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jnk1 sirna  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology jnk1 sirna
ROCK2-mediated thermogenic gene expression may occur through the JNK/FOXO1/UCP1 axis (A) Western blotting and quantification of FOXO1 in sWAT from male WT mice housed at room or cold temperature for 3 h ( n = 4 mice per group). (B) Ucp1 expression in sWAT from male WT mice housed at 4 °C for 0, 3, 6, or 12 h ( n = 4 mice). (C) Ucp1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 4 μM FOXO1 inhibitor (AS1842856) for 6 h ( n = 4 wells per group). (D) Foxo1 expression in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 4 mice). (E) Western blotting and quantification of nuclear FOXO1 (nFOXO1), cytoplasmic FOXO1 (cFOXO1), and total FOXO1 (tFOXO1) in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (F) Western blotting and quantification of phosphorylated JNK (pJNK) and total JNK (tJNK) in sWAT from male WT mice housed at RT or cold for 3 h ( n = 3 mice). (G) Foxo1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 100 μM JNK inhibitor (SP600125) for 6 h ( n = 6 wells per group). (H) Western blotting and quantification of pJNK and tJNK in sWAT from control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (I) Foxo1 and (J) Ucp1 expression in differentiated primary adipocytes from sWAT of control and AdR2KO mice. After differentiation for 8 days, mature adipocytes were treated with or without 10 μM isoproterenol (Iso), 1 μM AS1842856, or 50 μM SP600125 for 6 h n = 5–6 wells in (I); n = 3–8 wells in (J). (K) The mRNA levels of Mapk8 (encodes <t>JNK1),</t> Foxo1 , Ppargc1a , and Ucp1 in mature mouse adipocyte cells, 3T3-L1. Adipocytes were transfected with siRNAs for 72 h and then treated with 10 μM isoproterenol (Iso) for 6 h ( n = 6 wells per group). (L) The mRNA levels of Foxo1 , Ppargc1a , and Ucp1 in differentiated mouse primary adipocytes from sWAT of control and AdR2KO mice. Adipocytes were transduced with low ( Foxo1L ) and high ( Foxo1H ) MOI of AAV-8 containing mouse Foxo1 plasmid for 7 days and then treated with 20 μM isoproterenol (Iso) for 16 h ( n = 8 wells per group). The immunoblot images are representative of at least three independent experiments. p values were determined by the two-tailed Student’s t test (A and F) or one-way ANOVA with Tukey’s multiple comparisons test (B-E and G-L). All data are presented as the mean ± SEM of at least three independent biological replicates. See also and . AS: AS1842856; SP: SP600125.
Jnk1 Sirna, 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/product/jnk+sirna/JNK1+siRNA/pmc13014674-95-0-4
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anti phospho jnk  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology anti phospho jnk
ROCK2-mediated thermogenic gene expression may occur through the JNK/FOXO1/UCP1 axis (A) Western blotting and quantification of FOXO1 in sWAT from male WT mice housed at room or cold temperature for 3 h ( n = 4 mice per group). (B) Ucp1 expression in sWAT from male WT mice housed at 4 °C for 0, 3, 6, or 12 h ( n = 4 mice). (C) Ucp1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 4 μM FOXO1 inhibitor (AS1842856) for 6 h ( n = 4 wells per group). (D) Foxo1 expression in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 4 mice). (E) Western blotting and quantification of nuclear FOXO1 (nFOXO1), cytoplasmic FOXO1 (cFOXO1), and total FOXO1 (tFOXO1) in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (F) Western blotting and quantification of phosphorylated JNK (pJNK) and total JNK (tJNK) in sWAT from male WT mice housed at RT or cold for 3 h ( n = 3 mice). (G) Foxo1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 100 μM JNK inhibitor (SP600125) for 6 h ( n = 6 wells per group). (H) Western blotting and quantification of pJNK and tJNK in sWAT from control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (I) Foxo1 and (J) Ucp1 expression in differentiated primary adipocytes from sWAT of control and AdR2KO mice. After differentiation for 8 days, mature adipocytes were treated with or without 10 μM isoproterenol (Iso), 1 μM AS1842856, or 50 μM SP600125 for 6 h n = 5–6 wells in (I); n = 3–8 wells in (J). (K) The mRNA levels