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dvl2 orf (Addgene inc)

Name: dvl2 orf
Brand: Addgene inc
Rating: 93 (21 reviews)

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DIXDC1 upregulates VEGFR2 via <t>Dvl2.</t> A DIXDC1 or control vector, and VEGFR2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and VEGFR2 result revealed that no direct interaction between DIXDC1 and VEGFR2. B DIXDC1 or control vector, and Dvl2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and Dvl2 result revealed that there is an interaction between DIXDC1 and Dvl2. C Endogenous immunoprecipitation with antibodies against Dvl2 and VEGFR2 and there is an interaction between the two proteins in HUVEC. D Control siRNA or siDIX1 is transfected to HUVEC and subjected to immunoprecipitation antibody against Dvl2. E, F, G, and H Quantification of relative intensity of immunoprecipitated VEGFR2, Dvl2, and input VEGFR2 and Dvl2 of D . I DIXDC1 was overexpressed and there was a positive correlation between the expression level of DIXDC1 and Dvl2. J Quantification of relative intensity of Dvl2 in I . K DIXDC1, Dvl2, and VEGFR2 were co-overexpressed in HEK293T and the expression level of VEGFR2 and Dvl2 was observed. L Quantification of relative intensity of VEGFR2 in K . All Experiments were repeated at least 4 different sets. *p < 0.05, **p < 0.005, and ***p < 0.0001, by paired, 2-tailed Student’s t test and one-way ANOVA. Error bars represent the mean ± SD. Individual values can be found in Additional file : Fig 5

Dvl2 Orf, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "DIX domain containing 1 (DIXDC1) modulates VEGFR2 level in vasculatures to regulate embryonic and postnatal retina angiogenesis"

Article Title: DIX domain containing 1 (DIXDC1) modulates VEGFR2 level in vasculatures to regulate embryonic and postnatal retina angiogenesis

Journal: BMC Biology

doi: 10.1186/s12915-022-01240-3

DIXDC1 upregulates VEGFR2 via Dvl2. A DIXDC1 or control vector, and VEGFR2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and VEGFR2 result revealed that no direct interaction between DIXDC1 and VEGFR2. B DIXDC1 or control vector, and Dvl2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and Dvl2 result revealed that there is an interaction between DIXDC1 and Dvl2. C Endogenous immunoprecipitation with antibodies against Dvl2 and VEGFR2 and there is an interaction between the two proteins in HUVEC. D Control siRNA or siDIX1 is transfected to HUVEC and subjected to immunoprecipitation antibody against Dvl2. E, F, G, and H Quantification of relative intensity of immunoprecipitated VEGFR2, Dvl2, and input VEGFR2 and Dvl2 of D . I DIXDC1 was overexpressed and there was a positive correlation between the expression level of DIXDC1 and Dvl2. J Quantification of relative intensity of Dvl2 in I . K DIXDC1, Dvl2, and VEGFR2 were co-overexpressed in HEK293T and the expression level of VEGFR2 and Dvl2 was observed. L Quantification of relative intensity of VEGFR2 in K . All Experiments were repeated at least 4 different sets. *p < 0.05, **p < 0.005, and ***p < 0.0001, by paired, 2-tailed Student’s t test and one-way ANOVA. Error bars represent the mean ± SD. Individual values can be found in Additional file : Fig 5

Figure Legend Snippet: DIXDC1 upregulates VEGFR2 via Dvl2. A DIXDC1 or control vector, and VEGFR2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and VEGFR2 result revealed that no direct interaction between DIXDC1 and VEGFR2. B DIXDC1 or control vector, and Dvl2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and Dvl2 result revealed that there is an interaction between DIXDC1 and Dvl2. C Endogenous immunoprecipitation with antibodies against Dvl2 and VEGFR2 and there is an interaction between the two proteins in HUVEC. D Control siRNA or siDIX1 is transfected to HUVEC and subjected to immunoprecipitation antibody against Dvl2. E, F, G, and H Quantification of relative intensity of immunoprecipitated VEGFR2, Dvl2, and input VEGFR2 and Dvl2 of D . I DIXDC1 was overexpressed and there was a positive correlation between the expression level of DIXDC1 and Dvl2. J Quantification of relative intensity of Dvl2 in I . K DIXDC1, Dvl2, and VEGFR2 were co-overexpressed in HEK293T and the expression level of VEGFR2 and Dvl2 was observed. L Quantification of relative intensity of VEGFR2 in K . All Experiments were repeated at least 4 different sets. *p < 0.05, **p < 0.005, and ***p < 0.0001, by paired, 2-tailed Student’s t test and one-way ANOVA. Error bars represent the mean ± SD. Individual values can be found in Additional file : Fig 5

