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prolong gold anti-fade mountant dapi (Thermo Fisher)

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Thermo Fisher prolong gold anti-fade mountant dapi
Prolong Gold Anti Fade Mountant Dapi, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prolong+gold+anti-fade+mountant+with+dapi/pm39435643-332-22-28
Average 90 stars, based on 1 article reviews

prolong gold anti-fade mountant dapi - by Bioz Stars, 2026-10

90/100 stars

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Article Title: Characterization of RAN Translation and Antisense Transcription in Primary Cell Cultures of Patients with Myotonic Dystrophy Type 1
Article Snippet: After another round of washes, the cells were mounted with ProLong Gold Anti-Fade Mountant with DAPI (Thermo Fisher Scientific, Waltham, MA, USA).

Article Title: Harnessing the power of antibodies to fight bone metastasis
Article Snippet: Sections were mounted with Prolong gold anti-fade mountant with DAPI (from Thermo Fisher Scientific), sealed with a coverslip, and then used for confocal imaging.

Article Title: EZH2 inhibitors promote β-like cell regeneration in young and adult type 1 diabetes donors.
Article Snippet: Coverslips were rinsed in PBG and mounted using Prolong Gold Anti-Fade mountant with DAPI (ThermoFisher).

Article Title: Characterization of RAN Translation and Antisense Transcription in Primary Cell Cultures of Patients with Myotonic Dystrophy Type 1
Article Snippet: After another round of washes in 1× PBS, coverslips were mounted with ProLong Gold Anti-Fade Mountant with DAPI (Thermo Fisher Scientific, Waltham, MA, USA).

Article Title: Characterization of RAN Translation and Antisense Transcription in Primary Cell Cultures of Patients with Myotonic Dystrophy Type 1
Article Snippet: The following day, the coverslips were washed with 30% formamide in 2× SSC buffer at 45 °C, 1× SSC buffer at 37 °C and 1× PBS at room temperature, and mounted with ProLong Gold Anti-Fade Mountant with DAPI (Thermo Fisher Scientific, Waltham, MA, USA).

Article Title: Platelet-rich plasma enhances mechanical strength of strattice in rat model of ventral hernia repair.
Article Snippet: Division of Trauma, Acute, and Critical Care Surgery, Department of Surgery, Duke University School of Medicine, Durham, North Carolina, USA Department of Surgery, Houston Methodist Hospital, Houston, Texas, USA Department of Nanomedicine, Surgical Advanced Technologies Lab, Houston Methodist Research Institute, Houston, Texas, USA Department of Biomedical Engineering, Duke University, Durham, North Carolina, USA Department of Medicine, Renal Division, HarvardMedical School, BrighamandWomen's Hospital, Boston, Massachusetts, USA Department of Orthopedic Surgery, Houston Methodist Hospital, Houston, Texas, USA Department of Mechanical Engineering, Texas A&M College of Medicine, Bryan, Texas, USA IRCCS San Raffaele, University San Raffaele, Rome, Italy 3R Biotech, Milan, Italy

Incubation:

Article Title: Pericytes Modulate Third‐Generation Tyrosine Kinase Inhibitor Sensitivity in EGFR‐Mutated Lung Cancer Cells Through IL32‐β5‐Integrin Paracrine Signaling
Article Snippet: Sections were washed in PBS and blocked in 1% normal goat serum (NGS) with 0.1% Triton X‐100 for 1 h. Subsequently, sections were triple‐immunostained using anti‐alpha‐smooth muscle actin Cy3‐conjugated (Sigma–Aldrich‐#C6198), anti‐CD34 (Biolegend‐#343610), and either anti‐IL32 (Abcam‐#ab37158), anti‐Integrin β5 (Cell Signaling Technology‐#3629S) or anti‐YY1 antibodies (Cell Signaling Technology‐#46395). .. After three PBS washes, sections were incubated with secondary antibodies diluted 1:200 in 1% NGS 0.1% TX‐100, washed thrice, and mounted with Prolong Gold Anti‐Fade Mountant with DAPI (ThermoFisher Scientific‐#P36931). ..

