time crl 4025 cell lines Search Results


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  • 96
    JASCO Inc jasco hplc
    Jasco Hplc, supplied by JASCO Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    ATCC shakt1 stable cell lines telomerase
    (A) Representative confocal images showing immunofluorescence staining of VE-cadherin on HMEC monolayers transfected with either scrambled ShRNA or ShRNA targeting Akt1. (B) Representative Western blot images and band densitometry quantification of stable ShControl and <t>ShAkt1</t> HMEC lysates showing reduced Akt1 expression in ShAkt1 HMEC compared to ShControl HMEC (n=3). (C) Quantification of the gap area in control and Akt1 knockdown HMEC monolayers normalized to the total area (n=4). (D) Quantification of the number of gaps in control and Akt1 knockdown HMEC monolayers normalized to the number of nuclei per field (n=4). (E) Representative confocal images showing VE-cadherin staining on the vehicle (DMSO), Src inhibitor (PP2) and Akt inhibitor (TCBN) treated HMEC monolayers 24 hours after treatment. (F) Quantification of the number of gaps in the vehicle (DMSO), Src inhibitor (PP2) and Akt inhibitor (TCBN) treated HMEC monolayers 24 hours after treatment (n=4). Data are represented as mean ± SD. *P<0.01, #P<0.05, scale bar 20 μm.
    Shakt1 Stable Cell Lines Telomerase, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/shakt1 stable cell lines telomerase/product/ATCC
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    96
    Cell Signaling Technology Inc phospho nf κb p65 ser536
    miR-205-5p Can Mitigate the Cisplatin Tolerance of TNBC by Suppressing <t>the</t> <t>TRAF2/NF-κB/TNFAIP8</t> Pathway MDA-MB-231 cells were untransfected or transfected with negative control miRNA (miR-NC), miR-205-5p mimics, or both miR-205-5p mimics and TNFAIP8-overexpressing plasmid, while BT549 cells were untransfected or transfected with miR-NC inhibitor (anti-miR-NC), miR-205-5p inhibitor (anti-miR205-5p), or both miR-205-5p inhibitor and shTRAF2. (A) The expression of TRAF2 and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (B–D) After transfection, MDA-MB-231 and BT549 cells were then treated with cisplatin, and untransfected and nontreated cells were used as the control. (B) The relative expression of miR-205-5p, TRAF2, and TNFAIP8 was assessed by qPCR. The mRNA levels were normalized to the GAPDH mRNA level, and the experiments were performed in triplicate. n = 3. (C) The expression of TRAF2, phosphorylated <t>p65</t> (p-p65), p65, and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (D) The apoptosis of TNBC cells upon DDP treatment was assessed by PI/Annexin V-FITC staining and flow cytometric analysis. The cell apoptosis data are shown in the right histograms. n = 3. (A–D) The results are representative of three independent experiments. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05. Error bar = SD value.
    Phospho Nf κb P65 Ser536, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    ATCC human telomerase htert
    miR-205-5p Can Mitigate the Cisplatin Tolerance of TNBC by Suppressing <t>the</t> <t>TRAF2/NF-κB/TNFAIP8</t> Pathway MDA-MB-231 cells were untransfected or transfected with negative control miRNA (miR-NC), miR-205-5p mimics, or both miR-205-5p mimics and TNFAIP8-overexpressing plasmid, while BT549 cells were untransfected or transfected with miR-NC inhibitor (anti-miR-NC), miR-205-5p inhibitor (anti-miR205-5p), or both miR-205-5p inhibitor and shTRAF2. (A) The expression of TRAF2 and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (B–D) After transfection, MDA-MB-231 and BT549 cells were then treated with cisplatin, and untransfected and nontreated cells were used as the control. (B) The relative expression of miR-205-5p, TRAF2, and TNFAIP8 was assessed by qPCR. The mRNA levels were normalized to the GAPDH mRNA level, and the experiments were performed in triplicate. n = 3. (C) The expression of TRAF2, phosphorylated <t>p65</t> (p-p65), p65, and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (D) The apoptosis of TNBC cells upon DDP treatment was assessed by PI/Annexin V-FITC staining and flow cytometric analysis. The cell apoptosis data are shown in the right histograms. n = 3. (A–D) The results are representative of three independent experiments. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05. Error bar = SD value.
    Human Telomerase Htert, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human telomerase htert/product/ATCC
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    93
    JASCO Inc jasco fluorescence detectors
    miR-205-5p Can Mitigate the Cisplatin Tolerance of TNBC by Suppressing <t>the</t> <t>TRAF2/NF-κB/TNFAIP8</t> Pathway MDA-MB-231 cells were untransfected or transfected with negative control miRNA (miR-NC), miR-205-5p mimics, or both miR-205-5p mimics and TNFAIP8-overexpressing plasmid, while BT549 cells were untransfected or transfected with miR-NC inhibitor (anti-miR-NC), miR-205-5p inhibitor (anti-miR205-5p), or both miR-205-5p inhibitor and shTRAF2. (A) The expression of TRAF2 and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (B–D) After transfection, MDA-MB-231 and BT549 cells were then treated with cisplatin, and untransfected and nontreated cells were used as the control. (B) The relative expression of miR-205-5p, TRAF2, and TNFAIP8 was assessed by qPCR. The mRNA levels were normalized to the GAPDH mRNA level, and the experiments were performed in triplicate. n = 3. (C) The expression of TRAF2, phosphorylated <t>p65</t> (p-p65), p65, and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (D) The apoptosis of TNBC cells upon DDP treatment was assessed by PI/Annexin V-FITC staining and flow cytometric analysis. The cell apoptosis data are shown in the right histograms. n = 3. (A–D) The results are representative of three independent experiments. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05. Error bar = SD value.
    Jasco Fluorescence Detectors, supplied by JASCO Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    (A) Representative confocal images showing immunofluorescence staining of VE-cadherin on HMEC monolayers transfected with either scrambled ShRNA or ShRNA targeting Akt1. (B) Representative Western blot images and band densitometry quantification of stable ShControl and ShAkt1 HMEC lysates showing reduced Akt1 expression in ShAkt1 HMEC compared to ShControl HMEC (n=3). (C) Quantification of the gap area in control and Akt1 knockdown HMEC monolayers normalized to the total area (n=4). (D) Quantification of the number of gaps in control and Akt1 knockdown HMEC monolayers normalized to the number of nuclei per field (n=4). (E) Representative confocal images showing VE-cadherin staining on the vehicle (DMSO), Src inhibitor (PP2) and Akt inhibitor (TCBN) treated HMEC monolayers 24 hours after treatment. (F) Quantification of the number of gaps in the vehicle (DMSO), Src inhibitor (PP2) and Akt inhibitor (TCBN) treated HMEC monolayers 24 hours after treatment (n=4). Data are represented as mean ± SD. *P<0.01, #P<0.05, scale bar 20 μm.

