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anti-Human PCK1 Antikörper:
anti-Mouse (Murine) PCK1 Antikörper:
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Downregulation of PCK2 (zeige PEPCK Antikörper) remodels tricarboxylic acid cycle in tumor-repopulating cells of melanoma
ApoA-IV (zeige APOA4 Antikörper) colocalizes with NR4A1 (zeige NR4A1 Antikörper), which suppresses G6Pase (zeige G6PC Antikörper) and PEPCK (zeige PEPCK Antikörper) gene expression at the transcriptional level, reducing hepatic glucose output and lowering blood glucose.
Results indicate that PEPCK (zeige PEPCK Antikörper) promotes tumor growth by increasing glucose and glutamine (zeige GFPT1 Antikörper) metabolism, increases anabolic metabolism and promotes mTORC1 activity.
Mitochondrial PCK2 (zeige PEPCK Antikörper) regulates metabolic adaptation and enables glucose-independent tumor growth in various neoplasms.
When autophagy was blocked, the level of glucose-6-phosphatase (G6Pase (zeige G6PC Antikörper)) and phosphoenolpyruvate carboxykinase (PEPCK (zeige PEPCK Antikörper)) was reduced in HepG2 cells and not in Hep3B cells.
PEPCK (zeige PEPCK Antikörper) 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 (zeige PEPCK Antikörper) gene transcription in tumor cell lines.
Expression of phosphoenolpyruvate carboxykinase (zeige PEPCK Antikörper) linked to chemoradiation susceptibility of human colon cancer cells.
expression of HCV nonstructural component NS5A in Huh7 or primary hepatocytes stimulated PEPCK (zeige PEPCK Antikörper) 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
Lactate maintains/induces populations of postnatal neuronal progenitors/neural stem cells in a PEPCK-M (zeige PEPCK Antikörper)-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 (zeige PEPCK Antikörper) message and protein were detected in islets.
Transition to lactation does not alter expression of the mitochondrial form of PEPCK (zeige PEPCK Antikörper).
Concurrent binding and modifications of AUF1 (zeige HNRNPD Antikörper) and HuR (zeige ELAVL1 Antikörper) mediate the pH-responsive stabilization of phosphoenolpyruvate carboxykinase (zeige PEPCK Antikörper) mRNA in kidney cells.
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