of Mapk8 (encodes <t>JNK1),</t> Foxo1 , Ppargc1a , and Ucp1 in mature mouse adipocyte cells, 3T3-L1. Adipocytes were transfected with siRNAs for 72 h and then treated with 10 μM isoproterenol (Iso) for 6 h ( n = 6 wells per group). (L) The mRNA levels of Foxo1 , Ppargc1a , and Ucp1 in differentiated mouse primary adipocytes from sWAT of control and AdR2KO mice. Adipocytes were transduced with low ( Foxo1L ) and high ( Foxo1H ) MOI of AAV-8 containing mouse Foxo1 plasmid for 7 days and then treated with 20 μM isoproterenol (Iso) for 16 h ( n = 8 wells per group). The immunoblot images are representative of at least three independent experiments. p values were determined by the two-tailed Student’s t test (A and F) or one-way ANOVA with Tukey’s multiple comparisons test (B-E and G-L). All data are presented as the mean ± SEM of at least three independent biological replicates. See also and . AS: AS1842856; SP: SP600125.
Anti Phospho Jnk, 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/product/jnk+sirna/LASS3+siRNA/pmc12767408-70-85-89
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sapk jnk sirna  (Cell Signaling Technology Inc)
86
Cell Signaling Technology Inc sapk jnk sirna
ROCK2-mediated thermogenic gene expression may occur through the JNK/FOXO1/UCP1 axis (A) Western blotting and quantification of FOXO1 in sWAT from male WT mice housed at room or cold temperature for 3 h ( n = 4 mice per group). (B) Ucp1 expression in sWAT from male WT mice housed at 4 °C for 0, 3, 6, or 12 h ( n = 4 mice). (C) Ucp1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 4 μM FOXO1 inhibitor (AS1842856) for 6 h ( n = 4 wells per group). (D) Foxo1 expression in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 4 mice). (E) Western blotting and quantification of nuclear FOXO1 (nFOXO1), cytoplasmic FOXO1 (cFOXO1), and total FOXO1 (tFOXO1) in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (F) Western blotting and quantification of phosphorylated JNK (pJNK) and total JNK (tJNK) in sWAT from male WT mice housed at RT or cold for 3 h ( n = 3 mice). (G) Foxo1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 100 μM JNK inhibitor (SP600125) for 6 h ( n = 6 wells per group). (H) Western blotting and quantification of pJNK and tJNK in sWAT from control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (I) Foxo1 and (J) Ucp1 expression in differentiated primary adipocytes from sWAT of control and AdR2KO mice. After differentiation for 8 days, mature adipocytes were treated with or without 10 μM isoproterenol (Iso), 1 μM AS1842856, or 50 μM SP600125 for 6 h n = 5–6 wells in (I); n = 3–8 wells in (J). (K) The mRNA levels of Mapk8 (encodes <t>JNK1),</t> Foxo1 , Ppargc1a , and Ucp1 in mature mouse adipocyte cells, 3T3-L1. Adipocytes were transfected with siRNAs for 72 h and then treated with 10 μM isoproterenol (Iso) for 6 h ( n = 6 wells per group). (L) The mRNA levels of Foxo1 , Ppargc1a , and Ucp1 in differentiated mouse primary adipocytes from sWAT of control and AdR2KO mice. Adipocytes were transduced with low ( Foxo1L ) and high ( Foxo1H ) MOI of AAV-8 containing mouse Foxo1 plasmid for 7 days and then treated with 20 μM isoproterenol (Iso) for 16 h ( n = 8 wells per group). The immunoblot images are representative of at least three independent experiments. p values were determined by the two-tailed Student’s t test (A and F) or one-way ANOVA with Tukey’s multiple comparisons test (B-E and G-L). All data are presented as the mean ± SEM of at least three independent biological replicates. See also and . AS: AS1842856; SP: SP600125.
Sapk Jnk Sirna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/jnk+sirna/pm41319747-57-28-38
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mapk8 rat pre designed sirna  (MedChemExpress)
93
MedChemExpress mapk8 rat pre designed sirna
