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sk mes 1  (DSMZ)


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    DSMZ sk mes 1
    Sk Mes 1, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sk+mes+1/SK-MES-1/bio_rxiv__64898__2026__03__11__711115-176-73-90
    Average 94 stars, based on 8 article reviews
    sk mes 1 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Derivative Assay:

    Article Title: Proteasome inhibitors modulate chemokine production in lung epithelial and monocytic cells.
    Article Snippet: .. The epithelial cell lines: A549, derived from an alveolar lung carcinoma; SK-MES-1, derived from a lung squamous cell carcinoma; and Mono-Mac-6 and THP-1, which were isolated from patients with acute monocytic leukaemia; were obtained from DSMZ (Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH (a German collection of microorganisms and cell cultures) Braunschweig, Germany). .. NCI-H727, a bronchial epithelial carcinoid line, was obtained from the American Type Culture Collection (Manassas, Virginia, USA).

    Isolation:

    Article Title: Proteasome inhibitors modulate chemokine production in lung epithelial and monocytic cells.
    Article Snippet: .. The epithelial cell lines: A549, derived from an alveolar lung carcinoma; SK-MES-1, derived from a lung squamous cell carcinoma; and Mono-Mac-6 and THP-1, which were isolated from patients with acute monocytic leukaemia; were obtained from DSMZ (Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH (a German collection of microorganisms and cell cultures) Braunschweig, Germany). .. NCI-H727, a bronchial epithelial carcinoid line, was obtained from the American Type Culture Collection (Manassas, Virginia, USA).

    other:

    Article Title: Systematic Evaluation Defines the Limits of Ferroptosis in Cancer Therapy
    Article Snippet: TXNRD1 (SC-28321), GCLC (SC-166345) from Santa Cruz Goat Anti-mouse IgG (H+L), HRP (Invitrogen; 62-6520) Goat Anti-rabbit IgG (H+L), HRP (Invitrogen; 31460).

    Cell Culture:

    Article Title: TRAIL-coated lipid-nanoparticles overcome resistance to soluble recombinant TRAIL in non-small cell lung cancer cells.
    Article Snippet: Purpose.. Non-small cell lung cancer (NSCLC) is one the types of cancer with higher prevalence and mortality.. Apo2-Ligand/TRAIL is a TNF family member able to induce apoptosis in tumor cells but not in normal cells.



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    Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in <t>A549</t> <t>(LUAD),</t> <t>SK-MES-1</t> (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.
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    Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in <t>A549</t> <t>(LUAD),</t> <t>SK-MES-1</t> (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.
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    Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in <t>A549</t> <t>(LUAD),</t> <t>SK-MES-1</t> (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.
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    Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in <t>A549</t> <t>(LUAD),</t> <t>SK-MES-1</t> (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.
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    Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in <t>A549</t> <t>(LUAD),</t> <t>SK-MES-1</t> (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.
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    Transformation-induced changes to the protein composition of cell-derived sEVs (A) The morphology of isolated sEVs was assessed using transmission electron microscopy. Images of normal and transformed HBEC-derived sEVs (scale bars, 200 nm). (B) Nanoparticle analysis using tunable resistive pulse sensing of sEVs isolated from HBECs demonstrates that the majority of sEVs have a size range between 30 and 150 nm, and that transformation does not result in an increase in sEV secretion. (C) Western blot of sEVs from HBECs demonstrating the presence of sEV proteins HSP70 and CD63 and the absence of the cell marker calnexin. (D) Label-free mass spectrometry identified 148 proteins with greater abundance in sEVs derived from transformed HBECs (FDR <0.02), of which 15 were annotated as extracellular proteins. (E) Mass spectrometry results were confirmed using ELISA for THBS1, NID1, PTX3, and VCAN in sEVs derived from normal and transformed HBECs. (F) sEVs derived from 22 cancer cell lines including NSCLC <t>(SKMES1,</t> H1650, HCC4006, and H2170), glioblastoma ([GBM], D54, D270, U87, and U118), colorectal cancer ([CRC], HT29 and SW620), breast cancer ([BCa], BT549, MDA231, and MDA436), prostate cancer ([PCa], PC3 and LNCaP), melanoma ([MEL], A375, MAMEL65, and SKMEL28), esophageal cancer ([ECa], OE19), and ovarian cancer ([OVA], A2780, CAOV3, IGROV1, and OVCAR8) showed a clear increase in expression of THBS1, NID1, PTX3, and VCAN in relation to the average levels of sEVs from normal cells ([HBEC] 30KT, HOSE 6.3, and HOSE 17.1). Samples in mass spectrometry and ELISA were measured in triplicate. See also and .
    Sk Mes 1, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sk+mes+1/SK-MES-1/bio_rxiv__64898__2026__03__11__711115-176-73-90
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    sk mes 1  (ATCC)
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    ATCC sk mes 1
    Transformation-induced changes to the protein composition of cell-derived sEVs (A) The morphology of isolated sEVs was assessed using transmission electron microscopy. Images of normal and transformed HBEC-derived sEVs (scale bars, 200 nm). (B) Nanoparticle analysis using tunable resistive pulse sensing of sEVs isolated from HBECs demonstrates that the majority of sEVs have a size range between 30 and 150 nm, and that transformation does not result in an increase in sEV secretion. (C) Western blot of sEVs from HBECs demonstrating the presence of sEV proteins HSP70 and CD63 and the absence of the cell marker calnexin. (D) Label-free mass spectrometry identified 148 proteins with greater abundance in sEVs derived from transformed HBECs (FDR <0.02), of which 15 were annotated as extracellular proteins. (E) Mass spectrometry results were confirmed using ELISA for THBS1, NID1, PTX3, and VCAN in sEVs derived from normal and transformed HBECs. (F) sEVs derived from 22 cancer cell lines including NSCLC <t>(SKMES1,</t> H1650, HCC4006, and H2170), glioblastoma ([GBM], D54, D270, U87, and U118), colorectal cancer ([CRC], HT29 and SW620), breast cancer ([BCa], BT549, MDA231, and MDA436), prostate cancer ([PCa], PC3 and LNCaP), melanoma ([MEL], A375, MAMEL65, and SKMEL28), esophageal cancer ([ECa], OE19), and ovarian cancer ([OVA], A2780, CAOV3, IGROV1, and OVCAR8) showed a clear increase in expression of THBS1, NID1, PTX3, and VCAN in relation to the average levels of sEVs from normal cells ([HBEC] 30KT, HOSE 6.3, and HOSE 17.1). Samples in mass spectrometry and ELISA were measured in triplicate. See also and .
    Sk Mes 1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sk+mes+1/SK-MES-1/bio_rxiv__64898__2026__03__11__711115-176-73-78
    Average 96 stars, based on 1 article reviews
    sk mes 1 - by Bioz Stars, 2026-10
    96/100 stars
    		  Buy from Supplier

