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biological samples human ascites  (Vector Biolabs)


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    Vector Biolabs biological samples human ascites
    Biological Samples Human Ascites, supplied by Vector Biolabs, used in various techniques. Bioz Stars score: 96/100, based on 158 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Vector Biolabs human ift88
    ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. N = 6 replicates of 50 islets per genotype from 5 mice. *p<0.05, two-way ANOVA with Sidak’s multiple comparisons test. ( B–D ) Quantitative analysis of secretion traces. ( B ) Area under the curve (AUC) during liraglutide stimulation (minutes 30–50). ( C ) Total AUC of the entire perifusion (minutes 0-70). ( D ) AUC during KCl depolarization (minutes 60–70). βCKO islets secreted significantly less insulin in response to liraglutide and overall but showed no defect in KCl-induced secretion. Data are mean ± SEM. **p<0.01; ns, not significant, unpaired student’s t-test. ( E–J ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of male ( E–G ) and female ( H–J ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001; ns, not significant; one-way ANOVA with Tukey’s multiple comparisons test.
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    Vector Biolabs ad gfp u6 scrmb shrna
    ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. N = 6 replicates of 50 islets per genotype from 5 mice. *p<0.05, two-way ANOVA with Sidak’s multiple comparisons test. ( B–D ) Quantitative analysis of secretion traces. ( B ) Area under the curve (AUC) during liraglutide stimulation (minutes 30–50). ( C ) Total AUC of the entire perifusion (minutes 0-70). ( D ) AUC during KCl depolarization (minutes 60–70). βCKO islets secreted significantly less insulin in response to liraglutide and overall but showed no defect in KCl-induced secretion. Data are mean ± SEM. **p<0.01; ns, not significant, unpaired student’s t-test. ( E–J ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of male ( E–G ) and female ( H–J ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001; ns, not significant; one-way ANOVA with Tukey’s multiple comparisons test.
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    Vector Biolabs ad-gfp
    ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. N = 6 replicates of 50 islets per genotype from 5 mice. *p<0.05, two-way ANOVA with Sidak’s multiple comparisons test. ( B–D ) Quantitative analysis of secretion traces. ( B ) Area under the curve (AUC) during liraglutide stimulation (minutes 30–50). ( C ) Total AUC of the entire perifusion (minutes 0-70). ( D ) AUC during KCl depolarization (minutes 60–70). βCKO islets secreted significantly less insulin in response to liraglutide and overall but showed no defect in KCl-induced secretion. Data are mean ± SEM. **p<0.01; ns, not significant, unpaired student’s t-test. ( E–J ) <t>IFT88</t> knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of male ( E–G ) and female ( H–J ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001; ns, not significant; one-way ANOVA with Tukey’s multiple comparisons test.
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    A) Experimental scheme of organoid culture. B) Example immunostaining of H28126 line at DIV25. Scale bar is 500mm. C) Quantification using Imaris software of NKX2.1 protein expression at DIV21 (3 cell lines). D) ScRNA-seq analysis of MGE organoids with UMAP clustering revealing 29 distinct cell clusters based on principal component analysis (PCA). E) Proportion of MST divisions relative to non-MST divisions in organoids at DIV25 and DIV47 (3 cell lines). F) Average MST translocation length. G) Immunostaining of organoid slice following live imaging and infection with <t>Ad-CMV-GFP.</t>
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    Transcriptional regulation of LIN28A and LIN28B by developmental transcription factors. A) Schematic of transcription factors that orchestrate germ layer formation and early embryonic lineage specification and differentiation. B) Top: Schematic of morphogen-induced lung/endoderm formation from iPSCs through initiation of lung progenitors in vitro. Bottom: Gene expression analysis of single cell RNA-sequencing of roughly 10,000 cells (close 1200 for each day) throughout morphogen-directed lung endoderm formation from iPSCs. Data from manuscript (Ori et al., 2023). C) Fold change in gene expression of LIN28A and LIN28B upon infection of embryonic lung fibroblast WI-38, with <t>adenoviral</t> constructs: GFP, FOXA2, NKX2-1, SOX2 and SOX9 for 48–72 h before lysing in Trizol. Dots on the graph representative of n = 2 independent experiments in quadruplicate. D) Schematic of development of endoderm differentiation. Transient transfection of txrn factors into HEK293 with construct stably expressing dual luciferase construct; firefly and Renilla luciferase. Validation of a subset of factors that regulated human LIN28A and LIN28B promoter/enhancer sequences during screening experiments in panels B) and C) during E) pluripotency and F) endoderm/lung development. G) progenitor specification. Graphs in E), F) and G) are representative of n = 2 independent validation experiments out of 3. P values for C) were determined using 2-way ANOVA of normal distribution. P values of significance: In the order of left to right for panel C: LIN28A – FOXA2- ∗0.024, NKX2-1- ∗0.035, SOX9- ∗0.021; LIN28B – NKX2-1- ∗0.021, ∗SOX9- 0.021 P values for graphs E), F) and G) were determined using 1-way ANOVA of normal distribution in E) and 1-way ANOVA of lognormal distribution for F) and G). P values of significance: In the order of left to right for each panel: E)∗ 0.0375, ∗∗ 0.0021; ∗ 0.0184, ∗0.0321 F)∗ 0.0434, ∗0.0325; ∗0.0191, ∗0.0477 G)∗∗0.0097,∗ 0.0112; ∗∗0.0021, ∗∗0.0078; ∗∗ 0.0036, ∗∗0.0079; ∗∗0.0072, ∗0.0160. Schematics A), B), D) were made using BioRender.
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    Transcriptional regulation of LIN28A and LIN28B by developmental transcription factors. A) Schematic of transcription factors that orchestrate germ layer formation and early embryonic lineage specification and differentiation. B) Top: Schematic of morphogen-induced lung/endoderm formation from iPSCs through initiation of lung progenitors in vitro. Bottom: Gene expression analysis of single cell RNA-sequencing of roughly 10,000 cells (close 1200 for each day) throughout morphogen-directed lung endoderm formation from iPSCs. Data from manuscript (Ori et al., 2023). C) Fold change in gene expression of LIN28A and LIN28B upon infection of embryonic lung fibroblast WI-38, with <t>adenoviral</t> constructs: GFP, FOXA2, NKX2-1, SOX2 and SOX9 for 48–72 h before lysing in Trizol. Dots on the graph representative of n = 2 independent experiments in quadruplicate. D) Schematic of development of endoderm differentiation. Transient transfection of txrn factors into HEK293 with construct stably expressing dual luciferase construct; firefly and Renilla luciferase. Validation of a subset of factors that regulated human LIN28A and LIN28B promoter/enhancer sequences during screening experiments in panels B) and C) during E) pluripotency and F) endoderm/lung development. G) progenitor specification. Graphs in E), F) and G) are representative of n = 2 independent validation experiments out of 3. P values for C) were determined using 2-way ANOVA of normal distribution. P values of significance: In the order of left to right for panel C: LIN28A – FOXA2- ∗0.024, NKX2-1- ∗0.035, SOX9- ∗0.021; LIN28B – NKX2-1- ∗0.021, ∗SOX9- 0.021 P values for graphs E), F) and G) were determined using 1-way ANOVA of normal distribution in E) and 1-way ANOVA of lognormal distribution for F) and G). P values of significance: In the order of left to right for each panel: E)∗ 0.0375, ∗∗ 0.0021; ∗ 0.0184, ∗0.0321 F)∗ 0.0434, ∗0.0325; ∗0.0191, ∗0.0477 G)∗∗0.0097,∗ 0.0112; ∗∗0.0021, ∗∗0.0078; ∗∗ 0.0036, ∗∗0.0079; ∗∗0.0072, ∗0.0160. Schematics A), B), D) were made using BioRender.
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    Transcriptional regulation of LIN28A and LIN28B by developmental transcription factors. A) Schematic of transcription factors that orchestrate germ layer formation and early embryonic lineage specification and differentiation. B) Top: Schematic of morphogen-induced lung/endoderm formation from iPSCs through initiation of lung progenitors in vitro. Bottom: Gene expression analysis of single cell RNA-sequencing of roughly 10,000 cells (close 1200 for each day) throughout morphogen-directed lung endoderm formation from iPSCs. Data from manuscript (Ori et al., 2023). C) Fold change in gene expression of LIN28A and LIN28B upon infection of embryonic lung fibroblast WI-38, with <t>adenoviral</t> constructs: GFP, FOXA2, NKX2-1, SOX2 and SOX9 for 48–72 h before lysing in Trizol. Dots on the graph representative of n = 2 independent experiments in quadruplicate. D) Schematic of development of endoderm differentiation. Transient transfection of txrn factors into HEK293 with construct stably expressing dual luciferase construct; firefly and Renilla luciferase. Validation of a subset of factors that regulated human LIN28A and LIN28B promoter/enhancer sequences during screening experiments in panels B) and C) during E) pluripotency and F) endoderm/lung development. G) progenitor specification. Graphs in E), F) and G) are representative of n = 2 independent validation experiments out of 3. P values for C) were determined using 2-way ANOVA of normal distribution. P values of significance: In the order of left to right for panel C: LIN28A – FOXA2- ∗0.024, NKX2-1- ∗0.035, SOX9- ∗0.021; LIN28B – NKX2-1- ∗0.021, ∗SOX9- 0.021 P values for graphs E), F) and G) were determined using 1-way ANOVA of normal distribution in E) and 1-way ANOVA of lognormal distribution for F) and G). P values of significance: In the order of left to right for each panel: E)∗ 0.0375, ∗∗ 0.0021; ∗ 0.0184, ∗0.0321 F)∗ 0.0434, ∗0.0325; ∗0.0191, ∗0.0477 G)∗∗0.0097,∗ 0.0112; ∗∗0.0021, ∗∗0.0078; ∗∗ 0.0036, ∗∗0.0079; ∗∗0.0072, ∗0.0160. Schematics A), B), D) were made using BioRender.
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    Image Search Results


    ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. N = 6 replicates of 50 islets per genotype from 5 mice. *p<0.05, two-way ANOVA with Sidak’s multiple comparisons test. ( B–D ) Quantitative analysis of secretion traces. ( B ) Area under the curve (AUC) during liraglutide stimulation (minutes 30–50). ( C ) Total AUC of the entire perifusion (minutes 0-70). ( D ) AUC during KCl depolarization (minutes 60–70). βCKO islets secreted significantly less insulin in response to liraglutide and overall but showed no defect in KCl-induced secretion. Data are mean ± SEM. **p<0.01; ns, not significant, unpaired student’s t-test. ( E–J ) IFT88 knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of male ( E–G ) and female ( H–J ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001; ns, not significant; one-way ANOVA with Tukey’s multiple comparisons test.

    Journal: bioRxiv

    Article Title: Primary cilia regulate GLP-1 signaling in pancreatic β cells

    doi: 10.64898/2026.02.22.707280

    Figure Lengend Snippet: ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. N = 6 replicates of 50 islets per genotype from 5 mice. *p<0.05, two-way ANOVA with Sidak’s multiple comparisons test. ( B–D ) Quantitative analysis of secretion traces. ( B ) Area under the curve (AUC) during liraglutide stimulation (minutes 30–50). ( C ) Total AUC of the entire perifusion (minutes 0-70). ( D ) AUC during KCl depolarization (minutes 60–70). βCKO islets secreted significantly less insulin in response to liraglutide and overall but showed no defect in KCl-induced secretion. Data are mean ± SEM. **p<0.01; ns, not significant, unpaired student’s t-test. ( E–J ) IFT88 knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of male ( E–G ) and female ( H–J ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001; ns, not significant; one-way ANOVA with Tukey’s multiple comparisons test.

    Article Snippet: IFT88 knockdown in human islets: Healthy non-diabetic human islets were transduced with adenoviral vectors encoding either GFP-tagged shRNA targeting human IFT88 (Ad-GFP-h-IFT88-shRNA) or scrambled control (Ad-GFP-U6-scrmb-shRNA, #1122N; Vector Biolabs).

    Techniques: Knock-Out, Knockdown, Transduction, Control, shRNA, Incubation

    ( A ) Representative z-projected confocal images of human islets (28-year-old female donor) transduced with scrambled (Scr) or IFT88 -targeting shRNA adenovirus. GFP (green) marks transduced cells; ARL13B (red) labels primary cilia; DAPI (blue) stains nuclei. Scale bar = 20 µm. Cilia length was quantified from both conditions, showing significantly reduced mean length following IFT88 knockdown. n=132 cilia from 6 islets (Scr shRNA) and 467 cilia from 8 islets (IFT88 shRNA). ( B–C ) IFT88 knockdown efficiency was assessed across multiple donors to demonstrate reproducibility. ( B ) qPCR analysis of IFT88 mRNA levels in islets from two male donors (ages 27 and 44). ( C ) Immunoblot analysis of IFT88 protein levels in islets from three male donors (ages 36, 49 and 45), with corresponding quantifications. Bars represent scrambled control (gray) and IFT88 shRNA (pink). Data are mean ± SEM of duplicate or triplicate samples per donor. **p < 0.01, ****p < 0.0001, ns = not significant, by student’s unpaired t-test.

