PCK1 Antibodies

Phosphoenolpyruvate carboxykinase, cytosolic [GTP] (PCK1)

Catalyzes the conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP), the rate-limiting step in the metabolic pathway that produces glucose from lactate and other precursors derived from the citric acid cycle. .

Gene Information

Human
Gene Name:	PCK1
Uniprot:	P35558
Entrez:	5105

Family

Belongs to:
phosphoenolpyruvate carboxykinase [GTP] family

Alternative Names

EC 4.1.1.32; MGC22652; PCK1; PEPCK1; PEPCKC; PEPCK-C; PEPCK-CPEP carboxykinase; phosphoenolpyruvate carboxykinase 1 (soluble); phosphoenolpyruvate carboxykinase, cytosolic [GTP]; phosphoenolpyruvate carboxykinase, cytosolic; Phosphoenolpyruvate carboxylase; phosphopyruvate carboxylase

Molecular Weight

Mass (kDA):
69.195 kDA

Genomic Context

Human
Location:	20q13.31
Sequence:	20; NC_000020.11 (57561110..57568121)

Tissue Specificity

Major sites of expression are liver, kidney and adipocytes.

Subcellular Localizations

Cytoplasm.

Diseases

• Diabetes Mellitus
• Diabetes Mellitus, Non-insulin-dependent
• Insulin Resistance
• Obesity
• Hyperglycemia
• Insulin Sensitivity
• Liver Carcinoma
• Inflammation
• Alzheimer's Disease
• Dyslipidemias
• Impaired Glucose Tolerance
• Hypoglycemia

• Cholangiocarcinoma
• Dysequilibrium Syndrome
• Fatty Liver
• Hyperinsulinism
• Impaired Cognition
• Atherosclerosis
• Hypertensive Disease

Pathways

• Gluconeogenesis
• Localization
• Pathogenesis
• Glucose Homeostasis
• Glyoxylate Cycle
• Cell Cycle
• Glycolysis
• Secretion
• Urea Cycle
• Lipid Homeostasis
• Cognition
• Mating
• Cell Morphogenesis

• Lactation
• Energy Homeostasis
• Dna Replication
• Regulation Of Gluconeogenesis
• Transport
• Aging
• Hypersensitivity

PTMs

• Phosphorylation
• Oxidation
• Acetylation
• Methylation
• Ubiquitination

• Carboxylation
• Reduction
• Deacetylation
• Decarboxylation
• Dephosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/PCK1

Best Uses Of The PCK1 Marker

Polymorphic microsatellite markers for PCK1 have been the subject of numerous studies, and a polymorphic microsatellite marker for PCK1 is no exception. This marker can be used to screen for recombination between PCK1 and the MODY gene, a homologous gene on mouse chromosome 2.

Synthetic peptides corresponding to PCK1

PCK1 is a critical enzyme for the biosynthesis of lipids, but there is little known about how it functions. It undergoes self-acetylation under high acetyl-CoA levels and is also involved in the regulation of glycolytic genes. Synthetic peptides corresponding to PCK1 markers can be used as molecular probes to identify these proteins.

Biological activity of Pck1 can be evaluated by using synthetic peptides corresponding to the gene's middle region. The sequence was extracted from a 69-kDa phosphoenolpyruvate carboxykinase protein. In this study, we have developed a peptide that is specific to PCK1.

Our results also suggest that PCK1 and PCK2 expression levels are differentially regulated in LUSC. Unidentified protein phosphatases were responsible for the increased PCK2 expression. These findings suggest that unidentified protein phosphatases alter the correlation status between PCK1 and AKT pS473.

Several studies have shown that pigs with a single nucleotide polymorphism have lower meat quality and less fat in their backfat. In addition, pigs with the p.139L enzyme have significantly reduced kcat values in both glyceroneogenic and anaplerotic directions. Furthermore, the expression of the enzyme results in 30% lower glucose production in cell cultures.