ROCK2-mediated thermogenic gene expression may occur through the JNK/FOXO1/UCP1 axis (A) Western blotting and quantification of FOXO1 in sWAT from male WT mice housed at room or cold temperature for 3 h ( n = 4 mice per group). (B) Ucp1 expression in sWAT from male WT mice housed at 4 °C for 0, 3, 6, or 12 h ( n = 4 mice). (C) Ucp1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 4 μM FOXO1 inhibitor (AS1842856) for 6 h ( n = 4 wells per group). (D) Foxo1 expression in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 4 mice). (E) Western blotting and quantification of nuclear FOXO1 (nFOXO1), cytoplasmic FOXO1 (cFOXO1), and total FOXO1 (tFOXO1) in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (F) Western blotting and quantification of phosphorylated JNK (pJNK) and total JNK (tJNK) in sWAT from male WT mice housed at RT or cold for 3 h ( n = 3 mice). (G) Foxo1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 100 μM JNK inhibitor (SP600125) for 6 h ( n = 6 wells per group). (H) Western blotting and quantification of pJNK and tJNK in sWAT from control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (I) Foxo1 and (J) Ucp1 expression in differentiated primary adipocytes from sWAT of control and AdR2KO mice. After differentiation for 8 days, mature adipocytes were treated with or without 10 μM isoproterenol (Iso), 1 μM AS1842856, or 50 μM SP600125 for 6 h n = 5–6 wells in (I); n = 3–8 wells in (J). (K) The mRNA levels of Mapk8 (encodes <t>JNK1),</t> Foxo1 , Ppargc1a , and Ucp1 in mature mouse adipocyte cells, 3T3-L1. Adipocytes were transfected with siRNAs for 72 h and then treated with 10 μM isoproterenol (Iso) for 6 h ( n = 6 wells per group). (L) The mRNA levels of Foxo1 , Ppargc1a , and Ucp1 in differentiated mouse primary adipocytes from sWAT of control and AdR2KO mice. Adipocytes were transduced with low ( Foxo1L ) and high ( Foxo1H ) MOI of AAV-8 containing mouse Foxo1 plasmid for 7 days and then treated with 20 μM isoproterenol (Iso) for 16 h ( n = 8 wells per group). The immunoblot images are representative of at least three independent experiments. p values were determined by the two-tailed Student’s t test (A and F) or one-way ANOVA with Tukey’s multiple comparisons test (B-E and G-L). All data are presented as the mean ± SEM of at least three independent biological replicates. See also and . AS: AS1842856; SP: SP600125.
Mapk8 Rat Pre Designed Sirna, supplied by MedChemExpress, 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/product/jnk+sirna/Phospho-JNK1%2F2%2F3+(Thr183)+Antibody/bio_rxiv__2025__11__13__688209-95-11-16
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mapk8 rat pre designed sirna - by Bioz Stars, 2026-09
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jnk  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology jnk
Figure 3. MAPK pathway is regulated apelin-induced integrin expression and prostate cancer migration. (A&B) IPA pathway enrichment figure showing pathways that were changed in the GSE7930 dataset (Orange color indicated upregulated gene profile; blue color indicated downregulated gene profile). (C-H) Cells were treated with ERK (ERK II inhibitor; 10 <t>μM),</t> <t>p38</t> (SB203580; 10 μM) and <t>JNK</t> (SP600125; 10 μM) inhibitors or transfected with ERK, p38 and JNK siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (I) PC3 cells were stimulated with apelin and ERK, p38 and JNK phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.
Jnk, 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/product/jnk+sirna/JNK1+siRNA/10__7150_slash_ijbs__113161-45-22-41
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jnk sirna santa cruz biotechnology  (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology jnk sirna santa cruz biotechnology
Figure 3. MAPK pathway is regulated apelin-induced integrin expression and prostate cancer migration. (A&B) IPA pathway enrichment figure showing pathways that were changed in the GSE7930 dataset (Orange color indicated upregulated gene profile; blue color indicated downregulated gene profile). (C-H) Cells were treated with ERK (ERK II inhibitor; 10 <t>μM),</t> <t>p38</t> (SB203580; 10 μM) and <t>JNK</t> (SP600125; 10 μM) inhibitors or transfected with ERK, p38 and JNK siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (I) PC3 cells were stimulated with apelin and ERK, p38 and JNK phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.
Jnk Sirna Santa Cruz Biotechnology, 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/product/jnk+sirna/JNK1+siRNA/pmc11844289__ijbsv21p1378s1-0-150-152
