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rabbit anti cftr  (Alomone Labs)


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    Alomone Labs rabbit anti cftr
    Rabbit Anti Cftr, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+cftr/Anti-CFTR+Antibody/us12590288-3395-19-23
    Average 95 stars, based on 71 article reviews
    rabbit anti cftr - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Centrifugation:

    Article Title: Defective CFTR Expression and Function Are Detectable in Blood Monocytes: Development of a New Blood Test for Cystic Fibrosis
    Article Snippet: 200 μg of light membrane preparation was precleared by adding 100 μl of suspended 20% v/v Protein G-Sepharose 4 Fast flow conjugate (PGS: GE Healthcare, Uppsala Sweden) and incubated at 4°C on a rotating wheel for 30 minutes. .. After centrifugation at 16,000× g for 30 seconds at 4°C, the supernatant was transferred, to a new ice-cold microcentrifuge tube containing 2 μg rabbit anti-CFTR (ACL-006 Alomone Labs Ltd., Jerusalem, Israel; 0.8 mg/ml) and 2 μg mouse anti-CFTR (MAB 3482 clone MM13-4 Chemicon International, Temecula, California USA; 1 mg/ml) or non-immune rabbit and mouse IgG and incubated for 2 hours at 4°C. ..

    Incubation:

    Article Title: Defective CFTR Expression and Function Are Detectable in Blood Monocytes: Development of a New Blood Test for Cystic Fibrosis
    Article Snippet: 200 μg of light membrane preparation was precleared by adding 100 μl of suspended 20% v/v Protein G-Sepharose 4 Fast flow conjugate (PGS: GE Healthcare, Uppsala Sweden) and incubated at 4°C on a rotating wheel for 30 minutes. .. After centrifugation at 16,000× g for 30 seconds at 4°C, the supernatant was transferred, to a new ice-cold microcentrifuge tube containing 2 μg rabbit anti-CFTR (ACL-006 Alomone Labs Ltd., Jerusalem, Israel; 0.8 mg/ml) and 2 μg mouse anti-CFTR (MAB 3482 clone MM13-4 Chemicon International, Temecula, California USA; 1 mg/ml) or non-immune rabbit and mouse IgG and incubated for 2 hours at 4°C. ..

    Article Title: Olfactory microvillar tuft cells direct neurogenesis during allergic inflammation
    Article Snippet: For CFTR detection in cross sections, target retrieval was performed with a citrate buffer (Target Retrieval solution, pH 6, (Dako) for 30min after deparaffinization. .. The samples were blocked for 1 hour with 10% goat serum, then incubated overnight with a mix of primary antibodies, containing rabbit anti-CFTR (Alomone, 16 μg/ml) and chicken anti-GFP (Abcam, 35 μg/ml) at 4C. .. The slides were then treated with poly-HRP conjugated secondary antibody from Tyramide SuperBoostTM kit (Invitrogen) and the developed with tyramide working solution with Alexa Fluor 594 from Tyramide SuperBoostTM kit (Invitrogen) for 7 minutes.

    Article Title: Loss of endothelial CFTR drives barrier failure and edema formation in lung infection and can be targeted by CFTR potentiation.
    Article Snippet: Lasti Erfinanda1, Lin Zou1,2,3, Birgitt Gutbier4, Laura Kneller4, Sarah Weidenfeld1, Laura Michalick1, Disi Lei1,2, Katrin Reppe4†, Luiz Gustavo Teixeira Alves4, Bill Schneider4, Qi Zhang1, Caihong Li1, Diana Fatykhova4, Paul Schneider5, Wolfgang Liedtke6‡, Eisei Sohara7, Timothy J. Mitchell8, Achim D. Gruber9, Andreas Hocke4,10, Stefan Hippenstiel4,10, Norbert Suttorp4,10, Andrea Olschewski11, Marcus A. Mall10,12, Martin Witzenrath4,10, Wolfgang M. Kuebler1,10*

    Article Title: CFTR modulates aquaporin-mediated glycerol permeability in mouse Sertoli cells.
    Article Snippet: The cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel that is crucial for fluid homeodynamics throughout the male reproductive tract.. Previous evidence shed light on a potential molecular partnership between this channel and aquaporins (AQPs).. Herein, we explore the role of CFTR on AQPs-mediated glycerol permeability in mouse Sertoli cells (mSCs).

