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Phosphoenol-pyruvate carboxykinase isoform 2 (PCK2) causes metabolic defects in endothelial cells and angiogenesis.

ABSTRACT: Phosphoenol-pyruvate carboxykinase isoform 2 (PCK2) causes metabolic defects in endothelial cells and angiogenesis.

PROVIDER: PRJEB33275 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3407460.fastq.gz	Fastqsanger.gz
	ERR3407461.fastq.gz	Fastqsanger.gz
	ERR3407462.fastq.gz	Fastqsanger.gz
	ERR3407463.fastq.gz	Fastqsanger.gz
	ERR3407454.fastq.gz	Fastqsanger.gz

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Similar Datasets

Phosphoenol-pyruvate carboxykinase isoform 2 (PCK2) causes metabolic defects in endothelial cells and angiogenesis.

Project description:Given the prominent angiogenic defect in PCK2KD ECs, which could not be fully explained by its metabolic function as a cataplerotic enzyme, we performed an RNA-seq analysis of control versus PCK2KD ECs in normal versus glucose-deprived conditions.

2021-08-01 | E-MTAB-8104 | biostudies-arrayexpress

Glucose Metabolic Remodeling through Phosphoenolpyruvate Carboxykinase Isoform 2 Regulates Prostate Cancer Cell Tumorigenicity

Project description:Patients with aggressive prostate cancer generally present with poor outcomes. Identifying the factors regulating prostate cancer aggressiveness may open new avenues in therapy. Specifically, information from prostate cancer patient databases revealed that higher phosphoenolpyruvate carboxykinase isoform 2 (PCK2) levels correlate with more aggressive tumors and lower survival rates. Herein, we show that high tumorigenic prostate cancer cell clones express high levels of PCK2. We found that elevated levels of PCK2 are critical for the glucose metabolic remodeling and the maintenance of tumor-initiating cells (TICs) in aggressive prostate cancer. Our data suggest that PCK2 promotes tumorigenicity by lowering acetyl-CoA levels through reducing the mitochondrial tricarboxylic acid (TCA) cycle. Thus, PCK2 is a potential therapeutic target for aggressive prostate cancer.

2016-01-04 | GSE76470 | GEO

Glucose Metabolic Remodeling through Phosphoenolpyruvate Carboxykinase Isoform 2 Regulates Prostate Cancer Cell Tumorigenicity

2016-01-04 | E-GEOD-76470 | biostudies-arrayexpress

Catabolite repression of phosphoenolpyruvate carboxykinase by a zinc finger protein under biotin- and pyruvate carboxylase-deficient conditions in Pichia pastoris

Project description:We have identified a methanol- and biotin-starvation-inducible zinc finger protein named ROP [repressor of phosphoenolpyruvate carboxykinase (PEPCK)] in the methylotrophic yeast Pichia pastoris. When P.pastoris strain GS115 (wild-type, WT) is cultured in biotin-deficient, glucose ammonium (Bio-) medium, growth is suppressed due to the inhibition of anaplerotic synthesis of oxaloacetate, catalysed by the biotin-dependent enzyme pyruvate carboxylase (PC). Deletion of ROP results in a strain (∆ROP) that can grow under biotin-deficient conditions due to derepression of a biotin- and PC-independent pathway of anaplerotic synthesis of oxaloacetate. Northern analysis as well as microarray expression profiling of RNA isolated from WT and ∆ROP strains cultured in Bio(-) medium indicate that expression of the phosphoenolpyruvate carboxykinase gene (PEPCK) is induced in ∆ROP during biotin- or PC-deficiency even under glucose-abundant conditions. There is an excellent correlation between PEPCK expression and growth of ∆ROP in Bio(-) medium, suggesting that ROP-mediated regulation of PEPCK may have a crucial role in the biotin- and PC-independent growth of the ∆ROP strain. To our knowledge, ROP is the first example, of a zinc finger transcription factor involved in the catabolite repression of PEPCK in yeast cells cultured under biotin- or PC-deficient and glucose-abundant conditions.

