Anti-Glutaminase/GLS Antibody Picoband® Fluoro647 Conjugated

This gene encodes the K-type mitochondrial glutaminase. The encoded protein is an phosphate-activated amidohydrolase that catalyzes the hydrolysis of glutamine to glutamate and ammonia. This protein is primarily expressed in the brain and kidney plays an essential role in generating energy for metabolism, synthesizing the brain neurotransmitter glutamate and maintaining acid-base balance in the kidney. Alternate splicing results in multiple transcript variants.

Metabolism, Metabolism Of Carbohydrates, Methylation, Mitochondrial, Mitochondrial Markers, Mitochondrial Metabolism, Oncoproteins/Suppressors, Pathways and Processes, Signal Transduction, Tumor Suppressors

Kinase that plays a key role in regulation of glucose and fatty acid metabolism and homeostasis via phosphorylation of the pyruvate dehydrogenase subunits PDHA1 and PDHA2. This inhibits pyruvate dehydrogenase activity, and thereby regulates metabolite flux through the tricarboxylic acid cycle, down-regulates aerobic respiration and inhibits the formation of acetyl-coenzyme A from pyruvate. Plays an important role in cellular responses to hypoxia and is important for cell proliferation under hypoxia. Protects cells against apoptosis in response to hypoxia and oxidative stress.

1. Lynch, D. S., Chelban, V., Vandrovcova, J., Pittman, A., Wood, N. W., Houlden, H. GLS loss of function causes autosomal recessive spastic ataxia and optic atrophy. Ann. Clin. Transl. Neurol. 5: 216-221, 2018. 2. Modi, W. S., Pollock, D. D., Mock, B. A., Banner, C., Renauld, J.-C., Van Snick, J. Regional localization of the human glutaminase (GLS) and interleukin-9 (IL9) genes by in situ hybridization. Cytogenet. Cell Genet. 57: 114-116, 1991. 3. Rumping, L., Tessadori, F., Pouwels, P. J. W., Vringer, E., Wijnen, J. P., Bhogal, A. A., Savelberg, S. M. C., Duran, K. J., Bakkers, M. J. G., Ramos, R. J. J., Schellekens, P. A. W., Kroes, H. Y., and 16 others. GLS hyperactivity causes glutamate excess, infantile cataract and profound developmental delay. Hum. Molec. Genet. 28: 96-104, 2019.