    Blocking Assay:

    Article Title: Loss of endothelial CFTR drives barrier failure and edema formation in lung infection and can be targeted by CFTR potentiation.
    Article Snippet: Lasti Erfinanda1, Lin Zou1,2,3, Birgitt Gutbier4, Laura Kneller4, Sarah Weidenfeld1, Laura Michalick1, Disi Lei1,2, Katrin Reppe4†, Luiz Gustavo Teixeira Alves4, Bill Schneider4, Qi Zhang1, Caihong Li1, Diana Fatykhova4, Paul Schneider5, Wolfgang Liedtke6‡, Eisei Sohara7, Timothy J. Mitchell8, Achim D. Gruber9, Andreas Hocke4,10, Stefan Hippenstiel4,10, Norbert Suttorp4,10, Andrea Olschewski11, Marcus A. Mall10,12, Martin Witzenrath4,10, Wolfgang M. Kuebler1,10*



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    ( A ) Schema showing the process for generating PPDO. ( B – E ) Brightfield microscopy images of early passage PPDO and HPDO from Em- ( B ), EPN ( C ), LPN ( D ) and from a human donor ( E ). Scale bar: 500 µm. ( B’ – E’ ) Brightfield microscopy images of late passage PPDO and HPDO from Em ( B’ ), EPN ( C’ ), LPN ( D’ ) and from a human donor ( E ). Scale bar: 500 µm. ( F – H ) Single-plane confocal images of PPDO derived from EPN pig pancreas immunostained against <t>CFTR-Phalloidin-PDX1</t> ( F ), SOX9-GP2-NKX6-1/GCG ( G ), KRT7-CDH1 ( H ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 3. Scale bar: 50 µm. ( I – K ) Brightfield microscopy images of early passage Em PPDO at the beginning of the live imaging, treated with DMSO ( I ), forskolin ( J ), and secretin ( K ). Scale bar 500 µm. ( I’ –K’ ) Brightfield microscopy images of early passage Em PPDO at the end of the live imaging, treated with DMSO ( I’ ), forskolin ( J’ ) and secretin ( K’ ). Scale bar 500 µm. ( L ) Quantification of the lumen area expansion of PPDO following 4 h of live imaging and treatments with forskolin and secretin. n = 3 independent experiments with different PPDO lines (1 Em, 1 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. P val are: * Padj = 0.015 for DMSO vs forskolin and * Padj = 0.0140 for DMSO vs secretin. ( M ) Quantification of the lumen area expansion of HPDO following 4 h of live imaging and treatment with forskolin. n = 4 independent experiments with 4 HPDO lines. Data are shown as mean ± SD. Mann–Whitney test was used to assess significance. * P = 0.0286. .
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    ( A ) Schema showing the process for generating PPDO. ( B – E ) Brightfield microscopy images of early passage PPDO and HPDO from Em- ( B ), EPN ( C ), LPN ( D ) and from a human donor ( E ). Scale bar: 500 µm. ( B’ – E’ ) Brightfield microscopy images of late passage PPDO and HPDO from Em ( B’ ), EPN ( C’ ), LPN ( D’ ) and from a human donor ( E ). Scale bar: 500 µm. ( F – H ) Single-plane confocal images of PPDO derived from EPN pig pancreas immunostained against <t>CFTR-Phalloidin-PDX1</t> ( F ), SOX9-GP2-NKX6-1/GCG ( G ), KRT7-CDH1 ( H ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 3. Scale bar: 50 µm. ( I – K ) Brightfield microscopy images of early passage Em PPDO at the beginning of the live imaging, treated with DMSO ( I ), forskolin ( J ), and secretin ( K ). Scale bar 500 µm. ( I’ –K’ ) Brightfield microscopy images of early passage Em PPDO at the end of the live imaging, treated with DMSO ( I’ ), forskolin ( J’ ) and secretin ( K’ ). Scale bar 500 µm. ( L ) Quantification of the lumen area expansion of PPDO following 4 h of live imaging and treatments with forskolin and secretin. n = 3 independent experiments with different PPDO lines (1 Em, 1 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. P val are: * Padj = 0.015 for DMSO vs forskolin and * Padj = 0.0140 for DMSO vs secretin. ( M ) Quantification of the lumen area expansion of HPDO following 4 h of live imaging and treatment with forskolin. n = 4 independent experiments with 4 HPDO lines. Data are shown as mean ± SD. Mann–Whitney test was used to assess significance. * P = 0.0286. .
