Western Blot: Pyruvate Carboxylase Antibody [NBP1-49536] - Analysis of Pyruvate Carboxylase in A. Human liver extracts and B. Mouse liver extracts
Immunocytochemistry/ Immunofluorescence: Pyruvate Carboxylase Antibody [NBP1-49536] - Immunocytochemistry of Pyruvate Carboxylase in HeLa using NBP1-49536. Nuclei (Blue) are counterstained using Hoechst 33258.
Immunohistochemistry: Pyruvate Carboxylase Antibody [NBP1-49536] - Analysis of Pyruvate Carboxylase in mouse kidney and mouse fat.
Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.
PBS, 0.1% BSA, 50% glycerol
0.05% Sodium Azide
Immunogen affinity purified
This Pyruvate Carboxylase antibody is useful for Immunohistochemistry on paraffin-embedded sections, Immunocytochemistry/Immunofluorescence and Western blot, where a band is seen at ~129 kDa. The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
Read Publications using NBP1-49536 in the following applications:
Human and mouse. Immunogen has 96% identity to bovine and porcine. Rat reactivity reported in scientific literature (PMID: 24333689)
Alternate Names for Pyruvate Carboxylase Antibody
pyruvate carboxylase, mitochondrial
Pyruvate Carboxylase (PC) catalyzes an important 2-step reaction - (i) ATP-dependent carboxylation of covalently attached biotin (ii) transfer of carboxyl group to pyruvate, and this interconversion is essential for replenishment of TCA/citric acid cycle intermediates (anaplerosis). By extension, PC participates in many pathways that depend on oxaloacetate (OAA) such as gluconeogenesis, glycogen synthesis, lipogenesis, glycerogenesis, glucose-dependent insulin secretion, and synthesis of amino acids as well as neurotransmitters. With highest expression levels in liver, adipose tissue, kidney, lactating mammary gland, pancreatic islets etc, PC localize to cellular mitochondrial matrix and its activity is highly regulated by its allosteric activator acetyl-CoA. Enhanced acetyl-CoA levels indicate a need for increased OAA synthesis to replenish TCA cycle intermediates or a diversion of pyruvate for glucose synthesis in gluconeogenic tissues. PC's deficiency causes a fatal multiorgan metabolic imbalance that predominantly manifests with lactic acidemia and neurological dysfunction at an early age. Three clinical forms of PC deficiency include an infantile or mild form (Type A), a severe neonatal form (Type B), and a benign form (Type C), all of which exhibit clinical or biochemical parallals of impaired anaplerosis.
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.