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recombinant rat gdnf  (R&D Systems)


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    Structured Review

    R&D Systems recombinant rat gdnf
    Recombinant Rat Gdnf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/recombinant+gdnf/Recombinant+Rat+CNTF+Protein/pm41972906-64-17-23
    Average 93 stars, based on 42 article reviews
    recombinant rat gdnf - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    Cell Culture:

    Article Title: Restoring early postnatal synaptic dysregulation rescues motor neuron degeneration in a mouse model of Spinal and Bulbar Muscular Atrophy
    Article Snippet: .. Establishment and characterization of iPSCs from SBMA patients (SBMA1E12, SBMA2E16, SBMA3E10, and SBMA4E5 clones) and healthy controls (EKN3, TIGE9, YFE16, and YFE19 clones) were described elsewhere . iPSCs were differentiated into motor neurons through embryoid bodies (EBs) as previously described , , and dissociated EBs were plated onto dishes coated with growth factor reduced Matrigel (Corning, Corning, NY) at a density of 1 × 10 5 cells/cm 2 and cultured in motor neuron medium consisting of KBM Neural Stem Cell medium (Kohjin Bio, Saitama, Japan) or Media Hormone Mix (MHM) supplemented with 2% B27 supplement (Thermo Fisher Scientific), 1% non-essential amino acids (Thermo Fisher Scientific), 50 nM retinoic acid (Sigma-Aldrich), 500 nM purmorphamine (Calbiochem, Germany), 10 μM cyclic AMP (Sigma-Aldrich), 10 ng/mL recombinant BDNF (R&D systems, Minneapolis, MN), 10 ng/mL recombinant GDNF (R&D systems), 10 ng/mL recombinant human IGF-1 (R&D systems), and 200 ng/mL L-ascorbic acid (Sigma-Aldrich). .. Mouse tissues and cell lysates were homogenized in CelLytic lysis buffer (Sigma-Aldrich) containing Halt Protease and Phosphatase Inhibitor Cocktails (Thermo Fisher Scientific, Waltham, MA).

    Article Title: Modulation of oxygen tension, acidosis, and cell density is crucial for neural differentiation of human induced pluripotent stem cells.
    Article Snippet: Human induced pluripotent stem cell (hiPSC)-derived neural cells provide valuable disease models for pathophysiological analysis and drug discovery for intractable neurodegenerative diseases.. However, neural differentiation of hiPSCs requires a complex and long culture procedure, which has been a bottleneck for analysis.. We previously demonstrated rapid, efficient, and simple motor neuron differentiation from human pluripotent stem cells (hPSCs).

    Article Title: C9ORF72 dipeptide repeat proteins disrupt formation of GEM bodies and induce aberrant accumulation of survival of motor neuron protein
    Article Snippet: On day 14, hEBs were enzymatically dissociated into single cells using TrypLE Select (Thermo Fisher Scientific, USA). .. The dissociated cells were plated on growth factor-reduced Matrigel (33 × dilution, thin coating; Corning, USA)-coated dishes at a density of 2 × 10 4 cells/well (96-well imaging plate, Greiner Bio-One, Austria) and cultured in MN medium (MNM) consisting of KBM Neural Stem Cell medium (Kohjin Bio, Japan) supplemented with 2% B27 supplement (Thermo Fisher Scientific, USA), 1% NEAA, 50 nM RA, 500 nM purmorphamine, 10 μM cyclic AMP (cAMP) (Sigma-Aldrich, USA), 10 ng/mL recombinant BDNF (R&D Systems, USA), 10 ng/mL recombinant GDNF (R&D Systems, USA), 10 ng/mL recombinant human IGF-1 (R&D Systems, USA), and 200 ng/mL L-ascorbic acid (Sigma-Aldrich, USA) for up to 4 weeks. ..

