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anti-Human PCK1 Antibodies:
anti-Mouse (Murine) PCK1 Antibodies:
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ApoA-IV (show APOA4 Antibodies) colocalizes with NR4A1 (show NR4A1 Antibodies), which suppresses G6Pase (show G6PC Antibodies) and PEPCK (show PEPCK Antibodies) gene expression at the transcriptional level, reducing hepatic glucose output and lowering blood glucose.
Results indicate that PEPCK (show PEPCK Antibodies) promotes tumor growth by increasing glucose and glutamine (show GFPT1 Antibodies) metabolism, increases anabolic metabolism and promotes mTORC1 activity.
Mitochondrial PCK2 (show PEPCK Antibodies) regulates metabolic adaptation and enables glucose-independent tumor growth in various neoplasms.
When autophagy was blocked, the level of glucose-6-phosphatase (G6Pase (show G6PC Antibodies)) and phosphoenolpyruvate carboxykinase (PEPCK (show PEPCK Antibodies)) was reduced in HepG2 cells and not in Hep3B cells.
PEPCK (show PEPCK Antibodies) activity was elevated threefold in lung cancer samples over normal lungs and its activation mediates an adaptive response to glucose depletion in lung cancer.
Amino acid limitation and ER stress inducers, conditions that activate the amino acid response (AAR) and the unfolded protein response (UPR), stimulate PCK2 (show PEPCK Antibodies) gene transcription in tumor cell lines.
Expression of phosphoenolpyruvate carboxykinase (show PEPCK Antibodies) linked to chemoradiation susceptibility of human colon cancer cells.
expression of HCV nonstructural component NS5A in Huh7 or primary hepatocytes stimulated PEPCK (show PEPCK Antibodies) gene expression and glucose output in HepG2 cells.
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
Endoplasmic reticulum stress triggers suppression of AMPK (show PRKAA1 Antibodies) while increasing C/EBPbeta (show CEBPB Antibodies) and pCREB expression which activates PEPCK (show PEPCK Antibodies) gene transcription.
Lactate maintains/induces populations of postnatal neuronal progenitors/neural stem cells in a PEPCK-M (show PEPCK Antibodies)-dependent manner
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.
Data show that PEPCK-M (show PEPCK Antibodies) message and protein were detected in islets.
Concurrent binding and modifications of AUF1 (show HNRNPD Antibodies) and HuR (show ELAVL1 Antibodies) mediate the pH-responsive stabilization of phosphoenolpyruvate carboxykinase (show PEPCK Antibodies) mRNA in kidney cells.
Transition to lactation does not alter expression of the mitochondrial form of PEPCK (show PEPCK Antibodies).
This gene encodes a member of the phosphoenolpyruvate carboxykinase (GTP) family. The protein is a mitochondrial enzyme that catalyzes the conversion of oxaloacetate to phosphoenolpyruvate in the presence of GTP. A cytosolic form encoded by a different gene has also been characterized and is the key enzyme of gluconeogenesis in the liver. The encoded protein may serve a similar function, although it is constitutively expressed and not modulated by hormones such as glucagon and insulin that regulate the cytosolic form. Alternatively spliced transcript variants have been described.
, phosphoenolpyruvate carboxykinase [GTP], mitochondrial
, phosphoenolpyruvate carboxylase
, phosphopyruvate carboxylase