anti-PEPCK (PEPCK) Antikörper

Mouse (Murine) phosphoenolpyruvate Carboxykinase 2 (Mitochondrial) (PEPCK) Interaktionspartner

1. Downregulation of PCK2 remodels tricarboxylic acid cycle in tumor-repopulating cells of melanoma

2. Data (including data from studies in knockout mice) suggest that Pck1 (zeige PCK1 Antikörper) in liver plays role in glucose homeostasis; here, Pck1 (zeige PCK1 Antikörper) deficiency (in knockout mice) can be successfully treated by re-expression of Pck1 (zeige PCK1 Antikörper) in liver, thus partially rescuing pups from fatal neonatal hypoglycemia. Pck1 (zeige PCK1 Antikörper) appears to play roles in metabolism in lung and skeletal muscle.

3. Lactate maintains/induces populations of postnatal neuronal progenitors/neural stem cells in a PEPCK-M-dependent manner

4. Silencing PCK1 (zeige PCK1 Antikörper) or inhibiting its enzymatic activity slows the growth of tumor-repopulating cells in vitro and impedes tumorigenesis in vivo.

5. Amino acid limitation and ER stress inducers, conditions that activate the amino acid response (AAR) and the unfolded protein response (UPR), stimulate PCK2 gene transcription in tumor cell lines.

6. PEPCK-M expression partially rescued defects in lipid metabolism, gluconeogenesis and TCA cycle function impaired by PEPCK-C deletion, while approximately 10% re-expression of PEPCK-C normalized most parameters.

7. FAT/CD36 (zeige CD36 Antikörper) regulates PEPCK in adipose tissue and that this could be secondary to reductions in lipolysis.

8. PCB (zeige PC Antikörper) 126 blunted the forskolin-stimulated increase in phosphoenolpyruvate carboxykinase (PEPCK) mRNA levels.

9. the role of IL-6 (zeige IL6 Antikörper) signalling in adipose tissue during exercise

10. there are multiple cytokine pathways by which inflammation inhibits PEPCK expression in adipose tissue which could contribute to the increased mobilization of fatty acids during inflammation

Human phosphoenolpyruvate Carboxykinase 2 (Mitochondrial) (PEPCK) Interaktionspartner

1. Downregulation of PCK2 remodels tricarboxylic acid cycle in tumor-repopulating cells of melanoma

2. ApoA-IV (zeige APOA4 Antikörper) colocalizes with NR4A1 (zeige NR4A1 Antikörper), which suppresses G6Pase (zeige G6PC Antikörper) and PEPCK gene expression at the transcriptional level, reducing hepatic glucose output and lowering blood glucose.

3. Results indicate that PEPCK promotes tumor growth by increasing glucose and glutamine (zeige GFPT1 Antikörper) metabolism, increases anabolic metabolism and promotes mTORC1 activity.

4. Mitochondrial PCK2 regulates metabolic adaptation and enables glucose-independent tumor growth in various neoplasms.

5. When autophagy was blocked, the level of glucose-6-phosphatase (G6Pase (zeige G6PC Antikörper)) and phosphoenolpyruvate carboxykinase (PEPCK) was reduced in HepG2 cells and not in Hep3B cells.

6. PEPCK activity was elevated threefold in lung cancer samples over normal lungs and its activation mediates an adaptive response to glucose depletion in lung cancer.

7. Amino acid limitation and ER stress inducers, conditions that activate the amino acid response (AAR) and the unfolded protein response (UPR), stimulate PCK2 gene transcription in tumor cell lines.

8. Expression of phosphoenolpyruvate carboxykinase linked to chemoradiation susceptibility of human colon cancer cells.

9. expression of HCV nonstructural component NS5A in Huh7 or primary hepatocytes stimulated PEPCK gene expression and glucose output in HepG2 cells.

10. results reveal a novel link between glucose metabolism and the DNA damage signaling pathway and suggest a possible role for PEPCK and G6P in the DNA damage response

Cow (Bovine) phosphoenolpyruvate Carboxykinase 2 (Mitochondrial) (PEPCK) Interaktionspartner

1. Transition to lactation does not alter expression of the mitochondrial form of PEPCK.

Pig (Porcine) phosphoenolpyruvate Carboxykinase 2 (Mitochondrial) (PEPCK) Interaktionspartner

1. Concurrent binding and modifications of AUF1 (zeige HNRNPD Antikörper) and HuR (zeige ELAVL1 Antikörper) mediate the pH-responsive stabilization of phosphoenolpyruvate carboxykinase mRNA in kidney cells.