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Wählen Sie konfigurierbare Panels & Premixed-Kits - ODER - Kits für die zelluläre Signaltransduktion & MAPmates™
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Kits für die zelluläre Signaltransduktion & MAPmates™
Wählen Sie gebrauchsfertige Kits zur Erforschung gesamter Signalwege oder Prozesse. Oder konfigurieren Sie Ihre eigenen Kits mit Singleplex MAPmates™.
Die folgenden MAPmates™ sollten nicht zusammen analysiert werden: -MAPmates™, die einen unterschiedlichen Assaypuffer erfordern. -Phosphospezifische und MAPmate™ Gesamtkombinationen wie Gesamt-GSK3β und Gesamt-GSK3β (Ser 9). -PanTyr und locusspezifische MAPmates™, z.B. Phospho-EGF-Rezeptor und Phospho-STAT1 (Tyr701). -Mehr als 1 Phospho-MAPmate™ für ein einziges Target (Akt, STAT3). -GAPDH und β-Tubulin können nicht mit Kits oder MAPmates™, die panTyr enthalten, analysiert werden.
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Gewähltes Kit
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96-Well Plate
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Weitere Reagenzien hinzufügen (MAPmates erfordern die Verwendung eines Puffer- und Detektionskits)
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
Platzsparende Option Kunden, die mehrere Kits kaufen, können ihre Multiplex-Assaykomponenten in Kunststoffbeuteln anstelle von Packungen erhalten, um eine kompaktere Lagerung zu ermöglichen.
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Tumor suppressor p53-binding protein 1 (also known as 53BP1, p202, p53-binding protein 1, p53BP1) is encoded by the TP53BP1 gene (Entrez Gene ID 7158) in human. 53BP1 is a multidomain nonhomologous end joining (NHEJ) factor involved in the repair of double-strand DNA breaks (DSBs). The minimal region (residues 1,220–1,711) required for its recruitment includes the oligomerization domain, the tudor domain, and a carboxy-terminal extension termed the ubiquitination-dependent recruitment (UDR) motif. However, 53BP1 function must be inactivated during mitosis to prevent its interference with homologous recombination (NR). 53BP1 inactivation during mitosis is shown to be achieved by p38-dependent pT1609 and PLK-1-dependent pT1618 phosphorylation within the UDR motif. Reactivating 53BP1 function results in severe mitotic defects (PMID 24703952 & 24652939). Cat. No. ABE1446, Anti-phospho-53BP1 (Thr1609/Ser1618) is a rabbit polyclonal antiserum raised against human 53BP1-derived phosphopeptide encompassing pT1609/pS1618 phosphorylation site sequence (PMID 24703952) present in all three 53BP1 isoforms (UniProt Q12888). This antiserum recognizes 53BP1 only when both Thr1609/Ser1618 residues are phosphorylated, but not either one alone (PMID 24703952). The sequence surrounding the phosphorylation sites is 100% conserved among human, mouse, rat, equine, bovine species. Due to the large target protein size (~450 kDa), low percentage gels, such as 3% agarose or 6% polyacrylamide, are recommended to facilitate electrophoresis and transfer prior to Western blotting.
References
Product Information
Format
Serum
Presentation
Rabbit polyclonal serum with 0.09% sodium azide and 50% glycerol.
Anti-phospho-53BP1 Antibody is an antibody against phospho-53BP1 for use in Western Blotting.
Key Applications
Western Blotting
Application Notes
Western Blotting Analysis: A representative lot detected phospho-53BP1 (Thr1609/Ser1618) in HeLa cells synchronized in mitosis, HeLa cells expressing FH-53BP1 WT or phosphomutants were synchronized in mitosis and harvested by mitotic shake-off (Lee, D.H., et al. (2014). Mol. Cell. 54(3):512-525). Western Blotting Analysis: A representative lot detected phospho-53BP1 (Thr1609/Ser1618) in U2OS blocked at G1/S (Orthwein, A., et al. (2014). Science. 344:189-193).
Biological Information
Immunogen
Linear peptide corresponding to human phospho-53BP1 (Thr1609/Ser1618).
Epitope
Phosphorylated Thr1609 and phosphorylated Ser1618
Concentration
Please refer to lot specific datasheet.
Host
Rabbit
Species Reactivity
Human
Species Reactivity Note
Human. Predicted to react with Mouse, Bovine based on 100% sequence homology.
~430 kDa observed. Uncharacterized band(s) may appear in some lysates.
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blotting using G1 or mitotic HeLa cell lysate.
Western Blotting Analysis: A 1:5,000 dilution of this antibody detected phospho-53BP1 (Thr1609/Ser1618) in 10 µg from mitotic, but not G1, HeLa cell lysate.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Storage and Shipping Information
Storage Conditions
Stable for 1 year at -20°C from date of receipt. Handling Recommendations: Upon receipt and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerol containing solutions to become frozen during storage.
Mitotic cells inactivate DNA double-strand break (DSB) repair, but the rationale behind this suppression remains unknown. Here, we unravel how mitosis blocks DSB repair and determine the consequences of repair reactivation. Mitotic kinases phosphorylate the E3 ubiquitin ligase RNF8 and the nonhomologous end joining factor 53BP1 to inhibit their recruitment to DSB-flanking chromatin. Restoration of RNF8 and 53BP1 accumulation at mitotic DSB sites activates DNA repair but is, paradoxically, deleterious. Aberrantly controlled mitotic DSB repair leads to Aurora B kinase-dependent sister telomere fusions that produce dicentric chromosomes and aneuploidy, especially in the presence of exogenous genotoxic stress. We conclude that the capacity of mitotic DSB repair to destabilize the genome explains the necessity for its suppression during mitosis, principally due to the fusogenic potential of mitotic telomeres.
Excluding 53BP1 from chromatin is required to attenuate the DNA damage response during mitosis, yet the functional relevance and regulation of this exclusion are unclear. Here we show that 53BP1 is phosphorylated during mitosis on two residues, T1609 and S1618, located in its well-conserved ubiquitination-dependent recruitment (UDR) motif. Phosphorylating these sites blocks the interaction of the UDR motif with mononuclesomes containing ubiquitinated histone H2A and impedes binding of 53BP1 to mitotic chromatin. Ectopic recruitment of 53BP1-T1609A/S1618A to mitotic DNA lesions was associated with significant mitotic defects that could be reversed by inhibiting nonhomologous end-joining. We also reveal that protein phosphatase complex PP4C/R3β dephosphorylates T1609 and S1618 to allow the recruitment of 53BP1 to chromatin in G1 phase. Our results identify key sites of 53BP1 phosphorylation during mitosis, identify the counteracting phosphatase complex that restores the potential for DDR during interphase, and establish the physiological importance of this regulation.
