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96
Proteintech n cadherin
RPL3 reverses the effects of DUOX2 in vitro , and the different genes after DUOX2 knockdown were enriched in the AKT pathway, while RPL3 reversed this change partially. ( A ). Western blotting was performed to detect the DUOX2 protein in DUOX2-overexpressed (pcDNA3.1-DUOX2) and negative control (pcDNA3.1-Control) both in HCT116 and SW480 cells. ( B ) Transwell assays. The migration and invasion ability of the HCT116 and SW480 cells were significantly increased after overexpressing DUOX2, while the overexpression of RPL3 significantly reversed this trend. ( C ) Wound healing assay. The migration rate was derived from the ratio of the difference in wound area at different times to the initial wound area (200×). The tests were performed on SW480 cells. N.S. P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001. ( D ) Differentially expressed genes in DUOX2 knockdown (si1-DUOX2, si2-DUOX2) and negative control (si-NC) by next-generation sequencing as shown in the heatmap. ( E ) Different signaling pathways based on KEGG databases between si1-DUOX2 and si-NC group, or si2-DUOX2 and si-NC group. ( F ) Verification of related genes in PI3K–AKT pathway. ( G ) WB assay. The protein levels of <t>E-cadherin</t> (E-cad), EGFR, AKT, p-AKT, c-MYC after overexpression of DUOX2, or both of DUOX2 and RPL3.
N Cadherin, supplied by Proteintech, 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
Proteintech snail mab
RPL3 reverses the effects of DUOX2 in vitro , and the different genes after DUOX2 knockdown were enriched in the AKT pathway, while RPL3 reversed this change partially. ( A ). Western blotting was performed to detect the DUOX2 protein in DUOX2-overexpressed (pcDNA3.1-DUOX2) and negative control (pcDNA3.1-Control) both in HCT116 and SW480 cells. ( B ) Transwell assays. The migration and invasion ability of the HCT116 and SW480 cells were significantly increased after overexpressing DUOX2, while the overexpression of RPL3 significantly reversed this trend. ( C ) Wound healing assay. The migration rate was derived from the ratio of the difference in wound area at different times to the initial wound area (200×). The tests were performed on SW480 cells. N.S. P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001. ( D ) Differentially expressed genes in DUOX2 knockdown (si1-DUOX2, si2-DUOX2) and negative control (si-NC) by next-generation sequencing as shown in the heatmap. ( E ) Different signaling pathways based on KEGG databases between si1-DUOX2 and si-NC group, or si2-DUOX2 and si-NC group. ( F ) Verification of related genes in PI3K–AKT pathway. ( G ) WB assay. The protein levels of <t>E-cadherin</t> (E-cad), EGFR, AKT, p-AKT, c-MYC after overexpression of DUOX2, or both of DUOX2 and RPL3.
Snail Mab, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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snail mab - by Bioz Stars, 2025-01
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96
Proteintech mouse anti n cadherin
RPL3 reverses the effects of DUOX2 in vitro , and the different genes after DUOX2 knockdown were enriched in the AKT pathway, while RPL3 reversed this change partially. ( A ). Western blotting was performed to detect the DUOX2 protein in DUOX2-overexpressed (pcDNA3.1-DUOX2) and negative control (pcDNA3.1-Control) both in HCT116 and SW480 cells. ( B ) Transwell assays. The migration and invasion ability of the HCT116 and SW480 cells were significantly increased after overexpressing DUOX2, while the overexpression of RPL3 significantly reversed this trend. ( C ) Wound healing assay. The migration rate was derived from the ratio of the difference in wound area at different times to the initial wound area (200×). The tests were performed on SW480 cells. N.S. P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001. ( D ) Differentially expressed genes in DUOX2 knockdown (si1-DUOX2, si2-DUOX2) and negative control (si-NC) by next-generation sequencing as shown in the heatmap. ( E ) Different signaling pathways based on KEGG databases between si1-DUOX2 and si-NC group, or si2-DUOX2 and si-NC group. ( F ) Verification of related genes in PI3K–AKT pathway. ( G ) WB assay. The protein levels of <t>E-cadherin</t> (E-cad), EGFR, AKT, p-AKT, c-MYC after overexpression of DUOX2, or both of DUOX2 and RPL3.
Mouse Anti N Cadherin, supplied by Proteintech, 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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mouse anti n cadherin - by Bioz Stars, 2025-01
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96
Proteintech mouse monoclonal anti e cadherin
RPL3 reverses the effects of DUOX2 in vitro , and the different genes after DUOX2 knockdown were enriched in the AKT pathway, while RPL3 reversed this change partially. ( A ). Western blotting was performed to detect the DUOX2 protein in DUOX2-overexpressed (pcDNA3.1-DUOX2) and negative control (pcDNA3.1-Control) both in HCT116 and SW480 cells. ( B ) Transwell assays. The migration and invasion ability of the HCT116 and SW480 cells were significantly increased after overexpressing DUOX2, while the overexpression of RPL3 significantly reversed this trend. ( C ) Wound healing assay. The migration rate was derived from the ratio of the difference in wound area at different times to the initial wound area (200×). The tests were performed on SW480 cells. N.S. P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001. ( D ) Differentially expressed genes in DUOX2 knockdown (si1-DUOX2, si2-DUOX2) and negative control (si-NC) by next-generation sequencing as shown in the heatmap. ( E ) Different signaling pathways based on KEGG databases between si1-DUOX2 and si-NC group, or si2-DUOX2 and si-NC group. ( F ) Verification of related genes in PI3K–AKT pathway. ( G ) WB assay. The protein levels of <t>E-cadherin</t> (E-cad), EGFR, AKT, p-AKT, c-MYC after overexpression of DUOX2, or both of DUOX2 and RPL3.
Mouse Monoclonal Anti E Cadherin, supplied by Proteintech, 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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96/100 stars
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Image Search Results


