The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Specific Activity: 11 pmol/min/µg.
A 50 µl PKM2 reaction is conducted in a buffer containing 50 mM Tris (pH 7.4), 100mM MgCl2, 250 mM KCl, 40 mM ADP, 100 mM phosphoenolpyruvate (PEP) at room temperature for 15 min. ATP production is detected using Kinase-Glo Luminescent Kinase Assay Platform.
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Preparation and Storage
Stability and Storage
Shipped on Dry Ice. Upon delivery aliquot. Store at -80°C. Avoid freeze / thaw cycle.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Cytosolic thyroid hormone binding protein
Cytosolic thyroid hormone-binding protein
OPA interacting protein 3
Opa-interacting protein 3
PK muscle type
PK, muscle type
Pyruvate kinase 2/3
Pyruvate kinase 3
Pyruvate kinase isozymes M1/M2
Pyruvate kinase muscle
Pyruvate kinase muscle isozyme
pyruvate kinase PKM
Pyruvate kinase, muscle 2
Thyroid hormone binding protein 1
Thyroid hormone binding protein cytosolic
Thyroid hormone-binding protein 1
Tumor M2 PK
Glycolytic enzyme that catalyzes the transfer of a phosphoryl group from phosphoenolpyruvate (PEP) to ADP, generating ATP. Stimulates POU5F1-mediated transcriptional activation. Plays a general role in caspase independent cell death of tumor cells. The ratio between the highly active tetrameric form and nearly inactive dimeric form determines whether glucose carbons are channeled to biosynthetic processes or used for glycolytic ATP production. The transition between the 2 forms contributes to the control of glycolysis and is important for tumor cell proliferation and survival.
Specifically expressed in proliferating cells, such as embryonic stem cells, embryonic carcinoma cells, as well as cancer cells.
Carbohydrate degradation; glycolysis; pyruvate from D-glyceraldehyde 3-phosphate: step 5/5.
Belongs to the pyruvate kinase family.
Phosphorylated upon DNA damage, probably by ATM or ATR. ISGylated.
Cytoplasm. Nucleus. Translocates to the nucleus in response to different apoptotic stimuli. Nuclear translocation is sufficient to induce cell death that is caspase independent, isoform-specific and independent of its enzymatic actvity.