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    ( A ) Schema showing the process for generating PPDO. ( B – E ) Brightfield microscopy images of early passage PPDO and HPDO from Em- ( B ), EPN ( C ), LPN ( D ) and from a human donor ( E ). Scale bar: 500 µm. ( B’ – E’ ) Brightfield microscopy images of late passage PPDO and HPDO from Em ( B’ ), EPN ( C’ ), LPN ( D’ ) and from a human donor ( E ). Scale bar: 500 µm. ( F – H ) Single-plane confocal images of PPDO derived from EPN pig pancreas immunostained against <t>CFTR-Phalloidin-PDX1</t> ( F ), SOX9-GP2-NKX6-1/GCG ( G ), KRT7-CDH1 ( H ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 3. Scale bar: 50 µm. ( I – K ) Brightfield microscopy images of early passage Em PPDO at the beginning of the live imaging, treated with DMSO ( I ), forskolin ( J ), and secretin ( K ). Scale bar 500 µm. ( I’ –K’ ) Brightfield microscopy images of early passage Em PPDO at the end of the live imaging, treated with DMSO ( I’ ), forskolin ( J’ ) and secretin ( K’ ). Scale bar 500 µm. ( L ) Quantification of the lumen area expansion of PPDO following 4 h of live imaging and treatments with forskolin and secretin. n = 3 independent experiments with different PPDO lines (1 Em, 1 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. P val are: * Padj = 0.015 for DMSO vs forskolin and * Padj = 0.0140 for DMSO vs secretin. ( M ) Quantification of the lumen area expansion of HPDO following 4 h of live imaging and treatment with forskolin. n = 4 independent experiments with 4 HPDO lines. Data are shown as mean ± SD. Mann–Whitney test was used to assess significance. * P = 0.0286. .
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    ( A ) Schema showing the process for generating PPDO. ( B – E ) Brightfield microscopy images of early passage PPDO and HPDO from Em- ( B ), EPN ( C ), LPN ( D ) and from a human donor ( E ). Scale bar: 500 µm. ( B’ – E’ ) Brightfield microscopy images of late passage PPDO and HPDO from Em ( B’ ), EPN ( C’ ), LPN ( D’ ) and from a human donor ( E ). Scale bar: 500 µm. ( F – H ) Single-plane confocal images of PPDO derived from EPN pig pancreas immunostained against <t>CFTR-Phalloidin-PDX1</t> ( F ), SOX9-GP2-NKX6-1/GCG ( G ), KRT7-CDH1 ( H ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 3. Scale bar: 50 µm. ( I – K ) Brightfield microscopy images of early passage Em PPDO at the beginning of the live imaging, treated with DMSO ( I ), forskolin ( J ), and secretin ( K ). Scale bar 500 µm. ( I’ –K’ ) Brightfield microscopy images of early passage Em PPDO at the end of the live imaging, treated with DMSO ( I’ ), forskolin ( J’ ) and secretin ( K’ ). Scale bar 500 µm. ( L ) Quantification of the lumen area expansion of PPDO following 4 h of live imaging and treatments with forskolin and secretin. n = 3 independent experiments with different PPDO lines (1 Em, 1 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. P val are: * Padj = 0.015 for DMSO vs forskolin and * Padj = 0.0140 for DMSO vs secretin. ( M ) Quantification of the lumen area expansion of HPDO following 4 h of live imaging and treatment with forskolin. n = 4 independent experiments with 4 HPDO lines. Data are shown as mean ± SD. Mann–Whitney test was used to assess significance. * P = 0.0286. .
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    ( A ) Schema showing the process for generating PPDO. ( B – E ) Brightfield microscopy images of early passage PPDO and HPDO from Em- ( B ), EPN ( C ), LPN ( D ) and from a human donor ( E ). Scale bar: 500 µm. ( B’ – E’ ) Brightfield microscopy images of late passage PPDO and HPDO from Em ( B’ ), EPN ( C’ ), LPN ( D’ ) and from a human donor ( E ). Scale bar: 500 µm. ( F – H ) Single-plane confocal images of PPDO derived from EPN pig pancreas immunostained against <t>CFTR-Phalloidin-PDX1</t> ( F ), SOX9-GP2-NKX6-1/GCG ( G ), KRT7-CDH1 ( H ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 3. Scale bar: 50 µm. ( I – K ) Brightfield microscopy images of early passage Em PPDO at the beginning of the live imaging, treated with DMSO ( I ), forskolin ( J ), and secretin ( K ). Scale bar 500 µm. ( I’ –K’ ) Brightfield microscopy images of early passage Em PPDO at the end of the live imaging, treated with DMSO ( I’ ), forskolin ( J’ ) and secretin ( K’ ). Scale bar 500 µm. ( L ) Quantification of the lumen area expansion of PPDO following 4 h of live imaging and treatments with forskolin and secretin. n = 3 independent experiments with different PPDO lines (1 Em, 1 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. P val are: * Padj = 0.015 for DMSO vs forskolin and * Padj = 0.0140 for DMSO vs secretin. ( M ) Quantification of the lumen area expansion of HPDO following 4 h of live imaging and treatment with forskolin. n = 4 independent experiments with 4 HPDO lines. Data are shown as mean ± SD. Mann–Whitney test was used to assess significance. * P = 0.0286. .
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    Image Search Results


