mek3 6 Search Results


mek3  (Santa Cruz Biotechnology)
92
Santa Cruz Biotechnology mek3
The ECS cell phenotype and <t>MEK3/6</t> and p38 signaling. A-C) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA and the impact on p38 activity, and spheroid formation and invasive, were measured. D) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA, grown for 5 d as spheroids, and cell extracts (300 μg protein) were assayed for ability to enhance HUVEC tube formation as measured by junction, segment and node formation. E) Cells were electroporated with 3 μg of the indicated siRNA and p38 level and activity were measured at 48 h. F and G) Impact of p38 knockdown on spheroid formation and matrigel invasion. H and I) Treatment with SB203580, a p38α/β inhibitor, suppresses ECS cell spheroid formation and invasive potential. J and K) RhoA restores the ECS cell phenotype in NRP-1 knockdown cells. SCC-13 derived NRP-1 knockout cells were electroporated with 3 μg of empty vector or RhoA WT expression plasmid, and plated for spheroid formation (5 d). The immunoblot monitors NRP-1 knockdown, RhoA overexpression, and the impact on p38T and p38-P level. SCC-13 and SCC13-NRP-1-KOc8 cells were electroporated with 3 μg of the indicated plasmids and ability to form spheroids was monitored at 5 d. The asterisk indicates a significant reduction in spheroid formation in SCC13-NRP1-KOc8 cells versus SCC-13. The double asterisk indicates an increase in spheroid formation in RhoA WT expression plasmid-electroporated versus empty vector-electroporated SCC13-NRP1-KOc8 cells, n = 3, P ≤ 0.005. All bars = 100 μm. [Color figure can be viewed at wileyonlinelibrary.com]
Mek3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 92 stars, based on 1 article reviews
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mek3 6  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology mek3 6
The ECS cell phenotype and <t>MEK3/6</t> and p38 signaling. A-C) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA and the impact on p38 activity, and spheroid formation and invasive, were measured. D) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA, grown for 5 d as spheroids, and cell extracts (300 μg protein) were assayed for ability to enhance HUVEC tube formation as measured by junction, segment and node formation. E) Cells were electroporated with 3 μg of the indicated siRNA and p38 level and activity were measured at 48 h. F and G) Impact of p38 knockdown on spheroid formation and matrigel invasion. H and I) Treatment with SB203580, a p38α/β inhibitor, suppresses ECS cell spheroid formation and invasive potential. J and K) RhoA restores the ECS cell phenotype in NRP-1 knockdown cells. SCC-13 derived NRP-1 knockout cells were electroporated with 3 μg of empty vector or RhoA WT expression plasmid, and plated for spheroid formation (5 d). The immunoblot monitors NRP-1 knockdown, RhoA overexpression, and the impact on p38T and p38-P level. SCC-13 and SCC13-NRP-1-KOc8 cells were electroporated with 3 μg of the indicated plasmids and ability to form spheroids was monitored at 5 d. The asterisk indicates a significant reduction in spheroid formation in SCC13-NRP1-KOc8 cells versus SCC-13. The double asterisk indicates an increase in spheroid formation in RhoA WT expression plasmid-electroporated versus empty vector-electroporated SCC13-NRP1-KOc8 cells, n = 3, P ≤ 0.005. All bars = 100 μm. [Color figure can be viewed at wileyonlinelibrary.com]
Mek3 6, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mek3 6/product/Santa Cruz Biotechnology
Average 93 stars, based on 1 article reviews
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anti mkk3 6 sirnas  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology anti mkk3 6 sirnas
The ECS cell phenotype and <t>MEK3/6</t> and p38 signaling. A-C) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA and the impact on p38 activity, and spheroid formation and invasive, were measured. D) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA, grown for 5 d as spheroids, and cell extracts (300 μg protein) were assayed for ability to enhance HUVEC tube formation as measured by junction, segment and node formation. E) Cells were electroporated with 3 μg of the indicated siRNA and p38 level and activity were measured at 48 h. F and G) Impact of p38 knockdown on spheroid formation and matrigel invasion. H and I) Treatment with SB203580, a p38α/β inhibitor, suppresses ECS cell spheroid formation and invasive potential. J and K) RhoA restores the ECS cell phenotype in NRP-1 knockdown cells. SCC-13 derived NRP-1 knockout cells were electroporated with 3 μg of empty vector or RhoA WT expression plasmid, and plated for spheroid formation (5 d). The immunoblot monitors NRP-1 knockdown, RhoA overexpression, and the impact on p38T and p38-P level. SCC-13 and SCC13-NRP-1-KOc8 cells were electroporated with 3 μg of the indicated plasmids and ability to form spheroids was monitored at 5 d. The asterisk indicates a significant reduction in spheroid formation in SCC13-NRP1-KOc8 cells versus SCC-13. The double asterisk indicates an increase in spheroid formation in RhoA WT expression plasmid-electroporated versus empty vector-electroporated SCC13-NRP1-KOc8 cells, n = 3, P ≤ 0.005. All bars = 100 μm. [Color figure can be viewed at wileyonlinelibrary.com]
Anti Mkk3 6 Sirnas, supplied by Santa Cruz Biotechnology, 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/result/anti mkk3 6 sirnas/product/Santa Cruz Biotechnology
Average 90 stars, based on 1 article reviews
anti mkk3 6 sirnas - by Bioz Stars, 2026-03
90/100 stars
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Image Search Results


