Anti-AAG/MPG Antibody Picoband® Fluoro647 Conjugated

MPG (N-methylpurine-DNA glycosylase) also known as MDG, 3-METHYLADENINE DNA GLYCOSYLASE, 3MeAde DNA GLYCOSYLASE, AAG or APNG. The MPG gene is mapped to human chromosome 16 by analysis of a panel of DNAs from mouse/human and hamster/human hybrid cell lines.TheMPGgene was expressed in all cell lines and tissues examined, but was found at particularly high levels in a colon adenocarcinoma cell line (HT29) . The completely characterized humanMPGgene was found to span 7 to 8 kb of genomic DNA and to be localized 75 kb upstream of the embryonic zeta-globin gene. To assess the contribution of Apng to the repair of several mutagenic lesions in vivo, Hang et al. (1997) biochemically analyzed cell-free extracts of tissues from mice with a targeted deletion of the Apng gene. Following treatment with DNA-methylating agents, increased persistence of 7-methylguanine (meG) was found in liver sections of APNG knockout mice in comparison with wildtype mice, demonstrating an in vivo phenotype for the APNG-null animals.

Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs), cytokine KITLG/SCF and other cytokines and other growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize and associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of IFN- stimulated genes (ISG), which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN- gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4. .

1. Boosalis, M., Derfler, B., Call, K., Samson, L. Cloning of a human 3-methyladenine DNA glycosylase cDNA whose gene maps to human chromosome 16. (Abstract) Am. J. Hum. Genet. 49 (suppl.) : 399 only, 1991. 2. Engelward, B. P., Weeda, G., Wyatt, M. D., Broekhof, J. L. M., de Wit, J., Donker, I., Allan, J. M., Gold, B., Hoeijmakers, J. H. J., Samson, L. D.Base excision repair deficient mice lacking the Aag alkyladenine DNA glycosylase. Proc. Nat. Acad. Sci. 94: 13087-13092, 1997. 3. Kielman, M. F., Smits, R., Bernini, L. F. Localization and characterization of the mouse alpha-globin locus control region. Genomics 21: 431-433, 1994.

Cytoplasm . Nucleus . Translocated into the nucleus upon tyrosine phosphorylation and dimerization, in response to IFN-gamma and signaling by activated FGFR1, FGFR2, FGFR3 or FGFR4.