anonymized healthy control fibroblasts Search Results


anonymized healthy control fibroblasts  (Aladin Enterprises Inc)
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Aladin Enterprises Inc anonymized healthy control fibroblasts
( A ) Human adrenocortical NCI-H295R GFP and GFP-ALADIN over-expressing cells, NCI-H295R1-TR scrambled shRNA and AAAS shRNA ( AAAS knock-down) cells and human skin <t>fibroblasts</t> of healthy wild-type donors and triple A syndrome patients were stained with anti-PGRMC1 (green), anti-Aurora kinase A (AURKA) (red) and DAPI (blue). The different mutations in the human ALADIN protein are denoted as IVS14, S263P and W295X. Scale bars 5 μm, but for NCI-H295R GFP over-expressing cells: 10 μm. ( B ) Schematic drawing of the immunofluorescence staining of PGRMC1 and Aurora kinase A in (A).
Anonymized Healthy Control Fibroblasts, supplied by Aladin Enterprises Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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( A ) Human adrenocortical NCI-H295R GFP and GFP-ALADIN over-expressing cells, NCI-H295R1-TR scrambled shRNA and AAAS shRNA ( AAAS knock-down) cells and human skin fibroblasts of healthy wild-type donors and triple A syndrome patients were stained with anti-PGRMC1 (green), anti-Aurora kinase A (AURKA) (red) and DAPI (blue). The different mutations in the human ALADIN protein are denoted as IVS14, S263P and W295X. Scale bars 5 μm, but for NCI-H295R GFP over-expressing cells: 10 μm. ( B ) Schematic drawing of the immunofluorescence staining of PGRMC1 and Aurora kinase A in (A).

Journal: bioRxiv

Article Title: Triple A patient cells suffering from mitotic defects fail to localize PGRMC1 to mitotic kinetochore fibers

doi: 10.1101/381541

Figure Lengend Snippet: ( A ) Human adrenocortical NCI-H295R GFP and GFP-ALADIN over-expressing cells, NCI-H295R1-TR scrambled shRNA and AAAS shRNA ( AAAS knock-down) cells and human skin fibroblasts of healthy wild-type donors and triple A syndrome patients were stained with anti-PGRMC1 (green), anti-Aurora kinase A (AURKA) (red) and DAPI (blue). The different mutations in the human ALADIN protein are denoted as IVS14, S263P and W295X. Scale bars 5 μm, but for NCI-H295R GFP over-expressing cells: 10 μm. ( B ) Schematic drawing of the immunofluorescence staining of PGRMC1 and Aurora kinase A in (A).

Article Snippet: Here we show that fibroblasts from triple A patients carrying the ALADIN missense mutation S263P or the nonsense mutation W295X had about two-fold increased levels of PGRMC2 on mRNA and protein level compared to anonymized healthy control fibroblasts ( ).

Techniques: Expressing, shRNA, Knockdown, Staining, Immunofluorescence

( A ) Total RNA was isolated from human skin fibroblasts of healthy wild-type donors and patients with triple A syndrome. The different mutations in the human ALADIN protein are denoted on the x-axis of the diagram: IVS14, S263P and W295X. WT, wild-type. Significant differences were measured with unpaired Wilcoxon–Mann–Whitney U-test. Boxplot widths are proportional to the square root of the samples sizes. Whiskers indicate the range outside 1.5 times the inter-quartile range (IQR) above the upper quartile and below the lower quartile. Outliers were plotted as dots. ( B ) Total protein was isolated from human skin fibroblasts of healthy wild-type donors and triple A patients followed by western blot with indicated antibodies.

Journal: bioRxiv

Article Title: Triple A patient cells suffering from mitotic defects fail to localize PGRMC1 to mitotic kinetochore fibers

doi: 10.1101/381541

Figure Lengend Snippet: ( A ) Total RNA was isolated from human skin fibroblasts of healthy wild-type donors and patients with triple A syndrome. The different mutations in the human ALADIN protein are denoted on the x-axis of the diagram: IVS14, S263P and W295X. WT, wild-type. Significant differences were measured with unpaired Wilcoxon–Mann–Whitney U-test. Boxplot widths are proportional to the square root of the samples sizes. Whiskers indicate the range outside 1.5 times the inter-quartile range (IQR) above the upper quartile and below the lower quartile. Outliers were plotted as dots. ( B ) Total protein was isolated from human skin fibroblasts of healthy wild-type donors and triple A patients followed by western blot with indicated antibodies.

Article Snippet: Here we show that fibroblasts from triple A patients carrying the ALADIN missense mutation S263P or the nonsense mutation W295X had about two-fold increased levels of PGRMC2 on mRNA and protein level compared to anonymized healthy control fibroblasts ( ).

Techniques: Isolation, MANN-WHITNEY, Western Blot

Cells were cold-treated and stained with anti-PGRMC1 (green), anti-α-tubulin (TUBA) (red), anti-CENPB (red), anti-NDC80 (red), anti-TACC3 (red) and DAPI (blue). ( A ) Human adrenocortical NCI-H295R cells. ( B ) Human skin fibroblasts of healthy wild-type donors. ( C ) Human skin fibroblasts of triple A patients. The different mutations in the human ALADIN protein are denoted as IVS14, S263P and W295X. Scale bars 5 μm.

Journal: bioRxiv

Article Title: Triple A patient cells suffering from mitotic defects fail to localize PGRMC1 to mitotic kinetochore fibers

doi: 10.1101/381541

Figure Lengend Snippet: Cells were cold-treated and stained with anti-PGRMC1 (green), anti-α-tubulin (TUBA) (red), anti-CENPB (red), anti-NDC80 (red), anti-TACC3 (red) and DAPI (blue). ( A ) Human adrenocortical NCI-H295R cells. ( B ) Human skin fibroblasts of healthy wild-type donors. ( C ) Human skin fibroblasts of triple A patients. The different mutations in the human ALADIN protein are denoted as IVS14, S263P and W295X. Scale bars 5 μm.

Article Snippet: Here we show that fibroblasts from triple A patients carrying the ALADIN missense mutation S263P or the nonsense mutation W295X had about two-fold increased levels of PGRMC2 on mRNA and protein level compared to anonymized healthy control fibroblasts ( ).

Techniques: Staining