Metastases and primary tumors express PCK2 in a different manner. In addition, tumor-initiating cells also show heightened PCK2 expression than parental cells. The expression of PCK2 and GLUT1 were significantly associated with decreased tumor size and improved survival. It is important to note that PCK1/2 expression is closely regulated in the metabolic microenvironment in the tumor, including glucose levels and oxygenation.

Polymorphic microsatellite markers for PCK1

The genetic variation of PCK1 has been quantified by using 29 polymorphic microsatellite DNA loci in nine herds of plains and wood bison, two breeds of indicine cattle, and fourteen breeds of taurine cattle. Boster researchers have validated their product by using Western Blotting, Immunohistochemistry, and ELISA.

Gluconeogenesis

In the current study, we showed that PCK1 expression was upregulated in pancreatic cancer metastases and that tumor cells lacking this gene were more likely to be gluconeogenic. The mRNA of PCK1 was not upregulated in primary pancreatic cancer. Similarly, PCK2 expression was upregulated in pancreatic cancer metastases but not in skeletal muscle metastases. These results suggest that PCK1 and PCK2 may be regulated by similar mechanisms in hypoxia. More studies are needed to determine what regulates PCK1 and PCK2 expression in vivo.

Previous studies have shown that overexpression of the PCK1 gene results in excessive gluconeogenesis in the liver and kidney. Transgenic mice overexpressing the PCK1 gene in the liver develop a T2DM phenotype. Furthermore, PCK1 is considered a candidate gene for T2DM. These studies have implicated PCK1 as a potential gene for T2DM and suggest that overexpression of PCK1 leads to excessive gluconeogenesis in the liver.

Interestingly, PCK1 is closely associated with the incidence of type 2 diabetes. In the Guangxi minority, PCK1 has been associated with diabetes. It is therefore a genetic marker for this condition. The gene is primarily involved in glycolysis/gluconeogenesis. For example, a polymorphic PCK1 marker has been associated with type 2 diabetes in Guangxi, a minority population in China.

Moreover, a study in rats has shown that PEPCK mRNA levels are sixfold higher than normal in chronic acidosis-treated animals. In addition, the transcription rate of the PCK1 gene decreased over time in acidotic rats, plateauing at about twofold higher than normal ones. Therefore, a genetic test for PEPCK expression could be developed to identify the best targets for treatment.

AMPK

The PCK1 marker is a candidate gene for diabetes. It is an enzyme found in the liver, responsible for initiating the gluconeogenesis process. Glucocorticoids, glucagon, and insulin all control PCK1 expression. Several studies have also suggested that this gene is involved in the development of diabetes and obesity. The gene has also been implicated in obesity and type 2 diabetes.

Interestingly, the study also found an association between two PCK1 SNPs and T2D in a Chinese minority population. The findings suggest that interventions that lower the expression of the PCK1 gene may be effective in preventing or treating T2D. The role of oil tea consumption needs further study, especially in randomized controlled trials. Moreover, this study found that people who consumed oil tea had a higher risk of developing Type 2 diabetes than those who did not consume it.

The oil tea treatment reduced fasting blood glucose and total cholesterol levels. In addition, it reduced the expression of PCK1, a gene involved in the glycolysis/gluconeogenesis pathway. In a minority population of Guangxi, the PCK1 variant was significantly associated with type 2 diabetes. Thus, the PCK1 gene may serve as a marker for type 2 diabetes.

Insulin signaling pathway

The Moreoevaluated the role of the PCK1 gene in regulating the insulin signaling pathway. Cellular phenotypes were assessed using a phosphorylation assay. The expression of 48 genes involved in insulin signaling, lipolysis, and adipogenesis were studied. In addition, insulin receptor substrate 1 tyrosine phosphorylation was assessed. The results of the study indicate that OVE promotes a more positive energy balance, increased NEFA, and higher serum insulin concentration. Further, the mice that underwent OVE exhibited greater phosphorylation of the insulin receptors at a time point of day three compared with the mice who received the control treatment.