Luo, Bing ; Liu, Wen ; Gong, Zhiyuan ; Bi, Chunxia

An important feature of EBV-associated gastric cancer (EBVaGC) is extensive methylation of viral and host genomes. This study aims to analyze DNA methylation-driven genes (DMDG) in EBVaGC through bioinformatics methods, providing an important bioinformatics basis for the differential diagnosis and treatment of potential methylation biomarkers in EBVaGC. We downloaded the mRNA expression profiles and methylation datasets of EBVaGC and EBV-negative gastric cancer (EBVnGC) through the TCGA database to screen methylated-differentially expressed genes (MDEGs). DNA methylation-driver genes were identified based on MethylMix algorithm and key genes were further identified by LASSO regression and Random Forest algorithm. Then, we performed gene enrichment analysis for key genes and validated them by GEO database. Gene expression differences in EBVaGC and EBVnGC cell lines was determined by quantitative real-time PCR (qRT-PCR) and western blotting and in GT38 cell and SNU719 cell which all treated by 5-Aza-CdR. Finally, the effect of key gene on the migration and proliferation capacity of EBVaGC cells was determined by Transwells assay and Cell counting Kit-8 (CCK-8) assay. We obtained a total of 687 hypermethylation-low expression genes (Hyper-LGs) and further obtained 53 DNA methylation-driver genes based on the MethylMix algorithm. A total of six key genes (SCIN, ETNK2, PCDH20, PPP1R3C, MATN2, and HOXA5) were identified by LASSO regression and Random Forest algorithm. Among them, SCIN expression was significantly lower in EBVaGC cell lines than in EBVnGC cell lines, and its expression was significantly recovered in EBVaGC cell lines treated with 5-Aza-CdR. Overexpression of SCIN can promote the proliferation and migration capacity of EBVaGC cells. Our study will provide some bioinformatics basis for the study of EBVaGC-related methylation. SCIN may be used as potential methylation biomarkers for the diagnosis and treatment of EBVaGC.

01 Jan 2025·iScience

Effects of aging on diurnal transcriptome change in the mouse corpus callosum

Article

Author: Sakadzic, Sava ; Li, Wenlu ; Lo, Eng H ; Hoshino, Tomonori ; Arai, Ken ; Hamanaka, Gen ; Kimura, Shintaro ; Fukuda, Norito ; Shindo, Akihiro ; Ishikawa, Hidehiro ; Mandeville, Emiri T ; Guo, Shuzhen ; Harrington, Mary E

The corpus callosum, a major white matter region central to cognitive function, is vulnerable to aging. Using zeitgeber time (ZT) aligned with environmental light/dark cycles, we investigated temporal gene expression patterns in the corpus callosum of young (5-month-old) and aged (24-month-old) mice using RNA-seq. Comparative analysis revealed more differentially expressed genes across ZT pairs in young mice than aged mice. In addition, complement pathway genes, including C4b, C3, C1qa, C1qb, and C1qc, were consistently upregulated in aged mice regardless of ZT. Furthermore, genes such as Etnppl, Tinagl1, Hspa12b, Ppp1r3c, Thbd, Pla2g3, and Tsc22d3 exhibited ZT-dependent rhythmicity in young mice, but their rhythmic patterns were altered with age. This study provides an important dataset of the interplay between aging, diurnal rhythms, and gene expression in the corpus callosum, highlighting potential molecular mechanisms mediating white matter aging. Further investigation is warranted to dissect these gene's specific roles in neurological health during aging.

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PPP1R3C

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