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serum protein free cell freezing medium  (MedChemExpress)


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    Structured Review

    MedChemExpress serum protein free cell freezing medium
    Serum Protein Free Cell Freezing Medium, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/serum+protein+free+cell+freezing+medium/Serum%2FProtein-Free+Cell+Freezing+Medium/pm40683602-52-10-17
    Average 93 stars, based on 5 article reviews
    serum protein free cell freezing medium - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    Lysis:

    Article Title: GSK3β and UCHL3 govern RIPK4 homeostasis via deubiquitination to enhance tumor metastasis in ovarian cancer.
    Article Snippet: Receptor-interacting protein kinase 4 (RIPK4) is increasingly recognized as a pivotal player in ovarian cancer, promoting tumorigenesis and disease progression.. Despite its significance, the posttranslational modifications dictating RIPK4 stability in ovarian cancer remain largely uncharted.. In this study, we first established that RIPK4 levels are markedly higher in metastatic than in primary ovarian cancer tissues through single-cell sequencing.

    Luciferase:

    Article Title: GSK3β and UCHL3 govern RIPK4 homeostasis via deubiquitination to enhance tumor metastasis in ovarian cancer.
    Article Snippet: Receptor-interacting protein kinase 4 (RIPK4) is increasingly recognized as a pivotal player in ovarian cancer, promoting tumorigenesis and disease progression.. Despite its significance, the posttranslational modifications dictating RIPK4 stability in ovarian cancer remain largely uncharted.. In this study, we first established that RIPK4 levels are markedly higher in metastatic than in primary ovarian cancer tissues through single-cell sequencing.

    SYBR Green Assay:

    Article Title: GSK3β and UCHL3 govern RIPK4 homeostasis via deubiquitination to enhance tumor metastasis in ovarian cancer.
    Article Snippet: Receptor-interacting protein kinase 4 (RIPK4) is increasingly recognized as a pivotal player in ovarian cancer, promoting tumorigenesis and disease progression.. Despite its significance, the posttranslational modifications dictating RIPK4 stability in ovarian cancer remain largely uncharted.. In this study, we first established that RIPK4 levels are markedly higher in metastatic than in primary ovarian cancer tissues through single-cell sequencing.

    Real-time Polymerase Chain Reaction:

    Article Title: GSK3β and UCHL3 govern RIPK4 homeostasis via deubiquitination to enhance tumor metastasis in ovarian cancer.
    Article Snippet: Receptor-interacting protein kinase 4 (RIPK4) is increasingly recognized as a pivotal player in ovarian cancer, promoting tumorigenesis and disease progression.. Despite its significance, the posttranslational modifications dictating RIPK4 stability in ovarian cancer remain largely uncharted.. In this study, we first established that RIPK4 levels are markedly higher in metastatic than in primary ovarian cancer tissues through single-cell sequencing.



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    TCF7L2 promotes transcription of PLAUR in GC. a Representative image of the co-localization of TCF7L2 protein (green) and PLAUR (red) in MKN45 cell lines observed by confocal microscopy. b Representative image of the co-localization of TCF7L2 protein (green) and PLAUR (red) in 15 GC tissues (cohort 1) observed via confocal microscopy; the expression of TCF7L2 and PLAUR was positively correlated via fluorescence quantitative analysis. c-d TCF7L2 has a positive regulatory effect on the expression of PLAUR in GC cells. The effects of TCF7L2 silencing on PLAUR mRNA or protein expression in GC cells as detected by RT-qPCR (c) and western blot (d) , respectively. e Motif of the TCF7L2 binding site in the PLAUR promoter, predicted through the JASPAR dataset. f Schematic of the TCF7L2 binding site on the PLAUR promoter. g ChIP-qPCR analysis of TCF7L2 binding to the PLAUR promoter in MKN45 and 293T cell lines. The second position was the most important binding site. e Luciferase activity was determined after mutation of the second TCF7L2 site in the PLAUR promoter in MKN45 and 293T cell lines. The luciferase activity of the wild-type PLAUR promoter was significantly higher than that of mutant PLAUR promoter. Compared with the corresponding control group, * P < 0.001.

    Journal: International Journal of Biological Sciences

    Article Title: TCF7L2 promotes anoikis resistance and metastasis of gastric cancer by transcriptionally activating PLAUR

    doi: 10.7150/ijbs.69933

    Figure Lengend Snippet: TCF7L2 promotes transcription of PLAUR in GC. a Representative image of the co-localization of TCF7L2 protein (green) and PLAUR (red) in MKN45 cell lines observed by confocal microscopy. b Representative image of the co-localization of TCF7L2 protein (green) and PLAUR (red) in 15 GC tissues (cohort 1) observed via confocal microscopy; the expression of TCF7L2 and PLAUR was positively correlated via fluorescence quantitative analysis. c-d TCF7L2 has a positive regulatory effect on the expression of PLAUR in GC cells. The effects of TCF7L2 silencing on PLAUR mRNA or protein expression in GC cells as detected by RT-qPCR (c) and western blot (d) , respectively. e Motif of the TCF7L2 binding site in the PLAUR promoter, predicted through the JASPAR dataset. f Schematic of the TCF7L2 binding site on the PLAUR promoter. g ChIP-qPCR analysis of TCF7L2 binding to the PLAUR promoter in MKN45 and 293T cell lines. The second position was the most important binding site. e Luciferase activity was determined after mutation of the second TCF7L2 site in the PLAUR promoter in MKN45 and 293T cell lines. The luciferase activity of the wild-type PLAUR promoter was significantly higher than that of mutant PLAUR promoter. Compared with the corresponding control group, * P < 0.001.

    Article Snippet: Lysis buffer was used to extract MKN45 and 293T cell total protein, and a BCA kit (Solarbio, Beijing, China) was used to measure the protein concentration.

    Techniques: Confocal Microscopy, Expressing, Fluorescence, Quantitative RT-PCR, Western Blot, Binding Assay, ChIP-qPCR, Luciferase, Activity Assay, Mutagenesis, Control