j1 1 cells Search Results


j1.1 cells  (CEM Corporation)
90
CEM Corporation j1.1 cells
9AA inhibits viral replication in cells with mutant p53 . HIV-1 infected (J1.1 and <t>ACH2)</t> T-cells were treated with 0.5, 1, and 5 μM of 9AA. A) RT activity was determined by at seven day post treatment. B) Cell viability was determined by trypan blue staining (~100/sample) seven days post treatment. C) J1.1 cells were treated with DMSO, 1, 2.5, and 5 μM 9AA and collected after 48 hours. Western blots were performed with anti-p21WAF1, anti-p53, anti-p53-phospho-S15, and actin antibodies.
J1.1 Cells, supplied by CEM Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/j1+1+cells/pmc02723079-45-0-2?v=CEM+Corporation
Average 90 stars, based on 1 article reviews
j1.1 cells - by Bioz Stars, 2026-08
90/100 stars
  Buy from Supplier

Image Search Results


9AA inhibits viral replication in cells with mutant p53 . HIV-1 infected (J1.1 and ACH2) T-cells were treated with 0.5, 1, and 5 μM of 9AA. A) RT activity was determined by at seven day post treatment. B) Cell viability was determined by trypan blue staining (~100/sample) seven days post treatment. C) J1.1 cells were treated with DMSO, 1, 2.5, and 5 μM 9AA and collected after 48 hours. Western blots were performed with anti-p21WAF1, anti-p53, anti-p53-phospho-S15, and actin antibodies.

Journal: Virology Journal

Article Title: 9-aminoacridine Inhibition of HIV-1 Tat Dependent Transcription

doi: 10.1186/1743-422X-6-114

Figure Lengend Snippet: 9AA inhibits viral replication in cells with mutant p53 . HIV-1 infected (J1.1 and ACH2) T-cells were treated with 0.5, 1, and 5 μM of 9AA. A) RT activity was determined by at seven day post treatment. B) Cell viability was determined by trypan blue staining (~100/sample) seven days post treatment. C) J1.1 cells were treated with DMSO, 1, 2.5, and 5 μM 9AA and collected after 48 hours. Western blots were performed with anti-p21WAF1, anti-p53, anti-p53-phospho-S15, and actin antibodies.

Article Snippet: ACH2, J1.1, CEM, and Jurkat cells were grown in RPMI-1640 media containing 10% fetal bovine serum (FBS), 1% L-glutamine, and 1% streptomycin/penicillin.

Techniques: Mutagenesis, Infection, Activity Assay, Staining, Western Blot

9AA does not inhibit proliferation of uninfected cells . Uninfected (CEM and Jurkat) and HIV-1 infected (ACH2 and J1.1) T-cells were treated with DMSO, 1, 10, or 50 μM of A) 9AA, B) 2AA, C) 4AA, D) AH. Cell proliferation/viability was determined by MTT assays. Treatments were performed in triplicate and samples analyzed at 48 hours.

Journal: Virology Journal

Article Title: 9-aminoacridine Inhibition of HIV-1 Tat Dependent Transcription

doi: 10.1186/1743-422X-6-114

Figure Lengend Snippet: 9AA does not inhibit proliferation of uninfected cells . Uninfected (CEM and Jurkat) and HIV-1 infected (ACH2 and J1.1) T-cells were treated with DMSO, 1, 10, or 50 μM of A) 9AA, B) 2AA, C) 4AA, D) AH. Cell proliferation/viability was determined by MTT assays. Treatments were performed in triplicate and samples analyzed at 48 hours.

Article Snippet: ACH2, J1.1, CEM, and Jurkat cells were grown in RPMI-1640 media containing 10% fetal bovine serum (FBS), 1% L-glutamine, and 1% streptomycin/penicillin.

Techniques: Infection

9AA induces AKT activity and stabilization of p21WAF1 . Uninfected (CEM and Jurkat) and HIV-1 infected (ACH2 and J1.1) T-cells were treated with DMSO, 1, 2.5, or 5 μM of 9AA and collected 48 hours later. Western blot analysis was performed for Akt (pan), phospho-Akt (S473), phospho-Akt (T308), GSK3-β (pan), phospho-GSK3-β (S9), phospho-PDK1 (S241), phospho-p21WAF1 (S146), and actin.

Journal: Virology Journal

Article Title: 9-aminoacridine Inhibition of HIV-1 Tat Dependent Transcription

doi: 10.1186/1743-422X-6-114

Figure Lengend Snippet: 9AA induces AKT activity and stabilization of p21WAF1 . Uninfected (CEM and Jurkat) and HIV-1 infected (ACH2 and J1.1) T-cells were treated with DMSO, 1, 2.5, or 5 μM of 9AA and collected 48 hours later. Western blot analysis was performed for Akt (pan), phospho-Akt (S473), phospho-Akt (T308), GSK3-β (pan), phospho-GSK3-β (S9), phospho-PDK1 (S241), phospho-p21WAF1 (S146), and actin.

Article Snippet: ACH2, J1.1, CEM, and Jurkat cells were grown in RPMI-1640 media containing 10% fetal bovine serum (FBS), 1% L-glutamine, and 1% streptomycin/penicillin.

Techniques: Activity Assay, Infection, Western Blot

9AA treatment results in loss of cdk9 from the HIV-1 LTR . ACH2 cells were treated with either DMSO or 2.5 μM 9AA for 48 hours, cross-linked and collected for ChIP analysis. Antibodies against cdk9, histone H3-phospho-Ser10 (H3-pS10), RNA Polymerase II (Pol II), and rabbit IgG were utilized.

Journal: Virology Journal

Article Title: 9-aminoacridine Inhibition of HIV-1 Tat Dependent Transcription

doi: 10.1186/1743-422X-6-114

Figure Lengend Snippet: 9AA treatment results in loss of cdk9 from the HIV-1 LTR . ACH2 cells were treated with either DMSO or 2.5 μM 9AA for 48 hours, cross-linked and collected for ChIP analysis. Antibodies against cdk9, histone H3-phospho-Ser10 (H3-pS10), RNA Polymerase II (Pol II), and rabbit IgG were utilized.

Article Snippet: ACH2, J1.1, CEM, and Jurkat cells were grown in RPMI-1640 media containing 10% fetal bovine serum (FBS), 1% L-glutamine, and 1% streptomycin/penicillin.

Techniques: