pmd2 g lenti helper plasmid gift Search Results


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Thermo Fisher envelope plasmid dna
Envelope Plasmid Dna, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
P38 Shrna Lentivector, supplied by Addgene inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Pspax2, supplied by Polysciences inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Addgene inc envelope plasmid pmd2 g
Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Envelope Plasmid Pmd2 G, supplied by Addgene inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Genechem packaging plasmids pmd2 g
Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Packaging Plasmids Pmd2 G, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC second generation lentiviral system
Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Second Generation Lentiviral System, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Addgene inc pmd2 g
Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Pmd2 G, supplied by Addgene 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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Addgene inc pmd2 g prre
Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Pmd2 G Prre, supplied by Addgene 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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Addgene inc pmd2 g vectors
Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Pmd2 G Vectors, supplied by Addgene 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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Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of <t>p38</t> inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.
Vsv G Envelope, supplied by Addgene 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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Image Search Results


Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of p38 inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: STING trafficking activates MAPK-CREB signaling to trigger regulatory T cell differentiation.

doi: 10.1073/pnas.2320709121

Figure Lengend Snippet: Fig. 5. MAPK–CREB is required for STING-mediated Treg differentiation. (A–C) WT Naïve CD4 T cells were activated with anti-CD3 + anti-CD28 antibodies for 2 d, followed by treatment with mock or DMXAA (2.5 μg/mL) for indicated hours. Cell lysates were then collected for the detection of MAPK–CREB signaling. Densitometry analysis was performed and normalized to the mock sample (B and C). (D and E) WT naïve CD4+ T cells were stimulated with mock or DMXAA (2.5 μg/mL) for 1 to 3 d, followed by Treg analysis. Representative FACS plots are shown in (D), and statistics are shown in (E). (F and G) Knockdown of p38 inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were transduced with lentiviral-mediated sh-luciferase control or sh-p38, followed by stimulation with mock, DMXAA (2.5 μg/mL), or cGAMP (20 μg/mL) for 3 d. Representative FACS plots are shown in (F), and statistics are shown in (G). (H and I) p38 or CREB inhibitor treatment inhibits STING-mediated Treg differentiation. WT naïve CD4+ T cells were treated with mock or cGAMP (20 μg/mL) in the presence or absence of p38 inhibitors sb203850 (10 μM) or sb202190 (10 μM), or CREB inhibitor 666-15 (1 μM), for 3 d. Treg differentiation was analyzed by intracellular staining of Foxp3 and FACS analysis. Representative FACS plots are shown in (H), and statistics are shown in (I). Error bars: SEM; *P < 0.05, ***P < 0.001, ****P < 0.0001; ns, not significant. Two-way ANOVA test. Data shown are representative of two independent experiments.

Article Snippet: For lentivirus production, the p38 shRNA lentivector, pMD2.G (Addgene #12259), and psPAX2 (Addgene #12260) were transfected at a 10:5:9 ratio in HEK293T cells.

Techniques: Knockdown, Transduction, Luciferase, Control, Staining