Anti-Glutaminase/GLS Antibody Picoband® (monoclonal, 9G6)

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.

Ubiquitin carboxyl-terminal hydrolase 7; Deubiquitinating enzyme 7; Herpesvirus-associated ubiquitin-specific protease; Ubiquitin thioesterase 7; Ubiquitin-specific-processing protease 7

Cancer, Cell Biology, Cell Cycle, Cell Cycle Inhibitors, Deubiquitination, Epigenetics and Nuclear Signaling, Host-Virus Interaction, Interspecies Interaction, Microbiology, p53 Pathway, Proteasome / Ubiquitin, Proteolysis/Ubiquitin, Ubiquitin & Ubiquitin Like Modifiers

Hydrolase that deubiquitinates target proteins such as FOXO4, p53/TP53, MDM2, ERCC6, DNMT1, UHRF1, PTEN, KMT2E/MLL5 and DAXX. Together with DAXX, prevents MDM2 self-ubiquitination and enhances the E3 ligase activity of MDM2 towards p53/TP53, thereby promoting p53/TP53 ubiquitination and proteasomal degradation. Deubiquitinates p53/TP53, preventing degradation of p53/TP53, and enhances p53/TP53-dependent transcription regulation, cell growth repression and apoptosis. Deubiquitinates p53/TP53 and MDM2 and strongly stabilizes p53/TP53 even in the presence of excess MDM2, and also induces p53/TP53-dependent cell growth repression and apoptosis. Deubiquitination of FOXO4 in presence of hydrogen peroxide is not dependent on p53/TP53 and inhibits FOXO4-induced transcriptional activity. In association with DAXX, is involved in the deubiquitination and translocation of PTEN from the nucleus to the cytoplasm, both processes that are counteracted by PML. Deubiquitinates KMT2E/MLL5 preventing KMT2E/MLL5 proteasomal-mediated degradation . Involved in cell proliferation during early embryonic development. Involved in transcription-coupled nucleotide excision repair (TC-NER) in response to UV damage: recruited to DNA damage sites following interaction with KIAA1530/UVSSA and promotes deubiquitination of ERCC6, preventing UV-induced degradation of ERCC6. Involved in maintenance of DNA methylation via its interaction with UHRF1 and DNMT1: acts by mediating deubiquitination of UHRF1 and DNMT1, preventing their degradation and promoting DNA methylation by DNMT1. Deubiquitinates alkylation repair enzyme ALKBH3. OTUD4 recruits USP7 and USP9X to stabilize ALKBH3, thereby promoting the repair of alkylated DNA lesions. Acts as a chromatin regulator via its association with the Polycomb group (PcG) multiprotein PRC1-like complex; may act by deubiquitinating components of the PRC1-like complex. Able to mediate deubiquitination of histone H2B; it is however unsure whether this activity takes place in vivo. Exhibits a preference towards 'Lys-48'-linked ubiquitin chains. Increases regulatory T-cells (Treg) suppressive capacity by deubiquitinating and stabilizing the transcription factor FOXP3 which is crucial for Treg cell function. (Microbial infection) Contributes to the overall stabilization and trans-activation capability of the herpesvirus 1 trans-acting transcriptional protein ICP0/VMW110 during HSV-1 infection.

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.

At -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freezing and thawing.