Next-Generation Sequencing:

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Human pancreatic ductal epithelial cells express β-cell indices in response to pharmacological EZH2 inhibition. a Cells were stimulated with GSK126 or Tazemetostat over a 48-hour period. Assays were then performed at the 48-hour time point as well as 48 h following drug free conditions at the 96-hour time point. b Histones were prepared by acid extraction. Quantification of H3K27me3 levels were calculated and adjusted to overall histone H3 using Li-COR Odyssey. The signal ratio for H3K27me3/total H3 was calculated at 48 and 96 h. Vehicle control is DMSO. Data are presented as mean with error bars as S.E.M of 3 replicates of stimulation. Statistical significance was calculated by comparing control vs inhibitor values using Student t -test, ** P < 0.01. c Regenerative TEI of CK19, NGN3, PDX1, INS, MAFA, GCK, NKX6.1, PCSK1 , and PCSK2 in pancreatic ductal cells after 48 h stimulation with GSK126 or Tazemetostat assessed by qRT-PCR, normalised to H3F3A and adjusted to controls. Data are represented as mean of 3 replicates. Statistical significance was calculated by comparing control vs inhibitor values using Student t -test, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, error bars are S.E.M. d Regenerative TEI of CK19, NGN3, PDX1, INS, MAFA, GCK, NKX6.1, PCSK1 , and PCSK2 in pancreatic ductal cells after 48 h stimulation with GSK126 or Tazemetostat followed by 48 h drug free conditions (96 h) assessed by qRT-PCR, normalised to H3F3A and adjusted to controls. Data are represented as mean of 3 replicates. Statistical significance was calculated by comparing control vs inhibitor values using Student t -test, ** P < 0.01, *** P < 0.001, **** P < 0.0001, error bars are S.E.M. e Chromatin immunoprecipitation of H3K27me3 content for regenerative genes include CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 , and PCSK2 in pancreatic ductal cells following 48 h of GSK126 or Taz stimulation assessed by qPCR and represented as fold change, normalised and adjusted to controls. Data are represented as mean ± S.E.M. of percent input (GSK126 or Taz stimulation; n = 3). Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. f Chromatin immunoprecipitation of H3K27me3 content for regenerative genes include CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 , and PCSK2 in pancreatic ductal cells after 48 h stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h) assessed by qPCR and represented as fold change, normalised and adjusted to controls. Data are represented as mean ± S.E.M. of percent input (GSK126 or Taz stimulation; n = 3). Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. g Immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz. Cells were stained for DAPI, CK19, and INS. Images across three replicates of stimulation were captured at 20x magnification using ThermoFisher EVOS and processed with ImageJ. Scale bar represents 200 μm. Arrows point to CK19 + INS + cells. h Immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h). Cells were stained for DAPI, CK19, and INS. Images across three replicates of stimulation were captured at 20x magnification using ThermoFisher EVOS and processed with ImageJ. Scale bar represents 200 μm. Arrows point to CK19 + INS + cells. i Quantifiction of immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz. Protein expression was quantified by normalizing the CK19+, INS+ and CK19+/INS+ signals relative to the nuclear DAPI signal. Insulin expressing cells were scored across a total of 1 × 10 5 cells seeded on coverslips. Data are represented as mean ± S.E.M. of 6 replicates. Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, **** P < 0.0001. j Quantifiction of immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h). Protein expression was quantified by normalizing the CK19+, INS+ and CK19+/INS+ signals relative to the nuclear DAPI signal. Insulin expressing cells were scored across a total of 1 × 10 5 cells seeded on coverslips. Data are represented as mean ± S.E.M. of 6 replicates. Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, **** P < 0.0001. k Glucose-stimulated insulin secretion assay assessed the regenerative capacity in human pancreatic ductal cells after 48-hour stimulation with GSK126 or Taz. Cells were exposed to low (2.8 mM) and high (28 mM) glucose conditions. Insulin secretion was quantified by ELISA. Fold changes in insulin release are shown for both glucose conditions. Data are of three replicate experiments represented as mean ± S.E.M of fold change relative to control. Statistical significance was calculated by comparing 2.8 mM vs 28 mM glucose using Student t -test, **** P < 0.0001. l Glucose-stimulated insulin secretion assay assessed the regenerative capacity in human pancreatic ductal cells after 48-hour stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h). Cells were exposed to low (2.8 mM) and high (28 mM) glucose conditions. Insulin secretion was quantified by ELISA. Fold changes in insulin release are shown for both glucose conditions. Data are of three replicate experiments represented as mean ± S.E.M of fold change relative to control. Statistical significance was calculated by comparing 2.8 mM vs 28 mM glucose using Student t -test, **** P < 0.0001