    ( A ) Schema showing the process for generating PPDO. ( B – E ) Brightfield microscopy images of early passage PPDO and HPDO from Em- ( B ), EPN ( C ), LPN ( D ) and from a human donor ( E ). Scale bar: 500 µm. ( B’ – E’ ) Brightfield microscopy images of late passage PPDO and HPDO from Em ( B’ ), EPN ( C’ ), LPN ( D’ ) and from a human donor ( E ). Scale bar: 500 µm. ( F – H ) Single-plane confocal images of PPDO derived from EPN pig pancreas immunostained against CFTR-Phalloidin-PDX1 ( F ), SOX9-GP2-NKX6-1/GCG ( G ), KRT7-CDH1 ( H ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 3. Scale bar: 50 µm. ( I – K ) Brightfield microscopy images of early passage Em PPDO at the beginning of the live imaging, treated with DMSO ( I ), forskolin ( J ), and secretin ( K ). Scale bar 500 µm. ( I’ –K’ ) Brightfield microscopy images of early passage Em PPDO at the end of the live imaging, treated with DMSO ( I’ ), forskolin ( J’ ) and secretin ( K’ ). Scale bar 500 µm. ( L ) Quantification of the lumen area expansion of PPDO following 4 h of live imaging and treatments with forskolin and secretin. n = 3 independent experiments with different PPDO lines (1 Em, 1 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. P val are: * Padj = 0.015 for DMSO vs forskolin and * Padj = 0.0140 for DMSO vs secretin. ( M ) Quantification of the lumen area expansion of HPDO following 4 h of live imaging and treatment with forskolin. n = 4 independent experiments with 4 HPDO lines. Data are shown as mean ± SD. Mann–Whitney test was used to assess significance. * P = 0.0286. .

    Journal: EMBO Molecular Medicine

    Article Title: Benchmarking porcine pancreatic ductal organoids for drug screening applications

    doi: 10.1038/s44321-025-00330-3

    Figure Lengend Snippet: ( A ) Schema showing the process for generating PPDO. ( B – E ) Brightfield microscopy images of early passage PPDO and HPDO from Em- ( B ), EPN ( C ), LPN ( D ) and from a human donor ( E ). Scale bar: 500 µm. ( B’ – E’ ) Brightfield microscopy images of late passage PPDO and HPDO from Em ( B’ ), EPN ( C’ ), LPN ( D’ ) and from a human donor ( E ). Scale bar: 500 µm. ( F – H ) Single-plane confocal images of PPDO derived from EPN pig pancreas immunostained against CFTR-Phalloidin-PDX1 ( F ), SOX9-GP2-NKX6-1/GCG ( G ), KRT7-CDH1 ( H ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 3. Scale bar: 50 µm. ( I – K ) Brightfield microscopy images of early passage Em PPDO at the beginning of the live imaging, treated with DMSO ( I ), forskolin ( J ), and secretin ( K ). Scale bar 500 µm. ( I’ –K’ ) Brightfield microscopy images of early passage Em PPDO at the end of the live imaging, treated with DMSO ( I’ ), forskolin ( J’ ) and secretin ( K’ ). Scale bar 500 µm. ( L ) Quantification of the lumen area expansion of PPDO following 4 h of live imaging and treatments with forskolin and secretin. n = 3 independent experiments with different PPDO lines (1 Em, 1 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. P val are: * Padj = 0.015 for DMSO vs forskolin and * Padj = 0.0140 for DMSO vs secretin. ( M ) Quantification of the lumen area expansion of HPDO following 4 h of live imaging and treatment with forskolin. n = 4 independent experiments with 4 HPDO lines. Data are shown as mean ± SD. Mann–Whitney test was used to assess significance. * P = 0.0286. .