Techniques Used: Control, Plasmid Preparation, Transfection, Immunoprecipitation, Expressing

DIXDC1 increases wnt/ β-catenin signaling and VEGFR2 stability via Dvl2. A knockdown of DIXDC1 affects the VEGF-induced signaling pathways (40 ng/ml) in HUVEC. B, C, and D Quantification of relative intensity of p-VEGFR2(Y1175), P-ERK1/2, and p-FAK of A . E Knockdown of DIXDC1 affects the wnt/β-catenin signaling pathways (200 ng/ml wnt3a) in HUVEC. F, G, H, and I Quantification of relative intensity of VEGFR2, non-p-β-catenin, β-catenin, and Dvl2 of E . J Interaction between Dvl2 and VEGFR2 is affected by DIXDC1 and wnt3a (200 ng/ml) in HUVEC. K, L Quantification of relative intensity of immunoprecipitated VEGFR2 and Dvl2. M Suppression of DIXDC1 affects the level of HIF1a in oxygen glucose-deprived condition in HUVEC. N, O, P, Q, R, and S Quantification of relative intensity of VEGFR2, HIF1a, non-p-β-catenin, β-catenin, Dvl2, and DIXDC1 of M . T VEGFR2, Dvl2, and DIXDC1 transfected to HEK293T and treated with MG132. Accumulation of VEGFR2 level was observed with MG132. U Quantification of relative intensity of VEGFR2 of T . All Experiments were repeated at least 4 different sets. *p < 0.05, **p < 0.005, and ***p < 0.0001, by one-way ANOVA. Error bars represent the mean ± SD. Individual values can be found in Additional file : Fig. 6

Figure Legend Snippet: DIXDC1 increases wnt/ β-catenin signaling and VEGFR2 stability via Dvl2. A knockdown of DIXDC1 affects the VEGF-induced signaling pathways (40 ng/ml) in HUVEC. B, C, and D Quantification of relative intensity of p-VEGFR2(Y1175), P-ERK1/2, and p-FAK of A . E Knockdown of DIXDC1 affects the wnt/β-catenin signaling pathways (200 ng/ml wnt3a) in HUVEC. F, G, H, and I Quantification of relative intensity of VEGFR2, non-p-β-catenin, β-catenin, and Dvl2 of E . J Interaction between Dvl2 and VEGFR2 is affected by DIXDC1 and wnt3a (200 ng/ml) in HUVEC. K, L Quantification of relative intensity of immunoprecipitated VEGFR2 and Dvl2. M Suppression of DIXDC1 affects the level of HIF1a in oxygen glucose-deprived condition in HUVEC. N, O, P, Q, R, and S Quantification of relative intensity of VEGFR2, HIF1a, non-p-β-catenin, β-catenin, Dvl2, and DIXDC1 of M . T VEGFR2, Dvl2, and DIXDC1 transfected to HEK293T and treated with MG132. Accumulation of VEGFR2 level was observed with MG132. U Quantification of relative intensity of VEGFR2 of T . All Experiments were repeated at least 4 different sets. *p < 0.05, **p < 0.005, and ***p < 0.0001, by one-way ANOVA. Error bars represent the mean ± SD. Individual values can be found in Additional file : Fig. 6

Techniques Used: Knockdown, Protein-Protein interactions, Immunoprecipitation, Transfection

Image Search Results

NOTCH1 intracellular domain (NICD1) and dishevelled (DVL) overexpression restored the tumorigenic potential of ASPM‐i1‐deficient HCC cells. (A) Relative Notch‐specific luciferase activity in SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of ASPM ‐v1 expression along with the lentivirus‐mediated overexpression of NICD1 or NICD1 (T2511A) ( n = 3 independent experiments). Data are shown as mean ± SEM. *** P < 0.001, NS, not significant, two‐tailed unpaired t test. (B) The relative transcript levels of representative Notch target genes in SNU‐449 cells transduced with non‐target shRNA or ASPM ‐v1 shRNA (construct #4) without (vector) or with the concurrent overexpression of NICD1 following stimulation with JAG1‐Fc (5 μg·mL −1 for 24 h) as measured by qRT‐PCR ( n = 3 independent experiments). Data are shown as mean ± SEM and statistically analyzed by two‐tailed unpaired t test. * P < 0.05, compared with non‐target shRNA; † P < 0.05, compared with ASPM ‐v1 shRNA #4 plus vector. (C) Line graphs showing the number of SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of ASPM ‐v1 expression without (vector) or with the lentivirus‐mediated NICD1 overexpression ( n = 3 independent experiments). Data are shown as mean ± SEM, and statistically analyzed by two‐tailed unpaired t test. * P < 0.05, *** P < 0.001 compared with non‐target shRNA. (D) The relative transcript level of NOTCH1 in SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of NOTCH1 expression as measured by qRT‐PCR ( n = 3 independent experiments). Two lentivirus shRNA constructs (TRCN0000350253 and TRCN0000350330) were used for the genetic knockdown. (E) Line graphs showing the number of SNU‐449 cells lentivirally transduced with a non‐target shRNA or the NOTCH1 ‐targeted shRNA as in (D) ( n = 4 independent experiments). Data are shown as mean ± SEM. * P < 0.05, *** P < 0.001 compared with non‐target shRNA in (D) and (E), two‐tailed unpaired t test. (F) Representative phase‐contrast images of the tumorspheres formed by SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of NOTCH1 expression as in (D). Scale bar denotes 100 μ m (top). Limiting dilution assay demonstrating the tumorsphere‐forming efficacy (bottom) ( n = 5 independent experiments). (G) Representative phase‐contrast images of tumorspheres formed by SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of ASPM ‐v1 expression without or with the lentivirus‐mediated overexpression of NICD1, NICD1, and DVL1, or NICD1 and DVL2. Scale bar denotes 100 μ m . (H) Limiting dilution assay demonstrating the tumorsphere‐forming efficacy of the cells in (G). Bars represent maximum likelihood estimates with a 95% confidence interval ( n = 16, control group; n = 8, experimental groups). * P < 0.05, *** P < 0.001, NS, not significant, the likelihood ratio test and Chi‐square test in (F) and (H).