    Image Search Results


    Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in A549 (LUAD), SK-MES-1 (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.

    Journal: Oncology Letters

    Article Title: LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches

    doi: 10.3892/ol.2026.15671

    Figure Lengend Snippet: Functional impact of LATS2 upregulation on LUAD/LUSC cell viability and apoptosis. (A) Baseline LATS2 expression comparison in A549 (LUAD), SK-MES-1 (LUSC) and Beas-2B (normal bronchial) cell lines. (B) Western blot validation of LATS2 protein overexpression post-transfection. (C) Transfection efficiency confirmation via fluorescence labeling (MOI=10; transfection rate=90.5 and 90% in LUAD and LUSC, respectively). Scale bar, 100 µm. (D) qPCR quantification of LATS2 mRNA induction post-transfection. (E) MTT assay evaluation of cell proliferation changes following LATS2 upregulation. (F) Flow cytometry analysis of apoptosis rate alterations after LATS2 upregulation. Data are presented as mean ± SD and all comparisons were conducted using independent samples t-test. *P<0.05, **P<0.01 and ***P<0.001. LATS2, large tumor suppressor kinase 2; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; BC, blank control; NC, negative control; OE, overexpression; OD, optical density; MOI, multiplicity of infection; qPCR, quantitative PCR.

    Article Snippet: The A549 and SK-MES-1 cells (Procell Life Science & Technology Co., Ltd.) were divided into BC (blank control (BC), negative control (NC) and overexpression (OE) groups.

    Techniques: Functional Assay, Expressing, Comparison, Western Blot, Biomarker Discovery, Over Expression, Transfection, Fluorescence, Labeling, MTT Assay, Flow Cytometry, Control, Negative Control, Infection, Real-time Polymerase Chain Reaction

    Influence of LATS2 overexpression on LUAD and LUSC cell migration and invasion. (A) Wound healing assay in A549 cells. (B) Wound healing assay in SK-MES-1 cell lines. (C) Transwell assay evaluating altered invasive capacity of A549 and SK-MES-1 cells. (D) Comparison of cell migration rates. (E) Comparison of number of invading cells. Scale bar, 100 µm, **P<0.01 and ***P<0.001. LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; LATS2, large tumor suppressor kinase 2; BC, blank control; NC, negative control; OE, overexpression.