    Recombinant:

    Article Title: Restoring early postnatal synaptic dysregulation rescues motor neuron degeneration in a mouse model of Spinal and Bulbar Muscular Atrophy
    Article Snippet: .. Establishment and characterization of iPSCs from SBMA patients (SBMA1E12, SBMA2E16, SBMA3E10, and SBMA4E5 clones) and healthy controls (EKN3, TIGE9, YFE16, and YFE19 clones) were described elsewhere . iPSCs were differentiated into motor neurons through embryoid bodies (EBs) as previously described , , and dissociated EBs were plated onto dishes coated with growth factor reduced Matrigel (Corning, Corning, NY) at a density of 1 × 10 5 cells/cm 2 and cultured in motor neuron medium consisting of KBM Neural Stem Cell medium (Kohjin Bio, Saitama, Japan) or Media Hormone Mix (MHM) supplemented with 2% B27 supplement (Thermo Fisher Scientific), 1% non-essential amino acids (Thermo Fisher Scientific), 50 nM retinoic acid (Sigma-Aldrich), 500 nM purmorphamine (Calbiochem, Germany), 10 μM cyclic AMP (Sigma-Aldrich), 10 ng/mL recombinant BDNF (R&D systems, Minneapolis, MN), 10 ng/mL recombinant GDNF (R&D systems), 10 ng/mL recombinant human IGF-1 (R&D systems), and 200 ng/mL L-ascorbic acid (Sigma-Aldrich). .. Mouse tissues and cell lysates were homogenized in CelLytic lysis buffer (Sigma-Aldrich) containing Halt Protease and Phosphatase Inhibitor Cocktails (Thermo Fisher Scientific, Waltham, MA).

    Article Title: LIN28A binds to meiotic gene transcripts and modulates their translation in male germ cells.
    Article Snippet: .. The medium was supplemented with 20 ng/ml recombinant GDNF (R&D Systems, Minneapolis, MN), 150 ng/ml GFRA1 (R&D Systems), and 1 ng/ml FGF2 (BD Biosciences, San Jose, CA). ..

    Article Title: Modulation of oxygen tension, acidosis, and cell density is crucial for neural differentiation of human induced pluripotent stem cells.
    Article Snippet: Human induced pluripotent stem cell (hiPSC)-derived neural cells provide valuable disease models for pathophysiological analysis and drug discovery for intractable neurodegenerative diseases.. However, neural differentiation of hiPSCs requires a complex and long culture procedure, which has been a bottleneck for analysis.. We previously demonstrated rapid, efficient, and simple motor neuron differentiation from human pluripotent stem cells (hPSCs).

    Article Title: Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense.
    Article Snippet: First release: 22 May 2024 science.org (Page numbers not final at time of first release) 1 Although the ENS is best known for coordinating essential physiologic functions like digestion and gut motility, recent evidence suggests it is a critical mediator in gut neuro-immune communication.. We and others have demonstrated that ENS neuropeptides—such as neuromedin U (NMU), calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP)— profoundly influence barrier immune responses and host defense against pathogens (1–4).. For instance, NMU acts on type 2 innate lymphoid cells (ILC2s) that express NMUR1, amplifying their production of the type 2 cytokines interleukin-13 (IL-13) and IL-5 and promoting allergic inflammation in the lung and gut (1–3).

    Article Title: Engineering kidney developmental trajectory using culture boundary conditions
    Article Snippet: .. GDNF overactivation was achieved by supplying 100 ng/ml recombinant GDNF (212-GD, R&D systems) in culture media at day 0 of 3D 0.5 C + M gel culture. .. Similarly, RET inhibition was carried out through adding Selpercatinib (76-961-0, Tocris) at 100 nM in the culture media.

    Article Title: C9ORF72 dipeptide repeat proteins disrupt formation of GEM bodies and induce aberrant accumulation of survival of motor neuron protein
    Article Snippet: On day 14, hEBs were enzymatically dissociated into single cells using TrypLE Select (Thermo Fisher Scientific, USA). .. The dissociated cells were plated on growth factor-reduced Matrigel (33 × dilution, thin coating; Corning, USA)-coated dishes at a density of 2 × 10 4 cells/well (96-well imaging plate, Greiner Bio-One, Austria) and cultured in MN medium (MNM) consisting of KBM Neural Stem Cell medium (Kohjin Bio, Japan) supplemented with 2% B27 supplement (Thermo Fisher Scientific, USA), 1% NEAA, 50 nM RA, 500 nM purmorphamine, 10 μM cyclic AMP (cAMP) (Sigma-Aldrich, USA), 10 ng/mL recombinant BDNF (R&D Systems, USA), 10 ng/mL recombinant GDNF (R&D Systems, USA), 10 ng/mL recombinant human IGF-1 (R&D Systems, USA), and 200 ng/mL L-ascorbic acid (Sigma-Aldrich, USA) for up to 4 weeks. ..