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p jnk1 2  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology p jnk1 2
Figure 3. MAPK pathway is regulated apelin-induced integrin expression and prostate cancer migration. (A&B) IPA pathway enrichment figure showing pathways that were changed in the GSE7930 dataset (Orange color indicated upregulated gene profile; blue color indicated downregulated gene profile). (C-H) Cells were treated with ERK (ERK II inhibitor; 10 <t>μM),</t> <t>p38</t> (SB203580; 10 μM) and <t>JNK</t> (SP600125; 10 μM) inhibitors or transfected with ERK, p38 and JNK siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (I) PC3 cells were stimulated with apelin and ERK, p38 and JNK phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.
P Jnk1 2, 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
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sirnas for jnk and negative control (nc)  (Shanghai GenePharma)
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Shanghai GenePharma sirnas for jnk and negative control (nc)
Figure 3. MAPK pathway is regulated apelin-induced integrin expression and prostate cancer migration. (A&B) IPA pathway enrichment figure showing pathways that were changed in the GSE7930 dataset (Orange color indicated upregulated gene profile; blue color indicated downregulated gene profile). (C-H) Cells were treated with ERK (ERK II inhibitor; 10 <t>μM),</t> <t>p38</t> (SB203580; 10 μM) and <t>JNK</t> (SP600125; 10 μM) inhibitors or transfected with ERK, p38 and JNK siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (I) PC3 cells were stimulated with apelin and ERK, p38 and JNK phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.
Sirnas For Jnk And Negative Control (Nc), supplied by Shanghai GenePharma, 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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ROCK2-mediated thermogenic gene expression may occur through the JNK/FOXO1/UCP1 axis (A) Western blotting and quantification of FOXO1 in sWAT from male WT mice housed at room or cold temperature for 3 h ( n = 4 mice per group). (B) Ucp1 expression in sWAT from male WT mice housed at 4 °C for 0, 3, 6, or 12 h ( n = 4 mice). (C) Ucp1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 4 μM FOXO1 inhibitor (AS1842856) for 6 h ( n = 4 wells per group). (D) Foxo1 expression in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 4 mice). (E) Western blotting and quantification of nuclear FOXO1 (nFOXO1), cytoplasmic FOXO1 (cFOXO1), and total FOXO1 (tFOXO1) in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (F) Western blotting and quantification of phosphorylated JNK (pJNK) and total JNK (tJNK) in sWAT from male WT mice housed at RT or cold for 3 h ( n = 3 mice). (G) Foxo1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 100 μM JNK inhibitor (SP600125) for 6 h ( n = 6 wells per group). (H) Western blotting and quantification of pJNK and tJNK in sWAT from control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (I) Foxo1 and (J) Ucp1 expression in differentiated primary adipocytes from sWAT of control and AdR2KO mice. After differentiation for 8 days, mature adipocytes were treated with or without 10 μM isoproterenol (Iso), 1 μM AS1842856, or 50 μM SP600125 for 6 h n = 5–6 wells in (I); n = 3–8 wells in (J). (K) The mRNA levels of Mapk8 (encodes JNK1), Foxo1 , Ppargc1a , and Ucp1 in mature mouse adipocyte cells, 3T3-L1. Adipocytes were transfected with siRNAs for 72 h and then treated with 10 μM isoproterenol (Iso) for 6 h ( n = 6 wells per group). (L) The mRNA levels of Foxo1 , Ppargc1a , and Ucp1 in differentiated mouse primary adipocytes from sWAT of control and AdR2KO mice. Adipocytes were transduced with low ( Foxo1L ) and high ( Foxo1H ) MOI of AAV-8 containing mouse Foxo1 plasmid for 7 days and then treated with 20 μM isoproterenol (Iso) for 16 h ( n = 8 wells per group). The immunoblot images are representative of at least three independent experiments. p values were determined by the two-tailed Student’s t test (A and F) or one-way ANOVA with Tukey’s multiple comparisons test (B-E and G-L). All data are presented as the mean ± SEM of at least three independent biological replicates. See also and . AS: AS1842856; SP: SP600125.