    Journal: Journal of cellular physiology

    Article Title: Modulation of long-term endothelial-barrier integrity is conditional to the cross-talk between Akt and Src signaling

    doi: 10.1002/jcp.25791

    Figure Lengend Snippet: (A) Representative confocal images showing immunofluorescence staining of VE-cadherin on HMEC monolayers transfected with either scrambled ShRNA or ShRNA targeting Akt1. (B) Representative Western blot images and band densitometry quantification of stable ShControl and ShAkt1 HMEC lysates showing reduced Akt1 expression in ShAkt1 HMEC compared to ShControl HMEC (n=3). (C) Quantification of the gap area in control and Akt1 knockdown HMEC monolayers normalized to the total area (n=4). (D) Quantification of the number of gaps in control and Akt1 knockdown HMEC monolayers normalized to the number of nuclei per field (n=4). (E) Representative confocal images showing VE-cadherin staining on the vehicle (DMSO), Src inhibitor (PP2) and Akt inhibitor (TCBN) treated HMEC monolayers 24 hours after treatment. (F) Quantification of the number of gaps in the vehicle (DMSO), Src inhibitor (PP2) and Akt inhibitor (TCBN) treated HMEC monolayers 24 hours after treatment (n=4). Data are represented as mean ± SD. *P<0.01, #P<0.05, scale bar 20 μm.

    Article Snippet: Cell culture and preparation of ShAkt1 stable cell lines Telomerase-immortalized HMECs (CRL-4025; ATCC, Manassas, VA) were maintained in EBM-2 with a Growth factor-2 Bullet Kit (Lonza; Walkersville, MD).