    Incubation:

    Article Title: Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense.
    Article Snippet: First release: 22 May 2024 science.org (Page numbers not final at time of first release) 1 Although the ENS is best known for coordinating essential physiologic functions like digestion and gut motility, recent evidence suggests it is a critical mediator in gut neuro-immune communication.. We and others have demonstrated that ENS neuropeptides—such as neuromedin U (NMU), calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP)— profoundly influence barrier immune responses and host defense against pathogens (1–4).. For instance, NMU acts on type 2 innate lymphoid cells (ILC2s) that express NMUR1, amplifying their production of the type 2 cytokines interleukin-13 (IL-13) and IL-5 and promoting allergic inflammation in the lung and gut (1–3).

    Imaging:

    Article Title: C9ORF72 dipeptide repeat proteins disrupt formation of GEM bodies and induce aberrant accumulation of survival of motor neuron protein
    Article Snippet: On day 14, hEBs were enzymatically dissociated into single cells using TrypLE Select (Thermo Fisher Scientific, USA). .. The dissociated cells were plated on growth factor-reduced Matrigel (33 × dilution, thin coating; Corning, USA)-coated dishes at a density of 2 × 10 4 cells/well (96-well imaging plate, Greiner Bio-One, Austria) and cultured in MN medium (MNM) consisting of KBM Neural Stem Cell medium (Kohjin Bio, Japan) supplemented with 2% B27 supplement (Thermo Fisher Scientific, USA), 1% NEAA, 50 nM RA, 500 nM purmorphamine, 10 μM cyclic AMP (cAMP) (Sigma-Aldrich, USA), 10 ng/mL recombinant BDNF (R&D Systems, USA), 10 ng/mL recombinant GDNF (R&D Systems, USA), 10 ng/mL recombinant human IGF-1 (R&D Systems, USA), and 200 ng/mL L-ascorbic acid (Sigma-Aldrich, USA) for up to 4 weeks. ..

    Article Title: Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense.
    Article Snippet: First release: 22 May 2024 science.org (Page numbers not final at time of first release) 1 Although the ENS is best known for coordinating essential physiologic functions like digestion and gut motility, recent evidence suggests it is a critical mediator in gut neuro-immune communication.. We and others have demonstrated that ENS neuropeptides—such as neuromedin U (NMU), calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP)— profoundly influence barrier immune responses and host defense against pathogens (1–4).. For instance, NMU acts on type 2 innate lymphoid cells (ILC2s) that express NMUR1, amplifying their production of the type 2 cytokines interleukin-13 (IL-13) and IL-5 and promoting allergic inflammation in the lung and gut (1–3).

    other:

    Article Title: Restoring early postnatal synaptic dysregulation rescues motor neuron degeneration in a mouse model of Spinal and Bulbar Muscular Atrophy.
    Article Snippet: Mouse tissues and cell lysates were homogenized in CelLytic lysis buffer (Sigma-Aldrich) containing Halt Protease and Phosphatase Inhibitor Cocktails (Thermo Fisher Scientific, Waltham, MA).