Journal: Signal Transduction and Targeted Therapy

Article Title: EZH2 inhibitors promote β-like cell regeneration in young and adult type 1 diabetes donors

doi: 10.1038/s41392-023-01707-x

Figure Lengend Snippet: Human pancreatic ductal epithelial cells express β-cell indices in response to pharmacological EZH2 inhibition. a Cells were stimulated with GSK126 or Tazemetostat over a 48-hour period. Assays were then performed at the 48-hour time point as well as 48 h following drug free conditions at the 96-hour time point. b Histones were prepared by acid extraction. Quantification of H3K27me3 levels were calculated and adjusted to overall histone H3 using Li-COR Odyssey. The signal ratio for H3K27me3/total H3 was calculated at 48 and 96 h. Vehicle control is DMSO. Data are presented as mean with error bars as S.E.M of 3 replicates of stimulation. Statistical significance was calculated by comparing control vs inhibitor values using Student t -test, ** P < 0.01. c Regenerative TEI of CK19, NGN3, PDX1, INS, MAFA, GCK, NKX6.1, PCSK1 , and PCSK2 in pancreatic ductal cells after 48 h stimulation with GSK126 or Tazemetostat assessed by qRT-PCR, normalised to H3F3A and adjusted to controls. Data are represented as mean of 3 replicates. Statistical significance was calculated by comparing control vs inhibitor values using Student t -test, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, error bars are S.E.M. d Regenerative TEI of CK19, NGN3, PDX1, INS, MAFA, GCK, NKX6.1, PCSK1 , and PCSK2 in pancreatic ductal cells after 48 h stimulation with GSK126 or Tazemetostat followed by 48 h drug free conditions (96 h) assessed by qRT-PCR, normalised to H3F3A and adjusted to controls. Data are represented as mean of 3 replicates. Statistical significance was calculated by comparing control vs inhibitor values using Student t -test, ** P < 0.01, *** P < 0.001, **** P < 0.0001, error bars are S.E.M. e Chromatin immunoprecipitation of H3K27me3 content for regenerative genes include CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 , and PCSK2 in pancreatic ductal cells following 48 h of GSK126 or Taz stimulation assessed by qPCR and represented as fold change, normalised and adjusted to controls. Data are represented as mean ± S.E.M. of percent input (GSK126 or Taz stimulation; n = 3). Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. f Chromatin immunoprecipitation of H3K27me3 content for regenerative genes include CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 , and PCSK2 in pancreatic ductal cells after 48 h stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h) assessed by qPCR and represented as fold change, normalised and adjusted to controls. Data are represented as mean ± S.E.M. of percent input (GSK126 or Taz stimulation; n = 3). Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. g Immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz. Cells were stained for DAPI, CK19, and INS. Images across three replicates of stimulation were captured at 20x magnification using ThermoFisher EVOS and processed with ImageJ. Scale bar represents 200 μm. Arrows point to CK19 + INS + cells. h Immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h). Cells were stained for DAPI, CK19, and INS. Images across three replicates of stimulation were captured at 20x magnification using ThermoFisher EVOS and processed with ImageJ. Scale bar represents 200 μm. Arrows point to CK19 + INS + cells. i Quantifiction of immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz. Protein expression was quantified by normalizing the CK19+, INS+ and CK19+/INS+ signals relative to the nuclear DAPI signal. Insulin expressing cells were scored across a total of 1 × 10 5 cells seeded on coverslips. Data are represented as mean ± S.E.M. of 6 replicates. Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, **** P < 0.0001. j Quantifiction of immunofluorescence staining of human pancreatic ductal cells stimulated after 48 h stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h). Protein expression was quantified by normalizing the CK19+, INS+ and CK19+/INS+ signals relative to the nuclear DAPI signal. Insulin expressing cells were scored across a total of 1 × 10 5 cells seeded on coverslips. Data are represented as mean ± S.E.M. of 6 replicates. Statistical significance was calculated by comparing control vs GSK126 or Taz using Student t -test, **** P < 0.0001. k Glucose-stimulated insulin secretion assay assessed the regenerative capacity in human pancreatic ductal cells after 48-hour stimulation with GSK126 or Taz. Cells were exposed to low (2.8 mM) and high (28 mM) glucose conditions. Insulin secretion was quantified by ELISA. Fold changes in insulin release are shown for both glucose conditions. Data are of three replicate experiments represented as mean ± S.E.M of fold change relative to control. Statistical significance was calculated by comparing 2.8 mM vs 28 mM glucose using Student t -test, **** P < 0.0001. l Glucose-stimulated insulin secretion assay assessed the regenerative capacity in human pancreatic ductal cells after 48-hour stimulation with GSK126 or Taz followed by 48 h drug free conditions (96 h). Cells were exposed to low (2.8 mM) and high (28 mM) glucose conditions. Insulin secretion was quantified by ELISA. Fold changes in insulin release are shown for both glucose conditions. Data are of three replicate experiments represented as mean ± S.E.M of fold change relative to control. Statistical significance was calculated by comparing 2.8 mM vs 28 mM glucose using Student t -test, **** P < 0.0001

Article Snippet: Slides were then incubated with 4′,6-diamidino-2-phenylindole (DAPI) (0.10 μg/ml; D8417 Sigma-Aldrich) for 10 min and coverslips were mounted using Prolong Gold Anti-Fade mountant with DAPI (ThermoFisher).

