Warburg Effect

Warburg Effect


In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed “the Warburg effect.” PKM2, but not PKM1, can be phosphorylated at Ser37 by ERK2 through the activation of EGF Receptor. The phosphorylated PKM2 translocates to nucleus and act as a coactivator of beta catenin to induce c-myc expression and results in PKM2-dependant GLUT1, LDHA and PTB upregulation.



TOP 3  WARBURG EFFECT must-haves

PKM2 Antibody

A: Jurkat, B: A549, C: U2OS

PKM2 is a glycolytic enzyme specifically over-expressed in cancer cells that catalyzes the transfer of a phosphoryl group from phosphoenolpyruvate (PEP) to ADP, generating ATP.

Reactivity: Human
Application: WB, IHC-P, IF/ICC



LDHA Antibody

LDHA catalyzes the conversion of L-lactate and NAD to pyruvate and NADH in the final step of anaerobic glycolysis. Mutation of LDHA has been found to be related to certain cancer types.

Reactivity: Human
Application: FACS, IHC, WB



GLUT1 Antibody

GLUT1 facilitates the transport of glucose across the plasma membranes of mammalian cells. Dysfunctional mutations may lead to GLUT1 deficiency syndrome, whereas overexpression of GLUT1 is a prognostic indicator for cancer.

Reactivity: Human, Mouse, Rat
Application: FACS, ICC/IF, WB, IHC-Fr, IHC-P