    Journal: Oncology Letters

    Article Title: LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches

    doi: 10.3892/ol.2026.15671

    Figure Lengend Snippet: Influence of LATS2 overexpression on LUAD and LUSC cell migration and invasion. (A) Wound healing assay in A549 cells. (B) Wound healing assay in SK-MES-1 cell lines. (C) Transwell assay evaluating altered invasive capacity of A549 and SK-MES-1 cells. (D) Comparison of cell migration rates. (E) Comparison of number of invading cells. Scale bar, 100 µm, **P<0.01 and ***P<0.001. LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; LATS2, large tumor suppressor kinase 2; BC, blank control; NC, negative control; OE, overexpression.

    Article Snippet: The A549 and SK-MES-1 cells (Procell Life Science & Technology Co., Ltd.) were divided into BC (blank control (BC), negative control (NC) and overexpression (OE) groups.

    Techniques: Over Expression, Migration, Wound Healing Assay, Transwell Assay, Comparison, Control, Negative Control

    Transformation-induced changes to the protein composition of cell-derived sEVs (A) The morphology of isolated sEVs was assessed using transmission electron microscopy. Images of normal and transformed HBEC-derived sEVs (scale bars, 200 nm). (B) Nanoparticle analysis using tunable resistive pulse sensing of sEVs isolated from HBECs demonstrates that the majority of sEVs have a size range between 30 and 150 nm, and that transformation does not result in an increase in sEV secretion. (C) Western blot of sEVs from HBECs demonstrating the presence of sEV proteins HSP70 and CD63 and the absence of the cell marker calnexin. (D) Label-free mass spectrometry identified 148 proteins with greater abundance in sEVs derived from transformed HBECs (FDR <0.02), of which 15 were annotated as extracellular proteins. (E) Mass spectrometry results were confirmed using ELISA for THBS1, NID1, PTX3, and VCAN in sEVs derived from normal and transformed HBECs. (F) sEVs derived from 22 cancer cell lines including NSCLC (SKMES1, H1650, HCC4006, and H2170), glioblastoma ([GBM], D54, D270, U87, and U118), colorectal cancer ([CRC], HT29 and SW620), breast cancer ([BCa], BT549, MDA231, and MDA436), prostate cancer ([PCa], PC3 and LNCaP), melanoma ([MEL], A375, MAMEL65, and SKMEL28), esophageal cancer ([ECa], OE19), and ovarian cancer ([OVA], A2780, CAOV3, IGROV1, and OVCAR8) showed a clear increase in expression of THBS1, NID1, PTX3, and VCAN in relation to the average levels of sEVs from normal cells ([HBEC] 30KT, HOSE 6.3, and HOSE 17.1). Samples in mass spectrometry and ELISA were measured in triplicate. See also and .

    Journal: Cell Reports Medicine

    Article Title: Early-stage multi-cancer detection through a plasma extracellular vesicle protein signature

    doi: 10.1016/j.xcrm.2026.102694

    Figure Lengend Snippet: Transformation-induced changes to the protein composition of cell-derived sEVs (A) The morphology of isolated sEVs was assessed using transmission electron microscopy. Images of normal and transformed HBEC-derived sEVs (scale bars, 200 nm). (B) Nanoparticle analysis using tunable resistive pulse sensing of sEVs isolated from HBECs demonstrates that the majority of sEVs have a size range between 30 and 150 nm, and that transformation does not result in an increase in sEV secretion. (C) Western blot of sEVs from HBECs demonstrating the presence of sEV proteins HSP70 and CD63 and the absence of the cell marker calnexin. (D) Label-free mass spectrometry identified 148 proteins with greater abundance in sEVs derived from transformed HBECs (FDR <0.02), of which 15 were annotated as extracellular proteins. (E) Mass spectrometry results were confirmed using ELISA for THBS1, NID1, PTX3, and VCAN in sEVs derived from normal and transformed HBECs. (F) sEVs derived from 22 cancer cell lines including NSCLC (SKMES1, H1650, HCC4006, and H2170), glioblastoma ([GBM], D54, D270, U87, and U118), colorectal cancer ([CRC], HT29 and SW620), breast cancer ([BCa], BT549, MDA231, and MDA436), prostate cancer ([PCa], PC3 and LNCaP), melanoma ([MEL], A375, MAMEL65, and SKMEL28), esophageal cancer ([ECa], OE19), and ovarian cancer ([OVA], A2780, CAOV3, IGROV1, and OVCAR8) showed a clear increase in expression of THBS1, NID1, PTX3, and VCAN in relation to the average levels of sEVs from normal cells ([HBEC] 30KT, HOSE 6.3, and HOSE 17.1). Samples in mass spectrometry and ELISA were measured in triplicate. See also and .

    Article Snippet: SKMES1 , ATCC , HTB-58; RRID: CVCL_0630.

    Techniques: Transformation Assay, Derivative Assay, Isolation, Transmission Assay, Electron Microscopy, Tunable Resistive Pulse Sensing, Western Blot, Marker, Mass Spectrometry, Enzyme-linked Immunosorbent Assay, Expressing