Techniques: Inhibition, Extraction, Quantitative RT-PCR, Chromatin Immunoprecipitation, Immunofluorescence, Staining, Expressing, Enzyme-linked Immunosorbent Assay

Characteristic transcriptional indices of β-cells show robust insulin signal underscored by reduced H3K27me3 gene content. a The expression of mRNA transcripts for CK19, NGN3, PDX1, INS, MAFA, GCK, PCSK1 and PCSK2 genes from mature EndoC-βH5 cells relative to H3F3A are displayed. Data are represented as mean of 3 replicates, error bars are S.E.M. b Chromatin immunoprecipitation for suppressive H3K27me3 chromatin content for CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 and PCSK2 genes derived from EndoC-βH5 cells. Data are represented as mean ± S.E.M. of percent input ( n = 3). c Chromatin immunoprecipitation for permissive H3K27ac chromatin content for CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 and PCSK2 genes derived from EndoC-βH5 cells. Data are represented as mean ± S.E.M. of percent input ( n = 3). d Chromatin immunoprecipitation for permissive H3K4me3 chromatin content for CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 and PCSK2 genes derived from EndoC-βH5 cells. Data are represented as mean ± S.E.M. of percent input ( n = 3). e Immunofluorescence staining confirms functionally mature EndoC-βH5 cells. Staining was performed for DAPI, CK19, and INS. Images across three replicates of stimulation were captured at 20x magnification using ThermoFisher EVOS and processed with ImageJ. Scale bar represents 200 μm. White arrows point to CK19 + INS + cells. f Protein signal of immunofluorescence staining positive for INS in the absence of CK19 in EndoC-βH5 cells. Staining was assessed by adjusting the CK19 or INS signals to the nuclear DAPI signal. Data are represented as mean ± S.E.M. g Glucose stimulated insulin assays assessed in EndoC-βH5 cells. Fold change of insulin release in low (2.8 mM) and high (28 mM) glucose conditions. Data are of three replicate experiments represented as mean ± S.E.M of insulin concentration

Journal: Signal Transduction and Targeted Therapy

Article Title: EZH2 inhibitors promote β-like cell regeneration in young and adult type 1 diabetes donors

doi: 10.1038/s41392-023-01707-x

Figure Lengend Snippet: Characteristic transcriptional indices of β-cells show robust insulin signal underscored by reduced H3K27me3 gene content. a The expression of mRNA transcripts for CK19, NGN3, PDX1, INS, MAFA, GCK, PCSK1 and PCSK2 genes from mature EndoC-βH5 cells relative to H3F3A are displayed. Data are represented as mean of 3 replicates, error bars are S.E.M. b Chromatin immunoprecipitation for suppressive H3K27me3 chromatin content for CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 and PCSK2 genes derived from EndoC-βH5 cells. Data are represented as mean ± S.E.M. of percent input ( n = 3). c Chromatin immunoprecipitation for permissive H3K27ac chromatin content for CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 and PCSK2 genes derived from EndoC-βH5 cells. Data are represented as mean ± S.E.M. of percent input ( n = 3). d Chromatin immunoprecipitation for permissive H3K4me3 chromatin content for CK19, NGN3, PDX1, INS-IGF2, MAFA, GCK, PCSK1 and PCSK2 genes derived from EndoC-βH5 cells. Data are represented as mean ± S.E.M. of percent input ( n = 3). e Immunofluorescence staining confirms functionally mature EndoC-βH5 cells. Staining was performed for DAPI, CK19, and INS. Images across three replicates of stimulation were captured at 20x magnification using ThermoFisher EVOS and processed with ImageJ. Scale bar represents 200 μm. White arrows point to CK19 + INS + cells. f Protein signal of immunofluorescence staining positive for INS in the absence of CK19 in EndoC-βH5 cells. Staining was assessed by adjusting the CK19 or INS signals to the nuclear DAPI signal. Data are represented as mean ± S.E.M. g Glucose stimulated insulin assays assessed in EndoC-βH5 cells. Fold change of insulin release in low (2.8 mM) and high (28 mM) glucose conditions. Data are of three replicate experiments represented as mean ± S.E.M of insulin concentration

Techniques: Expressing, Chromatin Immunoprecipitation, Derivative Assay, Immunofluorescence, Staining, Concentration Assay

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