β d arabinofuranoside arac

Manufactured by Merck Group

β-D-arabinofuranoside (AraC) is a nucleoside analog used as a laboratory reagent. It functions as a cytosine analog, inhibiting DNA synthesis.

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Lab products found in correlation

β actin, by Abcam (1 mentions) Mg132, by Merck Group (1 mentions)

Close spelling variants of this product

Cytosine β-D-arabinofuranoside hydrochloride (AraC; β-d-arabinofuranoside

2 protocols using β d arabinofuranoside arac

Huh-7 Cells Transfection with HCV NS3/5B

Cited 2 times

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Huh-7 cells were inoculated at MOI 10 with a recombinant vaccinia virus expressing the T7 phage RNA polymerase (VacT7) [104 (link)]. Two hours later, cells were transfected with the plasmid pTM-NS3/5B [16 (link), 58 (link)] (kindly provided by Dr. Lohmann; U. of Heidelberg) and Lipofectamine 2000 (ThermoFisher-Massachussets, USA) following the manufacturer´s recommendations in terms of total DNA per well (typically 4μg per 35mm dishes with 7.5 X 10⁵ cells/well) and 50% of the recommended lipofectamine:DNA ratio. Transfected cells were cultured in the presence of the DNA replication inhibitor cytosine β-D-arabinofuranoside (AraC; Sigma-Aldrich) for 16 hours to prevent VacT7 replication [105 (link)]. When indicated, media was also supplemented with 100nM daclatasvir (DCTV). Total cell extracts were used to determine viral protein accumulation by Western-blot using anti-NS3 antibody (clone 2E3; Biofront) and β-actin (Abcam; ab8226) as loading control.

Mingorance L., Castro V., Ávila-Pérez G., Calvo G., Rodriguez M.J., Carrascosa J.L., Pérez-del-Pulgar S., Forns X, & Gastaminza P. (2018). Host phosphatidic acid phosphatase lipin1 is rate limiting for functional hepatitis C virus replicase complex formation. PLoS Pathogens, 14(9), e1007284.

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Neonatal Rat Cardiomyocyte Isolation and Apoptosis

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Neonatal ventricular cardiomyocytes of Sprague Dawley rats were isolated from either postnatal day 1 or 3 and cultured as described previously [17 (link)]. Neonatal cardiomyocytes were cultured for 48 h in the presence of 5% horse serum and 20 μM of cytosine β-D-arabinofuranoside (AraC) (Sigma-Aldrich) before stimulation or adenovirus administration to prevent proliferation of non-myocytes (> 90% cardiomyocytes). Subsequently, cells were washed, serum starved for 12 h for synchronization, and then infected with adenovirus for 48 h. To induce apoptosis, cardiomyocytes were then exposed to hypoxic stress by culturing the cells in medium containing 750 μM Cobalt Chloride (CoCl₂) for 24 h (control: diluent DMSO). For inhibition of Hsp90, cardiomyocytes were treated for 1 h with 17-AAG (100 nM) (Alexis) prior to the addition of CoCl₂. To analyze protein degradation P1 cardiomyocytes were treated for 24 h with MG-132 (10 μM) (Sigma), which was added one hour before the addition of CoCl₂ (750 μM).

Sajjad A., Novoyatleva T., Vergarajauregui S., Troidl C., Schermuly R.T., Tucker H.O, & Engel F.B. (2014). Lysine methyltransferase Smyd2 suppresses p53-dependent cardiomyocyte apoptosis. Biochimica et biophysica acta, 1843(11), 2556-2562.

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