    Journal: bioRxiv

    Article Title: Primary cilia regulate GLP-1 signaling in pancreatic β cells

    doi: 10.64898/2026.02.22.707280

    Figure Lengend Snippet: ( A ) Representative z-projected confocal images of human islets (28-year-old female donor) transduced with scrambled (Scr) or IFT88 -targeting shRNA adenovirus. GFP (green) marks transduced cells; ARL13B (red) labels primary cilia; DAPI (blue) stains nuclei. Scale bar = 20 µm. Cilia length was quantified from both conditions, showing significantly reduced mean length following IFT88 knockdown. n=132 cilia from 6 islets (Scr shRNA) and 467 cilia from 8 islets (IFT88 shRNA). ( B–C ) IFT88 knockdown efficiency was assessed across multiple donors to demonstrate reproducibility. ( B ) qPCR analysis of IFT88 mRNA levels in islets from two male donors (ages 27 and 44). ( C ) Immunoblot analysis of IFT88 protein levels in islets from three male donors (ages 36, 49 and 45), with corresponding quantifications. Bars represent scrambled control (gray) and IFT88 shRNA (pink). Data are mean ± SEM of duplicate or triplicate samples per donor. **p < 0.01, ****p < 0.0001, ns = not significant, by student’s unpaired t-test.

    Article Snippet: IFT88 knockdown in human islets: Healthy non-diabetic human islets were transduced with adenoviral vectors encoding either GFP-tagged shRNA targeting human IFT88 (Ad-GFP-h-IFT88-shRNA) or scrambled control (Ad-GFP-U6-scrmb-shRNA, #1122N; Vector Biolabs).

    Techniques: Transduction, shRNA, Knockdown, Western Blot, Control

    A) Experimental scheme of organoid culture. B) Example immunostaining of H28126 line at DIV25. Scale bar is 500mm. C) Quantification using Imaris software of NKX2.1 protein expression at DIV21 (3 cell lines). D) ScRNA-seq analysis of MGE organoids with UMAP clustering revealing 29 distinct cell clusters based on principal component analysis (PCA). E) Proportion of MST divisions relative to non-MST divisions in organoids at DIV25 and DIV47 (3 cell lines). F) Average MST translocation length. G) Immunostaining of organoid slice following live imaging and infection with Ad-CMV-GFP.

    Journal: bioRxiv

    Article Title: Progenitor Diversity and Architecture of the Human Ganglionic Eminences Shaping the Basal Ganglia

    doi: 10.64898/2025.12.31.697063

    Figure Lengend Snippet: A) Experimental scheme of organoid culture. B) Example immunostaining of H28126 line at DIV25. Scale bar is 500mm. C) Quantification using Imaris software of NKX2.1 protein expression at DIV21 (3 cell lines). D) ScRNA-seq analysis of MGE organoids with UMAP clustering revealing 29 distinct cell clusters based on principal component analysis (PCA). E) Proportion of MST divisions relative to non-MST divisions in organoids at DIV25 and DIV47 (3 cell lines). F) Average MST translocation length. G) Immunostaining of organoid slice following live imaging and infection with Ad-CMV-GFP.

    Article Snippet: Slices were incubated floating in cell culture medium according to age of organoids with 1:1000 Ad-CMV-GFP (vectorbiolabs; #1060) at 37°C for 3-5 days.

    Techniques: Immunostaining, Software, Expressing, Translocation Assay, Imaging, Infection