    Article Snippet: Primary antibodies used in this study were: a-SOX9 (rabbit, 1:800, Millipore AB3555), a-KRT5 (rabbit, 1:200, abcam ab53121), a-KRT7 (mouse, 1:200, Agilent Technologies M701829-2), a-KRT8/18 (guinea pig, 1:1000, Origene BP5007), a-PAN-KRT (rabbit, 1:500, Agilent Z0622), a-BMPR1A (mouse, 1:400, LSBio LS-C191759), a-CDH1 (mouse, 1:800, BD Biosciences 610181), a-CDH1 (rat, 1:500, Takara M108), a-CFTR (rabbit, 1:100, Cell Signaling 78335), a-GP2 (mouse, 1:100, MBL D277-3), a-PDX1 (goat, 1:200, R&D Systems AF2419), a-GCG (mouse, 1:200, Sigma-Aldrich G2654), a-AGR2 (rabbit, 1:200, Cell Signaling 13062S), a-GCG (guinea pig, 1:800, Takara M182), a-NKX6-1 (mouse, 1:100, Developmental Studies Hybridoma Bank F55A10), a-NEUROG3 (sheep, R&D Systems AF3444), a-Pancreatic amylase (rabbit, 1:200, abcam 21156), a-INS (guinea pig, 1:200, LSBio (BIOZOL), LS-C85862-1), a-GCG (guinea pig, 1:1000, Takara, M182), Phalloidin Alexa Fluor 546 (Invitrogen A22283), a-cleaved-caspase3-ASP175 (1:200, Cell Signaling, 9661S), a-Ki67-Vio G570 (1:100, Miltenyi Biotec, 130-133-796).

    Techniques: Microscopy, Derivative Assay, Staining, Imaging, MANN-WHITNEY

    ( A – C ) Single-plane confocal images of PPDO derived from one Em pig pancreas immunostained against Pan-Cytokeratin (PAN-CK)-BMPR1A-CDH1 ( A ), SOX9-Phalloidin-NKX6-1 ( B ), CFTR-GP2-PDX1 ( C ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 2. Scale bar: 50 µm. ( D –F ) Single-plane confocal images of PPDO derived from an LPN pig pancreas immunostained against KRT5-BMPR1A-CDH1 ( D ), SOX9-GCG/NKX6-1-Phalloidin ( E ), CFTR-GP2-PDX1 ( F ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 4. Scale bar: 50 µm. ( G – I ) Single-plane confocal images of PPDO derived from an Ad pig pancreas immunostained against CFTR-GP2-PDX1 ( G ), SOX9-Phalloidin-CDH1 ( H ), AMY3A-KRT7-NEUROG3 ( I ), and counterstained with DAPI. PPDO were stained at passage 3. Insets show the individual channels of the merge image. Scale bar: 50 µm. ( J –L ) Single-plane confocal images of HPDO immunostained against KRT7-AGR2-CDH1 ( J ), CFTR-BMPR1A-NKX6.1 ( K ), SOX9-Phalloidin-PDX1 ( L ), and counterstained with DAPI. Insets show the individual channels of the merge image. HPDO were stained at passage 3. Scale bar: 50 µm. ( M , N ) Single-plane confocal images of porcine pancreas cryosections (Ad) immunostained against NKX6.1-SOX9-CDH1 ( M ) and phalloidin-555-PDX1 ( N ), and counterstained with DAPI. Scale bar: 50 µm. ( O ) Quantification of the organoid area of late passage (>5) PPDO following 4 h of live imaging and treatment with forskolin. n = 3 independent experiments with 3 PPDO lines (2 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. Not-significant (ns) P = 0.9010.