The ECS cell phenotype and MEK3/6 and p38 signaling. A-C) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA and the impact on p38 activity, and spheroid formation and invasive, were measured. D) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA, grown for 5 d as spheroids, and cell extracts (300 μg protein) were assayed for ability to enhance HUVEC tube formation as measured by junction, segment and node formation. E) Cells were electroporated with 3 μg of the indicated siRNA and p38 level and activity were measured at 48 h. F and G) Impact of p38 knockdown on spheroid formation and matrigel invasion. H and I) Treatment with SB203580, a p38α/β inhibitor, suppresses ECS cell spheroid formation and invasive potential. J and K) RhoA restores the ECS cell phenotype in NRP-1 knockdown cells. SCC-13 derived NRP-1 knockout cells were electroporated with 3 μg of empty vector or RhoA WT expression plasmid, and plated for spheroid formation (5 d). The immunoblot monitors NRP-1 knockdown, RhoA overexpression, and the impact on p38T and p38-P level. SCC-13 and SCC13-NRP-1-KOc8 cells were electroporated with 3 μg of the indicated plasmids and ability to form spheroids was monitored at 5 d. The asterisk indicates a significant reduction in spheroid formation in SCC13-NRP1-KOc8 cells versus SCC-13. The double asterisk indicates an increase in spheroid formation in RhoA WT expression plasmid-electroporated versus empty vector-electroporated SCC13-NRP1-KOc8 cells, n = 3, P ≤ 0.005. All bars = 100 μm. [Color figure can be viewed at wileyonlinelibrary.com]

Journal: Molecular carcinogenesis

Article Title: NRP-1 interacts with GIPC1 and SYX to activate p38 MAPK signaling and cancer stem cell survival

doi: 10.1002/mc.22943

Figure Lengend Snippet: The ECS cell phenotype and MEK3/6 and p38 signaling. A-C) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA and the impact on p38 activity, and spheroid formation and invasive, were measured. D) Cells were electroporated with 3 μg of Control-, MEK3-, or MEK6-siRNA, grown for 5 d as spheroids, and cell extracts (300 μg protein) were assayed for ability to enhance HUVEC tube formation as measured by junction, segment and node formation. E) Cells were electroporated with 3 μg of the indicated siRNA and p38 level and activity were measured at 48 h. F and G) Impact of p38 knockdown on spheroid formation and matrigel invasion. H and I) Treatment with SB203580, a p38α/β inhibitor, suppresses ECS cell spheroid formation and invasive potential. J and K) RhoA restores the ECS cell phenotype in NRP-1 knockdown cells. SCC-13 derived NRP-1 knockout cells were electroporated with 3 μg of empty vector or RhoA WT expression plasmid, and plated for spheroid formation (5 d). The immunoblot monitors NRP-1 knockdown, RhoA overexpression, and the impact on p38T and p38-P level. SCC-13 and SCC13-NRP-1-KOc8 cells were electroporated with 3 μg of the indicated plasmids and ability to form spheroids was monitored at 5 d. The asterisk indicates a significant reduction in spheroid formation in SCC13-NRP1-KOc8 cells versus SCC-13. The double asterisk indicates an increase in spheroid formation in RhoA WT expression plasmid-electroporated versus empty vector-electroporated SCC13-NRP1-KOc8 cells, n = 3, P ≤ 0.005. All bars = 100 μm. [Color figure can be viewed at wileyonlinelibrary.com]