    Transcriptional regulation of LIN28A and LIN28B by developmental transcription factors. A) Schematic of transcription factors that orchestrate germ layer formation and early embryonic lineage specification and differentiation. B) Top: Schematic of morphogen-induced lung/endoderm formation from iPSCs through initiation of lung progenitors in vitro. Bottom: Gene expression analysis of single cell RNA-sequencing of roughly 10,000 cells (close 1200 for each day) throughout morphogen-directed lung endoderm formation from iPSCs. Data from manuscript (Ori et al., 2023). C) Fold change in gene expression of LIN28A and LIN28B upon infection of embryonic lung fibroblast WI-38, with adenoviral constructs: GFP, FOXA2, NKX2-1, SOX2 and SOX9 for 48–72 h before lysing in Trizol. Dots on the graph representative of n = 2 independent experiments in quadruplicate. D) Schematic of development of endoderm differentiation. Transient transfection of txrn factors into HEK293 with construct stably expressing dual luciferase construct; firefly and Renilla luciferase. Validation of a subset of factors that regulated human LIN28A and LIN28B promoter/enhancer sequences during screening experiments in panels B) and C) during E) pluripotency and F) endoderm/lung development. G) progenitor specification. Graphs in E), F) and G) are representative of n = 2 independent validation experiments out of 3. P values for C) were determined using 2-way ANOVA of normal distribution. P values of significance: In the order of left to right for panel C: LIN28A – FOXA2- ∗0.024, NKX2-1- ∗0.035, SOX9- ∗0.021; LIN28B – NKX2-1- ∗0.021, ∗SOX9- 0.021 P values for graphs E), F) and G) were determined using 1-way ANOVA of normal distribution in E) and 1-way ANOVA of lognormal distribution for F) and G). P values of significance: In the order of left to right for each panel: E)∗ 0.0375, ∗∗ 0.0021; ∗ 0.0184, ∗0.0321 F)∗ 0.0434, ∗0.0325; ∗0.0191, ∗0.0477 G)∗∗0.0097,∗ 0.0112; ∗∗0.0021, ∗∗0.0078; ∗∗ 0.0036, ∗∗0.0079; ∗∗0.0072, ∗0.0160. Schematics A), B), D) were made using BioRender.

    Journal: Biochemistry and Biophysics Reports

    Article Title: LIN28-mediated gene regulatory loops synchronize transitions throughout organogenesis

    doi: 10.1016/j.bbrep.2025.102226

    Figure Lengend Snippet: Transcriptional regulation of LIN28A and LIN28B by developmental transcription factors. A) Schematic of transcription factors that orchestrate germ layer formation and early embryonic lineage specification and differentiation. B) Top: Schematic of morphogen-induced lung/endoderm formation from iPSCs through initiation of lung progenitors in vitro. Bottom: Gene expression analysis of single cell RNA-sequencing of roughly 10,000 cells (close 1200 for each day) throughout morphogen-directed lung endoderm formation from iPSCs. Data from manuscript (Ori et al., 2023). C) Fold change in gene expression of LIN28A and LIN28B upon infection of embryonic lung fibroblast WI-38, with adenoviral constructs: GFP, FOXA2, NKX2-1, SOX2 and SOX9 for 48–72 h before lysing in Trizol. Dots on the graph representative of n = 2 independent experiments in quadruplicate. D) Schematic of development of endoderm differentiation. Transient transfection of txrn factors into HEK293 with construct stably expressing dual luciferase construct; firefly and Renilla luciferase. Validation of a subset of factors that regulated human LIN28A and LIN28B promoter/enhancer sequences during screening experiments in panels B) and C) during E) pluripotency and F) endoderm/lung development. G) progenitor specification. Graphs in E), F) and G) are representative of n = 2 independent validation experiments out of 3. P values for C) were determined using 2-way ANOVA of normal distribution. P values of significance: In the order of left to right for panel C: LIN28A – FOXA2- ∗0.024, NKX2-1- ∗0.035, SOX9- ∗0.021; LIN28B – NKX2-1- ∗0.021, ∗SOX9- 0.021 P values for graphs E), F) and G) were determined using 1-way ANOVA of normal distribution in E) and 1-way ANOVA of lognormal distribution for F) and G). P values of significance: In the order of left to right for each panel: E)∗ 0.0375, ∗∗ 0.0021; ∗ 0.0184, ∗0.0321 F)∗ 0.0434, ∗0.0325; ∗0.0191, ∗0.0477 G)∗∗0.0097,∗ 0.0112; ∗∗0.0021, ∗∗0.0078; ∗∗ 0.0036, ∗∗0.0079; ∗∗0.0072, ∗0.0160. Schematics A), B), D) were made using BioRender.

    Article Snippet: Lin28a/b were knocked out post-neurosphere formation via adenoviral infection with Ad-Cre-GFP adenovirus (Vector Biolabs, 1700) or Ad-GFP adenovirus (Vector Biolabs, 1060).

    Techniques: In Vitro, Gene Expression, RNA Sequencing, Infection, Construct, Transfection, Stable Transfection, Expressing, Luciferase, Biomarker Discovery