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Documenti fondamentali

553510

Sigma-Aldrich

RAD51-Stimulatory Compound-1, RS-1

A cell-permeable sulfonamido-benzamide-based allosteric regulator that stimulates DNA binding and recombinase activities of hRAD51 by locking hRAD51 in an active conformation without affecting its active site ATP hydrolysis.

Sinonimo/i:

RAD51-Stimulatory Compound-1, RS-1, 3-((Benzylamino)sulfonyl)-4-bromo-N-(4-bromophenyl)-benzamide, RS-1

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About This Item

Formula empirica (notazione di Hill):
C20H16Br2N2O3S
Numero CAS:
Peso molecolare:
524.23
Numero MDL:
Codice UNSPSC:
12352200
NACRES:
NA.51

Livello qualitativo

Saggio

≥95% (HPLC)

Forma fisica

solid

Produttore/marchio commerciale

Calbiochem®

Condizioni di stoccaggio

OK to freeze
protect from light

Colore

light beige

Solubilità

ethanol: 10 mg/mL
DMSO: 100 mg/mL

Condizioni di spedizione

ambient

Temperatura di conservazione

2-8°C

InChI

1S/C20H16Br2N2O3S/c21-16-7-9-17(10-8-16)24-20(25)15-6-11-18(22)19(12-15)28(26,27)23-13-14-4-2-1-3-5-14/h1-12,23H,13H2,(H,24,25)
SWKAVEUTKGKHSR-UHFFFAOYSA-N

Descrizione generale

A cell-permeable sulfonamido-benzamide-based allosteric regulator that stimulates DNA binding and recombinase activities of hRAD51 by locking hRAD51 in an active conformation without affecting its active site ATP hydrolysis. Although RS-1 enhances hRAD51 filament formation on ssDNA with or without the cofactor NTP, active filaments and recombinase activity are only induced in the presence of ATP or AMP-PNP, but not with ADP or no cofactors. Shown to promote resistance of primary human neonatal dermal fibroblasts to Cisplatin- (Cat. No. 232120) induced death in a dose-dependent manner. RS-1 is inactive toward related DNA strand exchange proteins scRAD5 and scDMC1 of yeast origin or E. coli RedA.This HDR (homology-directed repair) enhancer, is shown to significantly increase both Cas9 & TALEN-mediated knock-in efficiencies.
A cell-permeable sulfonamido-benzamide-based allosteric regulator that stimulates DNA binding and recombinase activities of hRAD51 by locking hRAD51 in an active conformation without affecting its active site ATP hydrolysis. Although RS-1 enhances hRAD51 filament formation on ssDNA with or without the cofactor NTP, active filaments and recombinase activity are only induced in the presence of ATP or AMP-PNP, but not with ADP or no cofactors. Shown to promote resistance of primary human neonatal dermal fibroblasts to Cisplatin- (Cat. No. 232120) induced death in a dose-dependent manner. RS-1 is inactive toward related DNA strand exchange proteins scRAD5 and scDMC1 of yeast origin or E. coli RedA.This HDR (homology-directed repair) enhancer, is shown to significantly increase both Cas9 & TALEN-mediated knock-in efficiencies.

Confezionamento

Packaged under inert gas

Attenzione

Toxicity: Standard Handling (A)

Ricostituzione

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up 3 months at -20°C.

Altre note

Song, J., et al. 2016. Nat. Comm., In Press.
Jayathilaka, K., et al. 2008. Proc. Natl. Acad. Sci. USA.105, 15848.

Note legali

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

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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Nucleic acids research, 49(2), 969-985 (2021-01-06)
Investigations of CRISPR gene knockout editing profiles have contributed to enhanced precision of editing outcomes. However, for homology-directed repair (HDR) in particular, the editing dynamics and patterns in clinically relevant cells, such as human iPSCs and primary T cells, are
Jacqueline Severino et al.
The EMBO journal, 41(12), e109457-e109457 (2022-05-24)
The mammalian germline is characterized by extensive epigenetic reprogramming during its development into functional eggs and sperm. Specifically, the epigenome requires resetting before parental marks can be established and transmitted to the next generation. In the female germline, X-chromosome inactivation

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