FunctionCatalyzes 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.
Involvement in diseaseDefects in PCK2 are the cause of mitochondrial phosphoenolpyruvate carboxykinase deficiency (M-PEPCKD) [MIM:261650]. A metabolic disorder resulting from impaired gluconeogenesis. It is a rare disease with less than 10 cases reported in the literature. Clinical characteristics include hypotonia, hepatomegaly, failure to thrive, lactic acidosis and hypoglycemia. Autoposy reveals fatty infiltration of both the liver and kidneys. The disorder is transmitted as an autosomal recessive trait.
Sequence similaritiesBelongs to the phosphoenolpyruvate carboxykinase [GTP] family.
Post-translational modificationsPhosphorylated upon DNA damage, probably by ATM or ATR.
Anti-PCK2 antibody (ab77047) at 1/500 dilution + A-431 cell lysate at 25 µg
Secondary goat anti-kouse IgG (H&L)-HRP conjugate at 1/2500 dilution
Predicted band size : 71 kDa Observed band size : 71 kDa
References for Anti-PCK2 antibody (ab77047)
This product has been referenced in:
Leithner K et al. PCK2 activation mediates an adaptive response to glucose depletion in lung cancer. OncogeneN/A:N/A (2014).
Read more (PubMed: 24632615) »
Martin SA et al. Parallel high-throughput RNA interference screens identify PINK1 as a potential therapeutic target for the treatment of DNA mismatch repair-deficient cancers. Cancer Res71:1836-48 (2011).
Read more (PubMed: 21242281) »