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Anti-ATP Synthase subunit beta Antibody, clone 11/21-7-A8 clone 11/21-7-A8, from mouse

ITEM#: 3042-MABS1304

MFR#: MABS1304

ATP synthase subunit beta, mitochondrial (EC 3.6.3.14; UniProt P06576; also known as ATP synthase H+ transporting mitochondrial F1 complex beta polypeptide, beta-F1-ATPase, Epididymis secretory protein Li 271, Mitochondrial ATP synthase beta subunit,

ATP synthase subunit beta, mitochondrial (EC 3.6.3.14; UniProt P06576; also known as ATP synthase H+ transporting mitochondrial F1 complex beta polypeptide, beta-F1-ATPase, Epididymis secretory protein Li 271, Mitochondrial ATP synthase beta subunit, Mitochondrial ATP synthetase beta subunit) is encoded by the ATP5B (also known as ATPMB, ATPSB, HEL-S-271) gene (Gene ID 506) in human. Mitochondrial ATP synthase produces ATP from ADP in the presence of a proton gradient generated by electron transport complexes. This ATPase contains two structural domains, F1-containing extramembrane catalytic core, and F0-containing the membrane proton channel that are linked via a central stalk and a peripheral stalk. Subunits alpha and beta form the catalytic code in F1. Tumor development requires the selection of cancer cells with a repressed biogenesis and functional activity of mitochondria. Both beta-F1-ATPase/GAPDH and beta-F1-ATPase/Hsp60 ratios are found to be significantly lower in tumors than the corresponding normal tissues. Studies conducted in human colon cancer cell line HCT116 show the involvement of AMPK (AMP-activated protein kinase) and GCN2 (general control non-derepressible 2; eIF2alpha kinase) in the onset of colon cancer progression by repressing of beta-F1-ATPase synthesis and promoting the abnormal bioenergetics of mitochondria.