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    GDNF-RET signaling tunes branching in mouse and human ureteric bud tissues. A. GDNF-RET signaling interactions involved in kidney branching. B. Immunofluorescence of cleared E14 mouse kidney. Top left , ECAD and SIX2. Bottom left, RET and GFRA1. Top right , isolated RET. Bottom right , isolated GFRA1 signal. C. Air-liquid interface (ALI) culture of mouse embryonic kidney explants. D. Design of GDNF-RET signaling perturbation experiments in ALI culture. E. Immunofluorescence of E13 kidneys grown in ALI culture for 4 days in 100 nM Selpercatinib (+RETi), 100 ng ml -1 GDNF (+GDNF), or control media. Inset , close-up of tip domains. Explants are immunostained for EpCAM (epithelium), RET (tip cells), and JAG1 (early nephrons). F. Tip number on days 1-4 across all conditions, N = 4 kidneys per condition. P -values by one-way Kruskal-Wallis test with Dunn’s post hoc test. G. Differentiation of iUB organoids from hiPSCs H. Immunofluorescence of epithelial (ECAD) and tip (RET) markers in a day 12 iUB organoid. I. Design of GDNF-RET signaling perturbations for iUB organoids. J. Merged brightfield and GATA3:mCherry images of iUB organoids at days 9 and 12. Organoids were cultured in control (-GDNF) or complete branching medium (+GDNF, 50 ng ml -1 ), excess GDNF (++GDNF, 250 ng ml -1 ), or complete branching medium with 100 nM Selpercatinib (+RETi). See: Fig. S4F . K. Projected area (x10 4 µm 2 ) on days 9 and 12 for all conditions, n = 47, 56, 40, 46 iUB organoids (-GDNF, +RETi, +GDNF, ++GDNF) from 2 independent biological replicates. L. Circularity (a.u.) on days 9 and 12. M. Bud number on days 9 and 12. P -values in panels K, L, M by one-way ANOVA with Dunnett’s post hoc test using +GDNF as reference group.
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    Image Search Results


    The figures illustrate the docking interaction of paeoniflorin with the GDNF receptor (PDB ID: 1AGQ). (A) Shows a surface representation of the GDNF receptor, with the active site highlighted in yellow, where the ligand paeoniflorin (red) is bound. (B) 2D interaction diagram displays key interactions between paeoniflorin and the receptor, with hydrogen bonds and hydrophobic interactions clearly indicated. (C) Provides a 3D view of the docking, showing paeoniflorin (blue) interacting with GDNF, with hydrogen bonds represented by green dashed lines and key regions labeled. (D) Offers a zoomed-in view of the binding site, emphasizing hydrogen bonds and hydrophobic contacts, depicted within a ribbon structure for clarity.

    Journal: Frontiers in Pharmacology

    Article Title: Enhanced therapeutic potential of paeoniflorin and vitamin B12 in intracerebropeduncle ethidium bromide-induced multiple sclerosis-like pathology

    doi: 10.3389/fphar.2026.1792674

    Figure Lengend Snippet: The figures illustrate the docking interaction of paeoniflorin with the GDNF receptor (PDB ID: 1AGQ). (A) Shows a surface representation of the GDNF receptor, with the active site highlighted in yellow, where the ligand paeoniflorin (red) is bound. (B) 2D interaction diagram displays key interactions between paeoniflorin and the receptor, with hydrogen bonds and hydrophobic interactions clearly indicated. (C) Provides a 3D view of the docking, showing paeoniflorin (blue) interacting with GDNF, with hydrogen bonds represented by green dashed lines and key regions labeled. (D) Offers a zoomed-in view of the binding site, emphasizing hydrogen bonds and hydrophobic contacts, depicted within a ribbon structure for clarity.

    Article Snippet: The ELISA kits for evaluating cellular and molecular targets included GDNF [E-EL-H1495; Elabscience GFRA1 [PKSH033670; Elabscience]; RET [AN00810P; Elabscience], AKT [E-EL-R0807 98T, Elabscience, Wuhan, China] ( ); ERK1/2 [E-AB-70292; Elabscience] ( ); and GSK3-Beta [KLR0989, KRISHGEN, Maharashtra, India] ( ).

    Techniques: Labeling, Binding Assay

    (A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular and molecular targets in MS rat model: GDNF (A) , GFRA1 (B) , AKT (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.