    Journal: EMBO Molecular Medicine

    Article Title: Benchmarking porcine pancreatic ductal organoids for drug screening applications

    doi: 10.1038/s44321-025-00330-3

    Figure Lengend Snippet: ( A – C ) Single-plane confocal images of PPDO derived from one Em pig pancreas immunostained against Pan-Cytokeratin (PAN-CK)-BMPR1A-CDH1 ( A ), SOX9-Phalloidin-NKX6-1 ( B ), CFTR-GP2-PDX1 ( C ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 2. Scale bar: 50 µm. ( D –F ) Single-plane confocal images of PPDO derived from an LPN pig pancreas immunostained against KRT5-BMPR1A-CDH1 ( D ), SOX9-GCG/NKX6-1-Phalloidin ( E ), CFTR-GP2-PDX1 ( F ) and counterstained with DAPI. Insets show the individual channels of the merge image. PPDO were stained at passage 4. Scale bar: 50 µm. ( G – I ) Single-plane confocal images of PPDO derived from an Ad pig pancreas immunostained against CFTR-GP2-PDX1 ( G ), SOX9-Phalloidin-CDH1 ( H ), AMY3A-KRT7-NEUROG3 ( I ), and counterstained with DAPI. PPDO were stained at passage 3. Insets show the individual channels of the merge image. Scale bar: 50 µm. ( J –L ) Single-plane confocal images of HPDO immunostained against KRT7-AGR2-CDH1 ( J ), CFTR-BMPR1A-NKX6.1 ( K ), SOX9-Phalloidin-PDX1 ( L ), and counterstained with DAPI. Insets show the individual channels of the merge image. HPDO were stained at passage 3. Scale bar: 50 µm. ( M , N ) Single-plane confocal images of porcine pancreas cryosections (Ad) immunostained against NKX6.1-SOX9-CDH1 ( M ) and phalloidin-555-PDX1 ( N ), and counterstained with DAPI. Scale bar: 50 µm. ( O ) Quantification of the organoid area of late passage (>5) PPDO following 4 h of live imaging and treatment with forskolin. n = 3 independent experiments with 3 PPDO lines (2 EPN and 1 Ad). Data are shown as mean ± SD. One-way ANOVA followed by Dunnett’s multiple comparisons test was used to assess significance. Not-significant (ns) P = 0.9010.

    Article Snippet: Primary antibodies used in this study were: a-SOX9 (rabbit, 1:800, Millipore AB3555), a-KRT5 (rabbit, 1:200, abcam ab53121), a-KRT7 (mouse, 1:200, Agilent Technologies M701829-2), a-KRT8/18 (guinea pig, 1:1000, Origene BP5007), a-PAN-KRT (rabbit, 1:500, Agilent Z0622), a-BMPR1A (mouse, 1:400, LSBio LS-C191759), a-CDH1 (mouse, 1:800, BD Biosciences 610181), a-CDH1 (rat, 1:500, Takara M108), a-CFTR (rabbit, 1:100, Cell Signaling 78335), a-GP2 (mouse, 1:100, MBL D277-3), a-PDX1 (goat, 1:200, R&D Systems AF2419), a-GCG (mouse, 1:200, Sigma-Aldrich G2654), a-AGR2 (rabbit, 1:200, Cell Signaling 13062S), a-GCG (guinea pig, 1:800, Takara M182), a-NKX6-1 (mouse, 1:100, Developmental Studies Hybridoma Bank F55A10), a-NEUROG3 (sheep, R&D Systems AF3444), a-Pancreatic amylase (rabbit, 1:200, abcam 21156), a-INS (guinea pig, 1:200, LSBio (BIOZOL), LS-C85862-1), a-GCG (guinea pig, 1:1000, Takara, M182), Phalloidin Alexa Fluor 546 (Invitrogen A22283), a-cleaved-caspase3-ASP175 (1:200, Cell Signaling, 9661S), a-Ki67-Vio G570 (1:100, Miltenyi Biotec, 130-133-796).