    Techniques: Immunofluorescence, Staining, Transfection, shRNA, Western Blot, Expressing

    (A–B) Representative Western blot images and corresponding bar graph of Akt Ser473 phosphorylation and total-Akt in HMEC lysates treated in the presence and absence of 5 ng/ml TGFβ1 for 1–24 hours, respectively. (C–D) Representative Western blot images and corresponding bar graph of Src Tyr416 phosphorylation and total-Src in HMEC lysates treated in the presence and absence of 5 ng/ml TGFβ1 for 1–24 hours, respectively. (E–F) Real-time changes and a bar graph showing the quantification of changes in the ShControl and ShAkt1 HMEC-barrier resistance upon treatment with either vehicle (PBS) or 5 ng/ml TGFβ1 as measured using ECIS equipment. Data are represented as mean ± SD. (n=3), *p<0.01.

    Journal: Journal of cellular physiology

    Article Title: Modulation of long-term endothelial-barrier integrity is conditional to the cross-talk between Akt and Src signaling

    doi: 10.1002/jcp.25791

    Figure Lengend Snippet: (A–B) Representative Western blot images and corresponding bar graph of Akt Ser473 phosphorylation and total-Akt in HMEC lysates treated in the presence and absence of 5 ng/ml TGFβ1 for 1–24 hours, respectively. (C–D) Representative Western blot images and corresponding bar graph of Src Tyr416 phosphorylation and total-Src in HMEC lysates treated in the presence and absence of 5 ng/ml TGFβ1 for 1–24 hours, respectively. (E–F) Real-time changes and a bar graph showing the quantification of changes in the ShControl and ShAkt1 HMEC-barrier resistance upon treatment with either vehicle (PBS) or 5 ng/ml TGFβ1 as measured using ECIS equipment. Data are represented as mean ± SD. (n=3), *p<0.01.

    Article Snippet: Cell culture and preparation of ShAkt1 stable cell lines Telomerase-immortalized HMECs (CRL-4025; ATCC, Manassas, VA) were maintained in EBM-2 with a Growth factor-2 Bullet Kit (Lonza; Walkersville, MD).

    Techniques: Western Blot

    miR-205-5p Can Mitigate the Cisplatin Tolerance of TNBC by Suppressing the TRAF2/NF-κB/TNFAIP8 Pathway MDA-MB-231 cells were untransfected or transfected with negative control miRNA (miR-NC), miR-205-5p mimics, or both miR-205-5p mimics and TNFAIP8-overexpressing plasmid, while BT549 cells were untransfected or transfected with miR-NC inhibitor (anti-miR-NC), miR-205-5p inhibitor (anti-miR205-5p), or both miR-205-5p inhibitor and shTRAF2. (A) The expression of TRAF2 and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (B–D) After transfection, MDA-MB-231 and BT549 cells were then treated with cisplatin, and untransfected and nontreated cells were used as the control. (B) The relative expression of miR-205-5p, TRAF2, and TNFAIP8 was assessed by qPCR. The mRNA levels were normalized to the GAPDH mRNA level, and the experiments were performed in triplicate. n = 3. (C) The expression of TRAF2, phosphorylated p65 (p-p65), p65, and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (D) The apoptosis of TNBC cells upon DDP treatment was assessed by PI/Annexin V-FITC staining and flow cytometric analysis. The cell apoptosis data are shown in the right histograms. n = 3. (A–D) The results are representative of three independent experiments. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05. Error bar = SD value.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: TNFAIP8 Promotes Cisplatin Chemoresistance in Triple-Negative Breast Cancer by Repressing p53-Mediated miR-205-5p Expression

    doi: 10.1016/j.omtn.2020.09.025

    Figure Lengend Snippet: miR-205-5p Can Mitigate the Cisplatin Tolerance of TNBC by Suppressing the TRAF2/NF-κB/TNFAIP8 Pathway MDA-MB-231 cells were untransfected or transfected with negative control miRNA (miR-NC), miR-205-5p mimics, or both miR-205-5p mimics and TNFAIP8-overexpressing plasmid, while BT549 cells were untransfected or transfected with miR-NC inhibitor (anti-miR-NC), miR-205-5p inhibitor (anti-miR205-5p), or both miR-205-5p inhibitor and shTRAF2. (A) The expression of TRAF2 and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (B–D) After transfection, MDA-MB-231 and BT549 cells were then treated with cisplatin, and untransfected and nontreated cells were used as the control. (B) The relative expression of miR-205-5p, TRAF2, and TNFAIP8 was assessed by qPCR. The mRNA levels were normalized to the GAPDH mRNA level, and the experiments were performed in triplicate. n = 3. (C) The expression of TRAF2, phosphorylated p65 (p-p65), p65, and TNFAIP8 was measured by western blots. β-actin was used as the loading control. n = 3. (D) The apoptosis of TNBC cells upon DDP treatment was assessed by PI/Annexin V-FITC staining and flow cytometric analysis. The cell apoptosis data are shown in the right histograms. n = 3. (A–D) The results are representative of three independent experiments. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05. Error bar = SD value.

