NewEast Biosciences pioneered the research and development of the antibodies for GTPases and mutated Oncogene ten years ago. GTPases involve (1) signal transduction in response to activation of cell surface receptors, including transmembrane receptors such as those mediating taste, smell and vision, (2) protein biosynthesis at the ribosome, (3) regulation of cell differentiation, proliferation, division and movement, (4) translocation of proteins through membranes, (5) transport of vesicles within the cell, and vesicle-mediated secretion and uptake, through GTPase control of vesicle coat assembly. An oncogene is a gene that has the potential to cause cancer.
We offer three unique categories of antibodies, which (1) recognize only the active configuration of GTPase (not the inactive one), (2) mutated Oncogene (not mild type) and (3) have super affinity for cAMP and cGMP (no acetylation required). We have over one thousand peer reviewed articles cited our products.
$349.00
Cat.#: N262117 |
Product Name: Anti-DBC 1 Rabbit Monoclonal Antibody |
Synonyms: DBC1; DBC-1; NET35; p30DBC; p30 DBC; KIAA1967 |
UNIPROT ID: Q8N163 |
Background: Core component of the DBIRD complex, a multiprotein complex that acts at the interface between core mRNP particles and RNA polymerase II (RNAPII) and integrates transcript elongation with the regulation of alternative splicing: the DBIRD complex affects local transcript elongation rates and alternative splicing of a large set of exons embedded in (A + T)-rich DNA regions. Inhibits SIRT1 deacetylase activity leading to increasing levels of p53/TP53 acetylation and p53-mediated apoptosis. Inhibits SUV39H1 methyltransferase activity. As part of a histone H3-specific methyltransferase complex may mediate ligand-dependent transcriptional activation by nuclear hormone receptors. Plays a critical role in maintaining genomic stability and cellular integrity following UV-induced genotoxic stress. Regulates the circadian expression of the core clock components NR1D1 and ARNTL/BMAL1. Enhances the transcriptional repressor activity of NR1D1 through stabilization of NR1D1 protein levels by preventing its ubiquitination and subsequent degradation (PubMed:18235501, PubMed:18235502, PubMed:19131338, PubMed:19218236, PubMed:22446626, PubMed:23352644, PubMed:23398316). Represses the ligand-dependent transcriptional activation function of ESR2 (PubMed:20074560). Acts as a regulator of PCK1 expression and gluconeogenesis by a mechanism that involves, at least in part, both NR1D1 and SIRT1 (PubMed:24415752). Negatively regulates the deacetylase activity of HDAC3 and can alter its subcellular localization (PubMed:21030595). Positively regulates the beta-catenin pathway (canonical Wnt signaling pathway) and is required for MCC-mediated repression of the beta-catenin pathway (PubMed:24824780). Represses ligand-dependent transcriptional activation function of NR1H2 and NR1H3 and inhibits the interaction of SIRT1 with NR1H3 (PubMed:25661920). Plays an important role in tumor suppression through p53/TP53 regulation; stabilizes p53/TP53 by affecting its interaction with ubiquitin ligase MDM2 (PubMed:25732823). Represses the transcriptional activator activity of BRCA1 (PubMed:20160719). Inhibits SIRT1 in a CHEK2 and PSEM3-dependent manner and inhibits the activity of CHEK2 in vitro (PubMed:25361978). |
Immunogen: A synthetic peptide of human DBC-1 |
Applications: WB,IHC-F,IHC-P,ICC/IF,IP |
Recommended Dilutions: WB: 1/500-1/1000 IHC: 1/50-1/100 IF: 1/50-1/200 IP: 1/20 |
Host Species: Rabbit |
Clonality: Rabbit Monoclonal |
Clone ID: R09-8K9 |
MW: Calculated MW: 103 kDa; Observed MW: 130 kDa |
Isotype: IgG |
Purification: Affinity Purified |
Species Reactivity: Human |
Conjugation: Unconjugated |
Modification: Unmodified |
Constituents: PBS (without Mg2+ and Ca2+), pH 7.3 containing 50% glycerol, 0.5% BSA and 0.02% sodium azide |
Research Areas: Epigenetics and Nuclear Signaling |
Storage & Shipping: Store at -20°C. Avoid repeated freezing and thawing |
Western blot analysis of DBC1 in 293, Jurkat lysates using DBC 1 antibody. |