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NA13

Sigma-Aldrich

Anti-Replication Protein A (Ab-1) Mouse mAb (RPA70-9)

liquid, clone RPA70-9, Calbiochem®

Synonim(y):

Anti-RP-A

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About This Item

Kod UNSPSC:
12352203
NACRES:
NA.41

pochodzenie biologiczne

mouse

Poziom jakości

forma przeciwciała

purified antibody

rodzaj przeciwciała

primary antibodies

klon

RPA70-9, monoclonal

Postać

liquid

zawiera

≤0.1% sodium azide as preservative

reaktywność gatunkowa

human, yeast

producent / nazwa handlowa

Calbiochem®

warunki przechowywania

do not freeze

izotyp

IgG2a

Warunki transportu

wet ice

temp. przechowywania

2-8°C

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

human ... RPA1(6117)

Opis ogólny

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

Zastosowanie


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)

Opakowanie

Please refer to vial label for lot-specific concentration.

Ostrzeżenie

Toxicity: Standard Handling (A)

Postać fizyczna

In 0.05 M sodium phosphate buffer, 0.2% gelatin.

Komentarz do analizy

Positive Control
HeLa or U293 cells or colon carcinoma tissue

Inne uwagi

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.
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.

Informacje prawne

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

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Kod klasy składowania

11 - Combustible Solids

Klasa zagrożenia wodnego (WGK)

WGK 1

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable


Certyfikaty analizy (CoA)

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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

Laurent Miccoli et al.
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
Francis Rodier et al.
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
Ken-ichi Yoshioka et al.
Molecular cell, 22(4), 501-510 (2006-05-23)
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
Tom Stiff et al.
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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