Journal: iScience

Article Title: Induction of adipocyte thermogenic program by Rho-associated coiled-coil containing kinase 2

doi: 10.1016/j.isci.2026.115225

Figure Lengend Snippet: ROCK2-mediated thermogenic gene expression may occur through the JNK/FOXO1/UCP1 axis (A) Western blotting and quantification of FOXO1 in sWAT from male WT mice housed at room or cold temperature for 3 h ( n = 4 mice per group). (B) Ucp1 expression in sWAT from male WT mice housed at 4 °C for 0, 3, 6, or 12 h ( n = 4 mice). (C) Ucp1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 4 μM FOXO1 inhibitor (AS1842856) for 6 h ( n = 4 wells per group). (D) Foxo1 expression in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 4 mice). (E) Western blotting and quantification of nuclear FOXO1 (nFOXO1), cytoplasmic FOXO1 (cFOXO1), and total FOXO1 (tFOXO1) in sWAT from male control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (F) Western blotting and quantification of phosphorylated JNK (pJNK) and total JNK (tJNK) in sWAT from male WT mice housed at RT or cold for 3 h ( n = 3 mice). (G) Foxo1 expression in sWAT harvested from control mice and then treated with 40 μM isoproterenol (Iso) and/or 100 μM JNK inhibitor (SP600125) for 6 h ( n = 6 wells per group). (H) Western blotting and quantification of pJNK and tJNK in sWAT from control and AdR2KO mice housed at RT or cold for 3 h ( n = 3 mice). (I) Foxo1 and (J) Ucp1 expression in differentiated primary adipocytes from sWAT of control and AdR2KO mice. After differentiation for 8 days, mature adipocytes were treated with or without 10 μM isoproterenol (Iso), 1 μM AS1842856, or 50 μM SP600125 for 6 h n = 5–6 wells in (I); n = 3–8 wells in (J). (K) The mRNA levels of Mapk8 (encodes JNK1), Foxo1 , Ppargc1a , and Ucp1 in mature mouse adipocyte cells, 3T3-L1. Adipocytes were transfected with siRNAs for 72 h and then treated with 10 μM isoproterenol (Iso) for 6 h ( n = 6 wells per group). (L) The mRNA levels of Foxo1 , Ppargc1a , and Ucp1 in differentiated mouse primary adipocytes from sWAT of control and AdR2KO mice. Adipocytes were transduced with low ( Foxo1L ) and high ( Foxo1H ) MOI of AAV-8 containing mouse Foxo1 plasmid for 7 days and then treated with 20 μM isoproterenol (Iso) for 16 h ( n = 8 wells per group). The immunoblot images are representative of at least three independent experiments. p values were determined by the two-tailed Student’s t test (A and F) or one-way ANOVA with Tukey’s multiple comparisons test (B-E and G-L). All data are presented as the mean ± SEM of at least three independent biological replicates. See also and . AS: AS1842856; SP: SP600125.

