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- Antigen structure
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- Validations
- Western blot [1]
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- Other assay [3]
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- Product number
- PA5-103744 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- CMTM7 Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide
- Description
- Antibody detects endogenous levels of total CKLF7.
- Reactivity
- Human, Mouse
- Host
- Rabbit
- Isotype
- IgG
- Vial size
- 100 µL
- Concentration
- 1 mg/mL
- Storage
- -20°C
Submitted references Breast cancer cell-derived extracellular vesicles transfer miR-182-5p and promote breast carcinogenesis via the CMTM7/EGFR/AKT axis.
Lu C, Zhao Y, Wang J, Shi W, Dong F, Xin Y, Zhao X, Liu C
Molecular medicine (Cambridge, Mass.) 2021 Jul 16;27(1):78
Molecular medicine (Cambridge, Mass.) 2021 Jul 16;27(1):78
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Western blot analysis of CMTM7 in K562 cell lysate. Samples were incubated with CMTM7 polyclonal antibody (Product # PA5-103744).
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry analysis of paraffin-embedded CMTM7 in human Melanoma tissue. Antigen retrieval was performed using citrate buffer. Samples were blocked with blocking buffer (1.5 hr, 22°C), incubated with CMTM7 polyclonal antibody (Product # PA5-103744) using a dilution of 1:100 (1.5 hr, 22°C), followed by HRP conjugated goat anti-rabbit.
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Fig. 6 EVs-miR-182-5p induces proliferation, migration and angiogenesis of HUVECs through inhibition of CMTM7 and activation of the EGFR/AKT signaling pathway. A Venn diagram of genes related to CMTM7 expression in breast cancer tissue samples from dataset GSE50428, MEM database and LinkedOmics database; B PPI network of 98 intersection genes related to CMTM7 expression constructed using String (in the PPI network, the higher core degree is, the more red the circle color is; otherwise, the lower the core degree, the bluer the color is); C Expression of CMTM7, VEGF, p-EGFR, EGFR, p-AKT and AKT in HUVECs treated with EVs or combined with miR-182-5p inhibitor by Western blot analysis, the statistical power was 1; D Expression of CMTM7, VEGF, p-EGFR, EGFR, p-AKT and AKT in HUVECs treated with EVs or combined with GDC0068 detected by Western blot analysis, the statistical power was 1; E Proliferation of HUVECs treated with EVs or combined with GDC0068 detected by CCK-8 method, the statistical power was 1; F Migration of HUVECs treated with EVs or combined with GDC0068 detected by scratch test, the statistical power was 1; G Migration ability of HUVECs treated with EVs or combined with GDC0068 detected by Transwell assay, the statistical power was 1; H Vessel-like tube formation in vitro of HUVECs treated with EVs or combined with GDC0068, the statistical power was 1. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 compared with control HUVECs, or HUVECs treated with PBS or
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Fig. 7 EVs-miR-182-5p exerts promoting effect on tumorigenesis and metastasis of breast cancer cells in vivo by the CMTM7/EGFR/AKT axis. Mice were treated with EVs + inhibitor NC, EVs + miR-182-5p inhibitor, or EVs + miR-182-5p inhibitor + si-CMTM7. A Tumor volume of nude mice, the statistical power was 1; B Tumor weight of nude mice after 28 days of modeling, the statistical power was 1; C Expression of miR-182-5p in tumor tissues of nude mice detected by RT-qPCR, the statistical power was 1; D Expression of CMTM7, p-EGFR, EGFR, VEGF, p-AKT and AKT protein in tumor tissues of nude mice detected by Western blot analysis, the statistical power was 1; E - F Number E and size ( F ) of pulmonary metastasis in nude mice, the statistical power was 1; G - H CD31 ( G ) and Ki-67 ( H ) immunohistochemical staining of pulmonary metastasis tissues in nude mice, the statistical power was 1. N = 10 for mice following each treatment. **** p < 0.0001 compared with mice treated with EVs + inhibitor NC. #### p < 0.0001 compared with HUVECs treated with EVs + miR-182-5p inhibitor + si-NC. The experiment was conducted three times independently
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Additional file 3: Fig. S2. CMTM1 exerts suppressed HUVECs proliferation, migration and angiogenesis. HUVECs were treated with oe-CMTM7 or EVs or EVs + oe-CMTM7. The mRNA (A) and protein (B) expression of CMTM7 detected by RT-qPCR and Western blot analysis, respectively. The statistical power was 1; (C) The proliferation of HUVECs detected by CCK-8 assay, the statistical power was 1; (D) Migration ability of HUVECs detected by scratch test, the statistical power was 1; (E) Migration ability of HUVECs detected by Transwell assay, the statistical power was 1; (F) Vessel-like tube formation in vitro of HUVEC, the statistical power was 1. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 compared with HUVEC; # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.001compared with HUVEC treated with EVs. The experiment was conducted three times independently.
