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Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells [scRNA-seq]

ABSTRACT: Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells [scRNA-seq]

PROVIDER: PRJNA1224788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32370370_1.fastq.gz	Fastqsanger.gz
	SRR32370370_2.fastq.gz	Fastqsanger.gz
	SRR32370371_1.fastq.gz	Fastqsanger.gz
	SRR32370371_2.fastq.gz	Fastqsanger.gz
	SRR32370372_1.fastq.gz	Fastqsanger.gz

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Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells [scRNA-seq]

Project description:Human induced pluripotent stem cells (hiPSCs) hold significant potential for advancing our understanding of heart development. Differentiating hiPSCs into cardiac cells allows for modeling early cardiac developmental processes and exploring key signaling pathways. However, variations in differentiation efficiency and poor reproducibility of hiPSC-derived cardiomyocytes (hiPSC-CMs) production have remained a challenge. Here, we report a unique metabolic method to promote hiPSC-CM differentiation that involves marked suppression of the mitochondrial oxidative phosphorylation from the mesendoderm to the cardiac mesoderm, which is regulated by PHGDH, a rate-limiting enzyme in the serine synthesis pathway (SSP). Mechanistically, the analysis of scRNA-seq revealed that SSP inhibition promotes CM lineage differentiation by disrupting the cardiopharyngeal mesoderm lineage differentiation. Our findings show that SSP can regulate cardiac differentiation and have implications in elucidating the potential mechanisms of heart development and pathogenesis of heart disease.

2025-05-24 | GSE289789 | GEO

Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells [RNA-seq]

Project description:Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells [RNA-seq]

| PRJNA1227540 | ENA

Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells [RNA-seq]

Project description:Differences of metabolism-related gene expression profiles in human pluripotent stem cells (hPSCs) and hPSC-derived cardiomyocytes (hPSC-CMs) were analyzed and successfully identified.

2025-05-24 | GSE290355 | GEO

PHGDH Arginine Methylation by PRMT1 Promotes Serine Synthesis and Represents a Therapeutic Vulnerability in Hepatocellular Carcinoma

Project description:Serine synthesis is crucial for tumor growth and survival, but its regulatory mechanism in cancer remains elusive. Here, using integrative metabolomics and transcriptomics analyses, we show a heterogeneity between metabolite and transcript profiles. Specifically, the level of serine in HCC tissues is increased, whereas the expression of phosphoglycerate dehydrogenase (PHGDH), the first rate-limiting enzyme in serine biosynthesis pathway, is dramatically downregulated. Interestingly, the increased serine level is obtained by enhanced PHGDH catalytic activity due to protein arginine methyltransferase 1 (PRMT1)-mediated methylation of PHGDH at arginine 236. PRMT1-mediated PHGDH methylation and activation potentiates serine synthesis, ameliorates oxidative stress, and promotes HCC growth in vitro and in vivo. FBXO7, an E3 ubiquitin ligase which is downregulated in human HCC tissues, ubiquitinates and downregulates PRMT1 to suppress PHGDH methylation and serine synthesis, leading to the inhibition of HCC cell growth. Furthermore, PRMT1-mediated PHGDH methylation correlates with PHGDH hyperactivation and serine accumulation in human HCC tissues, and is predictive of poor prognosis of HCC patients. Notably, blocking PHGDH methylation with a TAT-tagged non-methylated peptide inhibits serine synthesis and restrains HCC growth, both in an HCC patient-derived xenograft (PDX) model and subcutaneous HCC cell-derived xenograft model. Overall, our findings reveal a novel regulatory mechanism of PHGDH activity and serine synthesis, and suggest PHGDH methylation as a potential therapeutic vulnerability in HCC.

