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Merck

NA13

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

liquid, clone RPA70-9, Calbiochem®

동의어(들):

Anti-RP-A

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제품정보 (DICE 배송 시 비용 별도)

NACRES:
NA.41
UNSPSC Code:
12352203
기술 서비스
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제품 이름

Anti-Replication Protein A (Ab-1) Mouse mAb (RPA70-9), liquid, clone RPA70-9, Calbiochem®

biological source

mouse

antibody form

purified antibody

antibody product type

primary antibodies

clone

RPA70-9, monoclonal

form

liquid

contains

≤0.1% sodium azide as preservative

species reactivity

human, yeast

manufacturer/tradename

Calbiochem®

storage condition

do not freeze

dilution

(Frozen Sections (2.5 µg/mL)
Immunoblotting (1-5 µg/mL)
Immunofluorescence (2.5 µg/mL)
Immunoprecipitation (1 µg/reaction)
Paraffin Sections (2.5 µg/mL, no pre-treatment required))

isotype

IgG2a

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... RPA1(6117)

Analysis Note

Positive Control
HeLa or U293 cells or colon carcinoma tissue

Application


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)

Disclaimer

Toxicity: Standard Handling (A)

General description

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

Other Notes

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.

Packaging

Please refer to vial label for lot-specific concentration.

Physical form

In 0.05 M sodium phosphate buffer, 0.2% gelatin.

Legal Information

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

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저장 등급

11 - Combustible Solids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


시험 성적서(COA)

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문서 라이브러리에서 최근에 구매한 제품에 대한 문서를 찾아보세요.

문서 라이브러리 방문

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
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
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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NA13-100UGCN04055977227659

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