Article Snippet: Antibodies to GIPC1 (sc-9648), MEK3 (sc-961), Syx (PLEKHG5, sc-130100), mouse IgG (sc-2025), rabbit IgG (sc-2028), and MEK3/6- P (sc-8407) were obtained from Santa Cruz (Dallas, TX).

Techniques: Activity Assay, Derivative Assay, Knock-Out, Plasmid Preparation, Expressing, Western Blot, Over Expression

Impact of NRP-1 and RhoA in tumor formation and p38 signaling. A and B) Spheroid-derived SCC-13 and SCC-13-NRP-1-KOc8 cells were injected (100 000 cells per each front flank) into NSG mice. Tumors were harvested at 4 wk and extracts prepared for immunoblot. C and D) Spheroid-derived SCC-13 cells were injected (100 000 per each front flank) into NSG mice and treated with 0 or 10 mg EG00229/kg body weight. Four week tumors were harvested, photographed and extracts were assayed by immunoblot. E–G) Spheroid-derived SCC-13 cells were injected (100 000 per each front flank) into NSG mice and treated with 0 or 10 mg Y27632/kg body weight. Tumors were harvested at 4 wk, photographed, and assayed by immunoblot. K) Proposed VEGF-A/NRP-1/RhoA/p38 signal transduction pathway. The VEGF-A/NRP-1 complex formation causes the NRP-1 PDZ binding domain to engage the PDZ domain of one subunit of the GIPC1 dimer while the second GIPC1 subunit engages the Syx PDZ binding domain. Syx then activates RhoA which interacts with ROCK to stimulate MAPK signaling. Although MEK3/6 is shown as an activator of p38 activity, this role appears to be context-dependent and we cannot rule out a role for other p38 activation mechanisms. The plotted values are mean ± SEM. The asterisks in each plot indicate a significant reducing in tumor volume, n = 10 tumors/group, P ≤ 0.001. [Color figure can be viewed at wileyonlinelibrary.com]

Journal: Molecular carcinogenesis

Article Title: NRP-1 interacts with GIPC1 and SYX to activate p38 MAPK signaling and cancer stem cell survival

doi: 10.1002/mc.22943

Figure Lengend Snippet: Impact of NRP-1 and RhoA in tumor formation and p38 signaling. A and B) Spheroid-derived SCC-13 and SCC-13-NRP-1-KOc8 cells were injected (100 000 cells per each front flank) into NSG mice. Tumors were harvested at 4 wk and extracts prepared for immunoblot. C and D) Spheroid-derived SCC-13 cells were injected (100 000 per each front flank) into NSG mice and treated with 0 or 10 mg EG00229/kg body weight. Four week tumors were harvested, photographed and extracts were assayed by immunoblot. E–G) Spheroid-derived SCC-13 cells were injected (100 000 per each front flank) into NSG mice and treated with 0 or 10 mg Y27632/kg body weight. Tumors were harvested at 4 wk, photographed, and assayed by immunoblot. K) Proposed VEGF-A/NRP-1/RhoA/p38 signal transduction pathway. The VEGF-A/NRP-1 complex formation causes the NRP-1 PDZ binding domain to engage the PDZ domain of one subunit of the GIPC1 dimer while the second GIPC1 subunit engages the Syx PDZ binding domain. Syx then activates RhoA which interacts with ROCK to stimulate MAPK signaling. Although MEK3/6 is shown as an activator of p38 activity, this role appears to be context-dependent and we cannot rule out a role for other p38 activation mechanisms. The plotted values are mean ± SEM. The asterisks in each plot indicate a significant reducing in tumor volume, n = 10 tumors/group, P ≤ 0.001. [Color figure can be viewed at wileyonlinelibrary.com]

Article Snippet: Antibodies to GIPC1 (sc-9648), MEK3 (sc-961), Syx (PLEKHG5, sc-130100), mouse IgG (sc-2025), rabbit IgG (sc-2028), and MEK3/6- P (sc-8407) were obtained from Santa Cruz (Dallas, TX).