Article Snippet: JNK1 siRNA (m) , Santa Cruz Biotechnology , Cat# sc-29381.

Techniques: Gene Expression, Western Blot, Expressing, Control, Transfection, Transduction, Plasmid Preparation, Two Tailed Test

Figure 3. MAPK pathway is regulated apelin-induced integrin expression and prostate cancer migration. (A&B) IPA pathway enrichment figure showing pathways that were changed in the GSE7930 dataset (Orange color indicated upregulated gene profile; blue color indicated downregulated gene profile). (C-H) Cells were treated with ERK (ERK II inhibitor; 10 μM), p38 (SB203580; 10 μM) and JNK (SP600125; 10 μM) inhibitors or transfected with ERK, p38 and JNK siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (I) PC3 cells were stimulated with apelin and ERK, p38 and JNK phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.

Journal: International Journal of Biological Sciences

Article Title: Apelin facilitates integrin αvβ3 production and enhances metastasis in prostate cancer by activating STAT3 and inhibiting miR-8070

doi: 10.7150/ijbs.113161

Figure Lengend Snippet: Figure 3. MAPK pathway is regulated apelin-induced integrin expression and prostate cancer migration. (A&B) IPA pathway enrichment figure showing pathways that were changed in the GSE7930 dataset (Orange color indicated upregulated gene profile; blue color indicated downregulated gene profile). (C-H) Cells were treated with ERK (ERK II inhibitor; 10 μM), p38 (SB203580; 10 μM) and JNK (SP600125; 10 μM) inhibitors or transfected with ERK, p38 and JNK siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (I) PC3 cells were stimulated with apelin and ERK, p38 and JNK phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.

Article Snippet: JNK (SC-474), p38 (SC-4972), ERK (SC-1647), STAT3 (SC-482), p-JNK (SC-6254), p-p38 (SC-166182), p-ERK (SC-7383) and integrin αvβ3 (SC-7312) antibodies as well as JNK (sc-29380), p38 (sc-29433), STAT3 (sc-29493), integrin αv (sc-29373), integrin β3 (sc-29375) and apelin (sc-44741) siRNA were purchased from Santa Cruz Biotechnology (CA, USA).

Techniques: Expressing, Migration, Transfection, Phospho-proteomics, Western Blot, Control

Figure 4. Apelin promotes integrin production and cell motility via the STAT3 pathway. (A-F) Cells were treated with STAT3 inhibitor (10 μM) or transfected with STAT3 siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (G&H) PC3 cells were treated with apelin or pretreated with ERK, p38 and JNK inhibitor then with apelin, the STAT3 phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.

Journal: International Journal of Biological Sciences

Article Title: Apelin facilitates integrin αvβ3 production and enhances metastasis in prostate cancer by activating STAT3 and inhibiting miR-8070

doi: 10.7150/ijbs.113161

Figure Lengend Snippet: Figure 4. Apelin promotes integrin production and cell motility via the STAT3 pathway. (A-F) Cells were treated with STAT3 inhibitor (10 μM) or transfected with STAT3 siRNA for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (G&H) PC3 cells were treated with apelin or pretreated with ERK, p38 and JNK inhibitor then with apelin, the STAT3 phosphorylation was examined by Western blotting (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.

Article Snippet: JNK (SC-474), p38 (SC-4972), ERK (SC-1647), STAT3 (SC-482), p-JNK (SC-6254), p-p38 (SC-166182), p-ERK (SC-7383) and integrin αvβ3 (SC-7312) antibodies as well as JNK (sc-29380), p38 (sc-29433), STAT3 (sc-29493), integrin αv (sc-29373), integrin β3 (sc-29375) and apelin (sc-44741) siRNA were purchased from Santa Cruz Biotechnology (CA, USA).