2022-07-11 | GSE207435 | GEO

Phosphoglycerate mutase regulates Treg differentiation through control of serine synthesis and one-carbon metabolism

Project description:The differentiation and suppressive functions of regulatory CD4 T cells (Tregs) are supported by a broad array of metabolic changes, providing potential therapeutic targets for immune modulation. In this study, we focused on the regulatory role of glycolytic enzymes in Tregs and identified phosphoglycerate mutase (PGAM) as being differentially overexpressed in Tregs and associated with a highly suppressive phenotype. Pharmacologic or genetic inhibition of PGAM reduced Treg differentiation and suppressive function while reciprocally inducing markers of a pro-inflammatory, T helper 17 (Th17)-like state. The regulatory role of PGAM was dependent on the contribution of 3-phosphoglycerate (3PG), the PGAM substrate, to de novo serine synthesis. Blocking de novo serine synthesis from 3PG reversed the effect of PGAM inhibition on Treg polarization, while exogenous serine directly inhibited Treg polarization. Addi-tionally, altering serine levels in vivo with a serine/glycine-free diet increased peripheral Tregs and at-tenuated autoimmunity in a murine model of multiple sclerosis. Mechanistically, we found that serine limits Treg polarization by contributing to one-carbon metabolism and methylation of Treg-associated genes. Inhibiting one-carbon metabolism increased Treg polarization and suppressive function both in vitro and in vivo in a murine model of autoimmune colitis. Our study identifies a novel physiologic role for PGAM and highlights the metabolic interconnectivity between glycolysis, serine synthesis, one-car-bon metabolism, and epigenetic regulation of Treg differentiation and suppressive function

2025-06-06 | GSE269846 | GEO

FBXO7 Ubiquitinates PRMT1 to Suppress Serine Synthesis and Tumor Growth in HCC

Project description:Cancer cells are often addicted to de novo serine synthesis to support their survival and rapid proliferation. However, how serine synthesis is regulated in cancer is not well understood. Our recent report demonstrated that protein arginine methyltransferase 1 (PRMT1) is upregulated in hepatocellular carcinoma (HCC) and methylates phosphoglycerate dehydrogenase (PHGDH, the first and rate-limiting enzyme in serine synthesis) at arginine 236, thereby activating PHGDH and promoting serine synthesis. Nevertheless, the mechanisms underlying upregulation of PRMT1 and regulation of PRMT1-PHGDH axis in HCC remain unknown. Here, using label-free quantitative proteomics analysis, we identified the potential interacting proteins of PRMT1.

2024-02-01 | PXD049069 |

Mutant p53 regulates serine-glycine synthesis and essential amino acids intake

Project description:Mutant p53 regulates serine-glycine synthesis and essential amino acids intake

| PRJNA885512 | ENA

Serine metabolism supports macrophage IL-1β production.

Project description:Serine is a substrate for nucleotides, NADPH and glutathione (GSH) synthesis. Previous studies in cancer cells and lymphocytes have shown that serine-dependent one-carbon units are necessary for nucleotide production to support proliferation. Presently, it is unknown whether serine metabolism impacts the function of non-proliferative cells, such as inflammatory macrophages. We find that in macrophages, serine is required for optimal lipopolysaccharide (LPS) induction of IL-1β mRNA expression, but not inflammasome activation. The mechanism involves a requirement for glycine, which is made from serine, to support macrophage glutathione (GSH) synthesis. Cell-permeable GSH, but not the one-carbon donor formate, rescues IL-1β mRNA expression. Pharmacological inhibition of de novo serine synthesis in vivo decreased LPS induction of IL-1β levels and improved survival in an LPS-driven model of sepsis in mice. Our study reveals that serine metabolism is necessary for GSH synthesis to support IL-1β cytokine production.

2019-01-15 | GSE125036 | GEO

PHGDH Arginine Methylation by PRMT1 Promotes Serine Synthesis and Represents a Therapeutic Vulnerability in Hepatocellular Carcinoma

Project description:Serine synthesis is crucial for tumor growth and survival, but its regulatory mechanism in cancer remains elusive. Here, we found that R236 methylation of PHGDH promotes its activity and stimulates serine synthesis in hepatocellular carcinoma.

2022-07-28 | PXD035061 |

FGFR3 alterations in bladder cancer stimulate serine synthesis to induce immune-inert macrophages that suppress T-cell recruitment and activation

Project description:Metabolic reprogramming of bladder cancer cells driven by mutant FGFR3 increases serine synthesis that suppresses macrophage immunostimulatory functions to generate an immunosuppressive tumor microenvironment, which can be overcome by targeting PI3K.

2023-09-18 | GSE243093 | GEO

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