    Article Snippet: Rabbit anti-human NF-κB p65 (D14E12), phospho-NF-κB p65 (Ser536) (93H1), Akt (pan) (11E7), phospho-Akt (Thr308) (D25E6), phospho-Akt (Ser473) (D9E), Cyclin D1 (92G2), and β-actin (13E5) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Transfection, Negative Control, Plasmid Preparation, Expressing, Western Blot, Staining

    TNFAIP8 Knockdown Can Enhance the Inhibitory Capacity of Cisplatin on Tumor Growth in a TNBC Transplantable Tumor Model by Suppressing the TRAF2-NF-κB and TGFA-Akt Pathways by miR-205-5p MDA-MB-231 cells were subcutaneously injected into nude mice and then grouped (n = 5) and intratumorally injected with shNC, shTNFAIP8, shTNFAIP8 plus miR-205-5p inhibitor, or shTNFAIP8 plus anti-miR-NC. Then, the cells were treated with DDP by intragastric administration. Tumor-bearing mice without any treatment were used as the control group. (A) The tumor volume was monitored every 5 days. n = 5. (B–E) Thirty days later, the mice were sacrificed, and the TNBC tumor tissues were dissected out. (B) Representative images of the TNBC tumor tissues in each group of mice. n = 5. (C) The weights of TNBC tumor tissues in each group of mice. n = 5. (D) The expression of TNFAIP8 and TRAF2 in the TNBC tumor tissues was measured by immunohistochemistry. n = 5. (E) The relative expression of miR-205-5p, TNFAIP8, and TRAF2 in the TNBC tumor tissues was assessed by qPCR. The mRNA levels were normalized to the GAPDH mRNA level, and the experiments were performed in triplicate. n = 5. (F) The expression of TNFAIP8, TRAF2, p-p65, p65, TGFA, p-Akt, and Akt was measured by western blots. β-actin was used as the loading control. n = 5. (A–F) The results are representative of three independent experiments. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05. Error bar = SD value.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: TNFAIP8 Promotes Cisplatin Chemoresistance in Triple-Negative Breast Cancer by Repressing p53-Mediated miR-205-5p Expression

    doi: 10.1016/j.omtn.2020.09.025

    Figure Lengend Snippet: TNFAIP8 Knockdown Can Enhance the Inhibitory Capacity of Cisplatin on Tumor Growth in a TNBC Transplantable Tumor Model by Suppressing the TRAF2-NF-κB and TGFA-Akt Pathways by miR-205-5p MDA-MB-231 cells were subcutaneously injected into nude mice and then grouped (n = 5) and intratumorally injected with shNC, shTNFAIP8, shTNFAIP8 plus miR-205-5p inhibitor, or shTNFAIP8 plus anti-miR-NC. Then, the cells were treated with DDP by intragastric administration. Tumor-bearing mice without any treatment were used as the control group. (A) The tumor volume was monitored every 5 days. n = 5. (B–E) Thirty days later, the mice were sacrificed, and the TNBC tumor tissues were dissected out. (B) Representative images of the TNBC tumor tissues in each group of mice. n = 5. (C) The weights of TNBC tumor tissues in each group of mice. n = 5. (D) The expression of TNFAIP8 and TRAF2 in the TNBC tumor tissues was measured by immunohistochemistry. n = 5. (E) The relative expression of miR-205-5p, TNFAIP8, and TRAF2 in the TNBC tumor tissues was assessed by qPCR. The mRNA levels were normalized to the GAPDH mRNA level, and the experiments were performed in triplicate. n = 5. (F) The expression of TNFAIP8, TRAF2, p-p65, p65, TGFA, p-Akt, and Akt was measured by western blots. β-actin was used as the loading control. n = 5. (A–F) The results are representative of three independent experiments. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05. Error bar = SD value.

    Article Snippet: Rabbit anti-human NF-κB p65 (D14E12), phospho-NF-κB p65 (Ser536) (93H1), Akt (pan) (11E7), phospho-Akt (Thr308) (D25E6), phospho-Akt (Ser473) (D9E), Cyclin D1 (92G2), and β-actin (13E5) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Injection, Expressing, Immunohistochemistry, Western Blot