RPL3 reverses the effects of DUOX2 in vitro , and the different genes after DUOX2 knockdown were enriched in the AKT pathway, while RPL3 reversed this change partially. ( A ). Western blotting was performed to detect the DUOX2 protein in DUOX2-overexpressed (pcDNA3.1-DUOX2) and negative control (pcDNA3.1-Control) both in HCT116 and SW480 cells. ( B ) Transwell assays. The migration and invasion ability of the HCT116 and SW480 cells were significantly increased after overexpressing DUOX2, while the overexpression of RPL3 significantly reversed this trend. ( C ) Wound healing assay. The migration rate was derived from the ratio of the difference in wound area at different times to the initial wound area (200×). The tests were performed on SW480 cells. N.S. P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001. ( D ) Differentially expressed genes in DUOX2 knockdown (si1-DUOX2, si2-DUOX2) and negative control (si-NC) by next-generation sequencing as shown in the heatmap. ( E ) Different signaling pathways based on KEGG databases between si1-DUOX2 and si-NC group, or si2-DUOX2 and si-NC group. ( F ) Verification of related genes in PI3K–AKT pathway. ( G ) WB assay. The protein levels of E-cadherin (E-cad), EGFR, AKT, p-AKT, c-MYC after overexpression of DUOX2, or both of DUOX2 and RPL3.

Journal: Carcinogenesis

Article Title: DUOX2 promotes the progression of colorectal cancer cells by regulating the AKT pathway and interacting with RPL3

doi: 10.1093/carcin/bgaa056

Figure Lengend Snippet: RPL3 reverses the effects of DUOX2 in vitro , and the different genes after DUOX2 knockdown were enriched in the AKT pathway, while RPL3 reversed this change partially. ( A ). Western blotting was performed to detect the DUOX2 protein in DUOX2-overexpressed (pcDNA3.1-DUOX2) and negative control (pcDNA3.1-Control) both in HCT116 and SW480 cells. ( B ) Transwell assays. The migration and invasion ability of the HCT116 and SW480 cells were significantly increased after overexpressing DUOX2, while the overexpression of RPL3 significantly reversed this trend. ( C ) Wound healing assay. The migration rate was derived from the ratio of the difference in wound area at different times to the initial wound area (200×). The tests were performed on SW480 cells. N.S. P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001. ( D ) Differentially expressed genes in DUOX2 knockdown (si1-DUOX2, si2-DUOX2) and negative control (si-NC) by next-generation sequencing as shown in the heatmap. ( E ) Different signaling pathways based on KEGG databases between si1-DUOX2 and si-NC group, or si2-DUOX2 and si-NC group. ( F ) Verification of related genes in PI3K–AKT pathway. ( G ) WB assay. The protein levels of E-cadherin (E-cad), EGFR, AKT, p-AKT, c-MYC after overexpression of DUOX2, or both of DUOX2 and RPL3.

Article Snippet: The antibodies for ubiquitin, GAPDH, E-cadherin and N-cadherin were purchased from Proteintech (Wuhan, China).

Techniques: In Vitro, Western Blot, Negative Control, Migration, Over Expression, Wound Healing Assay, Derivative Assay, Next-Generation Sequencing