2011-10-14 | GSE32948 | GEO

Catabolite repression of phosphoenolpyruvate carboxykinase by a zinc finger protein under biotin- and pyruvate carboxylase-deficient conditions in Pichia pastoris

2011-10-13 | E-GEOD-32948 | biostudies-arrayexpress

Overexpression of the non-muscle RBFOX2 isoform triggers cardiac conduction defects in myotonic dystrophy

Project description:Myotonic dystrophy type 1 (DM1) is a multisystemic genetic disorder caused by a CTG trinucleotide repeat expansion in the 3′ untranslated region of DMPK gene. Heart dysfunctions occur in nearly 80% of DM1 patients and are the second leading cause of disease-related deaths, yet, the underlying mechanisms remain unclear. Herein, we report that upregulation of a non-muscle splice isoform of RNA binding protein RBFOX2 in DM1 heart tissue—due to altered splicing factor and microRNA activities—induces the characteristic cardiac conduction defects detected in DM1 individuals. Mice engineered to express the non-muscle RBFOX2 isoform in heart via tetracycline- inducible transgenesis, or CRISPR/Cas9 targeted genome editing, reproduced DM1- related cardiac-conduction delay and spontaneous episodes of arrhythmia. Furthermore, by integrating RNA binding with cardiac transcriptome datasets of DM1 patients, and mice expressing the non-muscle RBFOX2 isoform, we identified a core network of RBFOX2-driven splicing defects in sodium, potassium, and calcium channels that can alter their rate of ion diffusion and electrophysiological properties. Thus, our results uncover a trans-dominant role for an aberrantly expressed RBFOX2 isoform in DM1 cardiac pathogenesis.

2020-03-10 | GSE126771 | GEO

Spontaneous metastasis xenograft models link CD44 isoform 4 to angiogenesis, hypoxia, EMT and mitochondria-related pathways in colorectal cancer

Project description:Objective: To determine the functional relevance of CD44 isoforms for distant metastasis formation in human colorectal cancer (CRC). Design: We used a pan-CD44 knockdown (kd) approach in a clinically relevant cell line/ xenograft model (HT-29) that spontaneously metastasizes to multiple sites in vivo. Transcriptomics, proteomics and kinomics were used in addition to corresponding validation steps to explain the observed effects. Findings were further corroborated by 3D in vitro culture, tissue microarray and bioinformatics analyses. Results: HT-29 cells mainly express the clinically relevant CD44 isoforms 3 and 4. CD44 kd impairs primary tumor formation and abrogates distant metastasis in vivo. Both CD44 isoforms are induced in the paranecrotic, hypoxic regions of the xenograft primary tumors but are largely absent in the corresponding lung metastases. Tumor angiogenesis is improved in the paranecrosis upon CD44 kd, accompanied by reduced HIF-1α, EMT, and CEACAM5 expression. Vice versa, mitochondrial genes and proteins are induced upon CD44 kd as is oxidative phosphorylation. Hypoxia increases VEGF release from 3D HT-29 spheres, which is strikingly enhanced in CD44 kd spheres. The metastasis-promoting role of CD44 is reflected by an unfavorable prognostic effect of CD44 isoform 4 in patients (as opposed to isoform 3). Accordingly, the genes regulated by the CD44 kd in vivo concordantly overlap specifically with the genes regulated by CD44 isoform 4 in patients. Conclusion: In CRC, CD44 kd (most probably isoform 4) evidently impairs metastasis formation by improving VEGF release and thus angiogenesis in hypoxic conditions, thereby decreasing hypoxia, EMT, stemness, and promoting mitochondrial metabolism.

2022-07-18 | GSE208310 | GEO

Pharmacological activation of pyruvate kinase M2 (PKM2) inhibits CD4+ T cell pathogenicity and suppresses autoimmunity

Project description:Pyruvate kinase (PK) catalyzes the conversion of phosphoenolpyruvate to pyruvate during glycolysis. The PK isoform PKM2 has additional roles in regulation of gene transcription and protein phosphorylation. PKM2 controls macrophage metabolic remodeling in inflammation, but its role in T cell biology is poorly understood. These results show that TEPP-46, an activator of PKM2, reduces CD4+ T cell activation, proliferation, and cytokine production by inhibiting essential signaling pathways and preventing glycolysis.

2019-11-26 | GSE139378 | GEO

Overexpression of the non-muscle RBFOX2 isoform triggers cardiac conduction defects in myotonic dystrophy

Project description:Overexpression of the non-muscle RBFOX2 isoform triggers cardiac conduction defects in myotonic dystrophy

| PRJNA523234 | ENA

suppression of Pyruvate carboxylase

Project description:suppression of Pyruvate carboxylase

| PRJNA821599 | ENA