Techniques: Transfection, Migration, Expressing, Phospho-proteomics, Western Blot, Control

Figure 5. Apelin enhances integrin expression and promotes cell migration by inhibiting miR-8070 expression. (A) The diagrams depict the selection of miRNA candidates targeting integrin αv and β3. (B) PC3 cells were treated with apelin, the miRNAs expression was examined by qPCR (n=3). (C) Cells were treated with apelin for 24 hours, the miR-8070 expression was examined by qPCR (n=3). (D-F) Cells were transfected with miR-8070 mimic for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (G-I) Cells were treated with ERK, p38 and JNK inhibitor or siRNA then with apelin, the 3’UTR activity and miRNA expression was examined by luciferase activity and qPCR (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.

Journal: International Journal of Biological Sciences

Article Title: Apelin facilitates integrin αvβ3 production and enhances metastasis in prostate cancer by activating STAT3 and inhibiting miR-8070

doi: 10.7150/ijbs.113161

Figure Lengend Snippet: Figure 5. Apelin enhances integrin expression and promotes cell migration by inhibiting miR-8070 expression. (A) The diagrams depict the selection of miRNA candidates targeting integrin αv and β3. (B) PC3 cells were treated with apelin, the miRNAs expression was examined by qPCR (n=3). (C) Cells were treated with apelin for 24 hours, the miR-8070 expression was examined by qPCR (n=3). (D-F) Cells were transfected with miR-8070 mimic for 24 hours then with apelin, the wound healing, cell migration and integrin mRNA expression was examined (n=3). (G-I) Cells were treated with ERK, p38 and JNK inhibitor or siRNA then with apelin, the 3’UTR activity and miRNA expression was examined by luciferase activity and qPCR (n=3). * p < 0.05 compared with the control group. # p < 0.05 compared with the apelin-treated group.

Article Snippet: JNK (SC-474), p38 (SC-4972), ERK (SC-1647), STAT3 (SC-482), p-JNK (SC-6254), p-p38 (SC-166182), p-ERK (SC-7383) and integrin αvβ3 (SC-7312) antibodies as well as JNK (sc-29380), p38 (sc-29433), STAT3 (sc-29493), integrin αv (sc-29373), integrin β3 (sc-29375) and apelin (sc-44741) siRNA were purchased from Santa Cruz Biotechnology (CA, USA).

Techniques: Expressing, Migration, Selection, Transfection, Activity Assay, Luciferase, Control

Figure 7. Schematic diagram illustrating the mechanism underlying the effects of apelin in prostate cancer metastasis. Apelin stimulation enhances integrin αvβ3-dependent prostate cancer migration and metastasis. The activation of STAT3 and inhibition of miR-8070 via the ERK, p38 and JNK pathways mediate apelin-facilitated integrin synthesis and cell motility.

Journal: International Journal of Biological Sciences

Article Title: Apelin facilitates integrin αvβ3 production and enhances metastasis in prostate cancer by activating STAT3 and inhibiting miR-8070

doi: 10.7150/ijbs.113161

Figure Lengend Snippet: Figure 7. Schematic diagram illustrating the mechanism underlying the effects of apelin in prostate cancer metastasis. Apelin stimulation enhances integrin αvβ3-dependent prostate cancer migration and metastasis. The activation of STAT3 and inhibition of miR-8070 via the ERK, p38 and JNK pathways mediate apelin-facilitated integrin synthesis and cell motility.

Article Snippet: JNK (SC-474), p38 (SC-4972), ERK (SC-1647), STAT3 (SC-482), p-JNK (SC-6254), p-p38 (SC-166182), p-ERK (SC-7383) and integrin αvβ3 (SC-7312) antibodies as well as JNK (sc-29380), p38 (sc-29433), STAT3 (sc-29493), integrin αv (sc-29373), integrin β3 (sc-29375) and apelin (sc-44741) siRNA were purchased from Santa Cruz Biotechnology (CA, USA).

Techniques: Migration, Activation Assay, Inhibition