Journal: Molecular Oncology

Article Title: ASPM stabilizes the NOTCH intracellular domain 1 and promotes oncogenesis by blocking FBXW7 binding in hepatocellular carcinoma cells

doi: 10.1002/1878-0261.13589

Figure Lengend Snippet: NOTCH1 intracellular domain (NICD1) and dishevelled (DVL) overexpression restored the tumorigenic potential of ASPM‐i1‐deficient HCC cells. (A) Relative Notch‐specific luciferase activity in SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of ASPM ‐v1 expression along with the lentivirus‐mediated overexpression of NICD1 or NICD1 (T2511A) ( n = 3 independent experiments). Data are shown as mean ± SEM. *** P < 0.001, NS, not significant, two‐tailed unpaired t test. (B) The relative transcript levels of representative Notch target genes in SNU‐449 cells transduced with non‐target shRNA or ASPM ‐v1 shRNA (construct #4) without (vector) or with the concurrent overexpression of NICD1 following stimulation with JAG1‐Fc (5 μg·mL −1 for 24 h) as measured by qRT‐PCR ( n = 3 independent experiments). Data are shown as mean ± SEM and statistically analyzed by two‐tailed unpaired t test. * P < 0.05, compared with non‐target shRNA; † P < 0.05, compared with ASPM ‐v1 shRNA #4 plus vector. (C) Line graphs showing the number of SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of ASPM ‐v1 expression without (vector) or with the lentivirus‐mediated NICD1 overexpression ( n = 3 independent experiments). Data are shown as mean ± SEM, and statistically analyzed by two‐tailed unpaired t test. * P < 0.05, *** P < 0.001 compared with non‐target shRNA. (D) The relative transcript level of NOTCH1 in SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of NOTCH1 expression as measured by qRT‐PCR ( n = 3 independent experiments). Two lentivirus shRNA constructs (TRCN0000350253 and TRCN0000350330) were used for the genetic knockdown. (E) Line graphs showing the number of SNU‐449 cells lentivirally transduced with a non‐target shRNA or the NOTCH1 ‐targeted shRNA as in (D) ( n = 4 independent experiments). Data are shown as mean ± SEM. * P < 0.05, *** P < 0.001 compared with non‐target shRNA in (D) and (E), two‐tailed unpaired t test. (F) Representative phase‐contrast images of the tumorspheres formed by SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of NOTCH1 expression as in (D). Scale bar denotes 100 μ m (top). Limiting dilution assay demonstrating the tumorsphere‐forming efficacy (bottom) ( n = 5 independent experiments). (G) Representative phase‐contrast images of tumorspheres formed by SNU‐449 cells without (non‐target shRNA) or with shRNA‐mediated knockdown of ASPM ‐v1 expression without or with the lentivirus‐mediated overexpression of NICD1, NICD1, and DVL1, or NICD1 and DVL2. Scale bar denotes 100 μ m . (H) Limiting dilution assay demonstrating the tumorsphere‐forming efficacy of the cells in (G). Bars represent maximum likelihood estimates with a 95% confidence interval ( n = 16, control group; n = 8, experimental groups). * P < 0.05, *** P < 0.001, NS, not significant, the likelihood ratio test and Chi‐square test in (F) and (H).