    Techniques: Derivative Assay, Staining, Imaging

    ( A , B ) Brightfield microscopy images of PPDO in complete ( A ) or porcine serum supplemented ( B ). Scale bar 500 µm. ( C , D ) Brightfield microscopy images of PPDO at the end of differentiation in complete ( C ) or at the end of the differentiation using S5 + S6 combination ( D ) media. Scale bar 500 µm. ( E –J ) Bar plots showing the fold change of gene expression analysis at the end of the differentiation after treatment with porcine serum. Gene expression was measured for CFTR ( E ), KRT7 ( F ), NEUROD1 ( G ), GCG ( H ), INS ( I ), and SST ( J ). n = 3 independent PPDO lines (1 Em and 2 EPN). Absence of samples from the plots indicate non-detectable amplification following the RT-PCR. Data are shown as mean ± SEM. Unpaired Student’s t-test was used to assess significance with * P = 0.0196 for NEUROD1 . ( K , L ) Single-plane confocal images of PPDO in growth media ( K ) or in differentiation media from Loomans et al ( L ) (see Methods). PPDO were immunostained against INS-KRT7-CHGA and counterstained with DAPI. Experiment was repeated with n = 3 biological replicates (1 Em-1 EPN-1 Ad). Scale bar: 50 µm. ( M , N ) Brightfield microscopy images of HPDO in differentiation media ( M ) or differentiation media supplemented with DAPT/DEAB small molecules ( N ). Experiment was repeated with n = 3 biological replicates. Scale bar 500 µm.

    Journal: EMBO Molecular Medicine

    Article Title: Benchmarking porcine pancreatic ductal organoids for drug screening applications

    doi: 10.1038/s44321-025-00330-3

    Figure Lengend Snippet: ( A , B ) Brightfield microscopy images of PPDO in complete ( A ) or porcine serum supplemented ( B ). Scale bar 500 µm. ( C , D ) Brightfield microscopy images of PPDO at the end of differentiation in complete ( C ) or at the end of the differentiation using S5 + S6 combination ( D ) media. Scale bar 500 µm. ( E –J ) Bar plots showing the fold change of gene expression analysis at the end of the differentiation after treatment with porcine serum. Gene expression was measured for CFTR ( E ), KRT7 ( F ), NEUROD1 ( G ), GCG ( H ), INS ( I ), and SST ( J ). n = 3 independent PPDO lines (1 Em and 2 EPN). Absence of samples from the plots indicate non-detectable amplification following the RT-PCR. Data are shown as mean ± SEM. Unpaired Student’s t-test was used to assess significance with * P = 0.0196 for NEUROD1 . ( K , L ) Single-plane confocal images of PPDO in growth media ( K ) or in differentiation media from Loomans et al ( L ) (see Methods). PPDO were immunostained against INS-KRT7-CHGA and counterstained with DAPI. Experiment was repeated with n = 3 biological replicates (1 Em-1 EPN-1 Ad). Scale bar: 50 µm. ( M , N ) Brightfield microscopy images of HPDO in differentiation media ( M ) or differentiation media supplemented with DAPT/DEAB small molecules ( N ). Experiment was repeated with n = 3 biological replicates. Scale bar 500 µm.

    Article Snippet: Primary antibodies used in this study were: a-SOX9 (rabbit, 1:800, Millipore AB3555), a-KRT5 (rabbit, 1:200, abcam ab53121), a-KRT7 (mouse, 1:200, Agilent Technologies M701829-2), a-KRT8/18 (guinea pig, 1:1000, Origene BP5007), a-PAN-KRT (rabbit, 1:500, Agilent Z0622), a-BMPR1A (mouse, 1:400, LSBio LS-C191759), a-CDH1 (mouse, 1:800, BD Biosciences 610181), a-CDH1 (rat, 1:500, Takara M108), a-CFTR (rabbit, 1:100, Cell Signaling 78335), a-GP2 (mouse, 1:100, MBL D277-3), a-PDX1 (goat, 1:200, R&D Systems AF2419), a-GCG (mouse, 1:200, Sigma-Aldrich G2654), a-AGR2 (rabbit, 1:200, Cell Signaling 13062S), a-GCG (guinea pig, 1:800, Takara M182), a-NKX6-1 (mouse, 1:100, Developmental Studies Hybridoma Bank F55A10), a-NEUROG3 (sheep, R&D Systems AF3444), a-Pancreatic amylase (rabbit, 1:200, abcam 21156), a-INS (guinea pig, 1:200, LSBio (BIOZOL), LS-C85862-1), a-GCG (guinea pig, 1:1000, Takara, M182), Phalloidin Alexa Fluor 546 (Invitrogen A22283), a-cleaved-caspase3-ASP175 (1:200, Cell Signaling, 9661S), a-Ki67-Vio G570 (1:100, Miltenyi Biotec, 130-133-796).

    Techniques: Microscopy, Gene Expression, Amplification, Reverse Transcription Polymerase Chain Reaction