Techniques: Derivative Assay, Injection, Western Blot, Transduction, Binding Assay, Activity Assay, Activation Assay

Role of NRP-1 and RhoA in HaCaT ECS cells. A and B) Cells, electroporated with 3 μg control- or NRP-1-siRNA, were tested for spheroid formation and extracts were prepared to assay NRP-1 and MEK3/6 and p38. C) Cells were electroporated with control- or NRP-1- siRNA. After 48 h, extracts were prepared to monitor RhoA level and RhoA activity. D–F) Cells were electroporated with 3 μg of control- or GIPC1-siRNA and tested for spheroid formation, invasion, and MAPK signaling. G–I) Cells were electroporated with 3 μg of control- or RhoA-siRNA and tested for spheroid formation, invasive potential, and MAPK signaling. J–L) Cells were electroporated with 3 μg of control- or NRP1-siRNA in the presence of empty vector (EV) or RhoA WT expression plasmid, and the impact on spheroid formation (3 d) and p38 activity was monitored. All graphical data is presented as the mean ± SEM. In panels A, D, and E, the single asterisk indicates a significant reduction in the treated group compared to control, n = 3, P ≤ 0.005. In panel J the asterisk indicates a significant reduction in spheroid formation in NRP1-siRNA treated versus control. The double asterisk indicates a significant increase in spheroid formation in NRP-1 knockout cells electroporated with RhoA WT expression plasmid versus cells electroporated with empty vector (EV), n = 3, P ≤ 0.005. All bars = 100 μm. [Color figure can be viewed at wileyonlinelibrary.com]

Journal: Molecular carcinogenesis

Article Title: NRP-1 interacts with GIPC1 and SYX to activate p38 MAPK signaling and cancer stem cell survival

doi: 10.1002/mc.22943

Figure Lengend Snippet: Role of NRP-1 and RhoA in HaCaT ECS cells. A and B) Cells, electroporated with 3 μg control- or NRP-1-siRNA, were tested for spheroid formation and extracts were prepared to assay NRP-1 and MEK3/6 and p38. C) Cells were electroporated with control- or NRP-1- siRNA. After 48 h, extracts were prepared to monitor RhoA level and RhoA activity. D–F) Cells were electroporated with 3 μg of control- or GIPC1-siRNA and tested for spheroid formation, invasion, and MAPK signaling. G–I) Cells were electroporated with 3 μg of control- or RhoA-siRNA and tested for spheroid formation, invasive potential, and MAPK signaling. J–L) Cells were electroporated with 3 μg of control- or NRP1-siRNA in the presence of empty vector (EV) or RhoA WT expression plasmid, and the impact on spheroid formation (3 d) and p38 activity was monitored. All graphical data is presented as the mean ± SEM. In panels A, D, and E, the single asterisk indicates a significant reduction in the treated group compared to control, n = 3, P ≤ 0.005. In panel J the asterisk indicates a significant reduction in spheroid formation in NRP1-siRNA treated versus control. The double asterisk indicates a significant increase in spheroid formation in NRP-1 knockout cells electroporated with RhoA WT expression plasmid versus cells electroporated with empty vector (EV), n = 3, P ≤ 0.005. All bars = 100 μm. [Color figure can be viewed at wileyonlinelibrary.com]

Article Snippet: Antibodies to GIPC1 (sc-9648), MEK3 (sc-961), Syx (PLEKHG5, sc-130100), mouse IgG (sc-2025), rabbit IgG (sc-2028), and MEK3/6- P (sc-8407) were obtained from Santa Cruz (Dallas, TX).

Techniques: Activity Assay, Plasmid Preparation, Expressing, Knock-Out