Article Snippet: The coding sequence of human DVL2 was PCR amplified from a DVL2 expression vector (Origene #RC202233; Rockville, MD, USA) and subcloned into the pLenti‐His lentivirus vector (Applied Biological Materials, ABM, Richmond, BC, Canada).

Techniques: Over Expression, Luciferase, Activity Assay, shRNA, Knockdown, Expressing, Two Tailed Test, Transduction, Construct, Plasmid Preparation, Quantitative RT-PCR, Limiting Dilution Assay, Control

Journal: BMC Biology

Article Title: DIX domain containing 1 (DIXDC1) modulates VEGFR2 level in vasculatures to regulate embryonic and postnatal retina angiogenesis

doi: 10.1186/s12915-022-01240-3

Figure Lengend Snippet: DIXDC1 upregulates VEGFR2 via Dvl2. A DIXDC1 or control vector, and VEGFR2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and VEGFR2 result revealed that no direct interaction between DIXDC1 and VEGFR2. B DIXDC1 or control vector, and Dvl2 was co-transfected in HEK293T. Immunoprecipitation with antibody against DIXDC1 and Dvl2 result revealed that there is an interaction between DIXDC1 and Dvl2. C Endogenous immunoprecipitation with antibodies against Dvl2 and VEGFR2 and there is an interaction between the two proteins in HUVEC. D Control siRNA or siDIX1 is transfected to HUVEC and subjected to immunoprecipitation antibody against Dvl2. E, F, G, and H Quantification of relative intensity of immunoprecipitated VEGFR2, Dvl2, and input VEGFR2 and Dvl2 of D . I DIXDC1 was overexpressed and there was a positive correlation between the expression level of DIXDC1 and Dvl2. J Quantification of relative intensity of Dvl2 in I . K DIXDC1, Dvl2, and VEGFR2 were co-overexpressed in HEK293T and the expression level of VEGFR2 and Dvl2 was observed. L Quantification of relative intensity of VEGFR2 in K . All Experiments were repeated at least 4 different sets. *p < 0.05, **p < 0.005, and ***p < 0.0001, by paired, 2-tailed Student’s t test and one-way ANOVA. Error bars represent the mean ± SD. Individual values can be found in Additional file : Fig 5

Article Snippet: The Dvl2 ORF-containing plasmid 3XFlag-Dvl2(Item #24802) was purchased from Addgene (Cambridge, MA, USA). pEGFP-C2 was used as a transfection control (Clontech).

Techniques: Control, Plasmid Preparation, Transfection, Immunoprecipitation, Expressing

Journal: BMC Biology

Article Title: DIX domain containing 1 (DIXDC1) modulates VEGFR2 level in vasculatures to regulate embryonic and postnatal retina angiogenesis

doi: 10.1186/s12915-022-01240-3

Figure Lengend Snippet: DIXDC1 increases wnt/ β-catenin signaling and VEGFR2 stability via Dvl2. A knockdown of DIXDC1 affects the VEGF-induced signaling pathways (40 ng/ml) in HUVEC. B, C, and D Quantification of relative intensity of p-VEGFR2(Y1175), P-ERK1/2, and p-FAK of A . E Knockdown of DIXDC1 affects the wnt/β-catenin signaling pathways (200 ng/ml wnt3a) in HUVEC. F, G, H, and I Quantification of relative intensity of VEGFR2, non-p-β-catenin, β-catenin, and Dvl2 of E . J Interaction between Dvl2 and VEGFR2 is affected by DIXDC1 and wnt3a (200 ng/ml) in HUVEC. K, L Quantification of relative intensity of immunoprecipitated VEGFR2 and Dvl2. M Suppression of DIXDC1 affects the level of HIF1a in oxygen glucose-deprived condition in HUVEC. N, O, P, Q, R, and S Quantification of relative intensity of VEGFR2, HIF1a, non-p-β-catenin, β-catenin, Dvl2, and DIXDC1 of M . T VEGFR2, Dvl2, and DIXDC1 transfected to HEK293T and treated with MG132. Accumulation of VEGFR2 level was observed with MG132. U Quantification of relative intensity of VEGFR2 of T . All Experiments were repeated at least 4 different sets. *p < 0.05, **p < 0.005, and ***p < 0.0001, by one-way ANOVA. Error bars represent the mean ± SD. Individual values can be found in Additional file : Fig. 6

Article Snippet: The Dvl2 ORF-containing plasmid 3XFlag-Dvl2(Item #24802) was purchased from Addgene (Cambridge, MA, USA). pEGFP-C2 was used as a transfection control (Clontech).

Techniques: Knockdown, Protein-Protein interactions, Immunoprecipitation, Transfection

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1) Product Images from "DIX domain containing 1 (DIXDC1) modulates VEGFR2 level in vasculatures to regulate embryonic and postnatal retina angiogenesis"

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