NA13
Anti-Replication Protein A (Ab-1) Mouse mAb (RPA70-9)
liquid, clone RPA70-9, Calbiochem®
Synonym(e):
Anti-RP-A
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Alle Fotos(1)
About This Item
UNSPSC-Code:
12352203
NACRES:
NA.41
Empfohlene Produkte
Biologische Quelle
mouse
Qualitätsniveau
Antikörperform
purified antibody
Antikörper-Produkttyp
primary antibodies
Klon
RPA70-9, monoclonal
Form
liquid
Enthält
≤0.1% sodium azide as preservative
Speziesreaktivität
human, yeast
Hersteller/Markenname
Calbiochem®
Lagerbedingungen
do not freeze
Isotyp
IgG2a
Versandbedingung
wet ice
Lagertemp.
2-8°C
Posttranslationale Modifikation Target
unmodified
Angaben zum Gen
human ... RPA1(6117)
Allgemeine Beschreibung
Purified mouse monoclonal antibody generated by immunizing BALB/c mice with the specified immunogen and fusing splenocytes with the NS1 myeloma cell line. Recognizes the ~70 kDa Replication Protein A.
Recognizes the ~70 kDa subunit of replication protein A in HeLa and u293 cells and colon carcinoma tissue.
This Anti-Replication Protein A (Ab-1) Mouse mAb (RPA70-9) is validated for use in Frozen Sections, Immunoblotting, IF, IP, Paraffin Sections for the detection of Replication Protein A (Ab-1).
Immunogen
Epitope: Within the p70 subunit of replication protein A
Human
replication protein A purified from U293 cells
Anwendung
Frozen Sections (2.5 g/ml)
Immunoblotting (1-5 g/ml)
Immunofluorescence (2.5 g/ml)
Immunoprecipitation (1 g/reaction)
Paraffin Sections (2.5 g/ml, no pre-treatment required)
Verpackung
Please refer to vial label for lot-specific concentration.
Warnhinweis
Toxicity: Standard Handling (A)
Physikalische Form
In 0.05 M sodium phosphate buffer, 0.2% gelatin.
Hinweis zur Analyse
Positive Control
HeLa or U293 cells or colon carcinoma tissue
HeLa or U293 cells or colon carcinoma tissue
Sonstige Hinweise
Din, S., et al. 1990. Genes Dev.4, 968.
Brill, S.J. and Stillman, B., 1989. Nature342, 92.
Stillman, B., 1989. Annu. Rev. Cell. Biol.5, 197.
Tsurimoto, T. and Stillman, B., 1989. EMBO J.8, 3883.
Wobbe, C.R., et al. 1987. Proc. Natl. Acad. Sci. USA84, 1834.
Brill, S.J. and Stillman, B., 1989. Nature342, 92.
Stillman, B., 1989. Annu. Rev. Cell. Biol.5, 197.
Tsurimoto, T. and Stillman, B., 1989. EMBO J.8, 3883.
Wobbe, C.R., et al. 1987. Proc. Natl. Acad. Sci. USA84, 1834.
Specific for the p70 subunit of replication protein A. This antibody can be used as a marker for proliferation. Antibody should be titrated for optimal results in individual systems.
Rechtliche Hinweise
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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Lagerklassenschlüssel
11 - Combustible Solids
WGK
WGK 1
Flammpunkt (°F)
Not applicable
Flammpunkt (°C)
Not applicable
Analysenzertifikate (COA)
Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.
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Molecular and cellular biology, 25(9), 3814-3830 (2005-04-16)
The human stress-activated protein kin17 accumulates in the nuclei of proliferating cells with predominant colocalization with sites of active DNA replication. The distribution of kin17 protein is in equilibrium between chromatin-DNA and the nuclear matrix. An increased association with nonchromatin
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Journal of cell science, 124(Pt 1), 68-81 (2010-12-02)
DNA damage can induce a tumor suppressive response termed cellular senescence. Damaged senescent cells permanently arrest growth, secrete inflammatory cytokines and other proteins and harbor persistent nuclear foci that contain DNA damage response (DDR) proteins. To understand how persistent damage
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S(N)1-type alkylating agents that produce cytotoxic O(6)-methyl-G (O(6)-meG) DNA adducts induce cell cycle arrest and apoptosis in a manner requiring the DNA mismatch repair (MMR) proteins MutSalpha and MutLalpha. Here, we show that checkpoint signaling in response to DNA methylation
S Buchsbaum et al.
Oncogene, 26(35), 5132-5144 (2007-02-22)
The mouse int6 gene is a frequent integration site of the mouse mammary tumor virus and INT6 silencing by RNA interference in HeLa cells causes an increased number of cells in the G2/M phases of the cell cycle, along with
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Human molecular genetics, 25(8), 1574-1587 (2016-02-26)
Mutations in ATR(ataxia telangiectasia and RAD3-related) cause Seckel syndrome (ATR-SS), a microcephalic primordial dwarfism disorder. Hitherto, the clinical manifestation of ATR deficiency has been attributed to its canonical role in DNA damage response signalling following replication fork stalling/collapse. Here, we
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