    Journal: Frontiers in Pharmacology

    Article Title: Enhanced therapeutic potential of paeoniflorin and vitamin B12 in intracerebropeduncle ethidium bromide-induced multiple sclerosis-like pathology

    doi: 10.3389/fphar.2026.1792674

    Figure Lengend Snippet: (A–H) PNN neuroprotective role in mitigating EBRO-induced alterations in levels of cellular and molecular targets in MS rat model: GDNF (A) , GFRA1 (B) , AKT (C) , ERK1/2 (D) , GSK3-Beta (E) , in brain homogenates, and GDNF, GFRA1, AKT, ERK1/2, GSK3-Beta in CSF levels (F–H) . Statistical analysis was performed using a one-way ANOVA followed by Tukey’s post hoc test to determine significant differences among groups (A–H) . Data were presented as mean ± standard deviation (SD), with statistical significance set at p < 0.01. Each experimental group consisted of eight wistar rats (n = 8). β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50. To identify significant differences between groups, a one-way ANOVA and Tukey’s post hoc test were used for statistical analysis (A–H) . The statistical significance level was set at p < 0.01, and the data were displayed as mean ± standard deviation (SD). There were eight wistar rats (n = 8) in each experimental group. β v/s Sham Control, Vehicle Control, and PNN Perse; δ v/s EBRO; δα1 v/s EBRO + PNN50; δα2 v/s EBRO + PNN100, EBRO + PNN50; and δα3 v/s EBRO + VB12 (30), EBRO + PNN100, EBRO + PNN50.

    Article Snippet: The ELISA kits for evaluating cellular and molecular targets included GDNF [E-EL-H1495; Elabscience GFRA1 [PKSH033670; Elabscience]; RET [AN00810P; Elabscience], AKT [E-EL-R0807 98T, Elabscience, Wuhan, China] ( ); ERK1/2 [E-AB-70292; Elabscience] ( ); and GSK3-Beta [KLR0989, KRISHGEN, Maharashtra, India] ( ).

    Techniques: Standard Deviation, Control

    GDNF-RET signaling tunes branching in mouse and human ureteric bud tissues. A. GDNF-RET signaling interactions involved in kidney branching. B. Immunofluorescence of cleared E14 mouse kidney. Top left , ECAD and SIX2. Bottom left, RET and GFRA1. Top right , isolated RET. Bottom right , isolated GFRA1 signal. C. Air-liquid interface (ALI) culture of mouse embryonic kidney explants. D. Design of GDNF-RET signaling perturbation experiments in ALI culture. E. Immunofluorescence of E13 kidneys grown in ALI culture for 4 days in 100 nM Selpercatinib (+RETi), 100 ng ml -1 GDNF (+GDNF), or control media. Inset , close-up of tip domains. Explants are immunostained for EpCAM (epithelium), RET (tip cells), and JAG1 (early nephrons). F. Tip number on days 1-4 across all conditions, N = 4 kidneys per condition. P -values by one-way Kruskal-Wallis test with Dunn’s post hoc test. G. Differentiation of iUB organoids from hiPSCs H. Immunofluorescence of epithelial (ECAD) and tip (RET) markers in a day 12 iUB organoid. I. Design of GDNF-RET signaling perturbations for iUB organoids. J. Merged brightfield and GATA3:mCherry images of iUB organoids at days 9 and 12. Organoids were cultured in control (-GDNF) or complete branching medium (+GDNF, 50 ng ml -1 ), excess GDNF (++GDNF, 250 ng ml -1 ), or complete branching medium with 100 nM Selpercatinib (+RETi). See: Fig. S4F . K. Projected area (x10 4 µm 2 ) on days 9 and 12 for all conditions, n = 47, 56, 40, 46 iUB organoids (-GDNF, +RETi, +GDNF, ++GDNF) from 2 independent biological replicates. L. Circularity (a.u.) on days 9 and 12. M. Bud number on days 9 and 12. P -values in panels K, L, M by one-way ANOVA with Dunnett’s post hoc test using +GDNF as reference group.

    Journal: bioRxiv

    Article Title: Synthetic budding morphogenesis by optogenetic receptor tyrosine kinase signaling

    doi: 10.64898/2026.03.31.715459

    Figure Lengend Snippet: GDNF-RET signaling tunes branching in mouse and human ureteric bud tissues. A. GDNF-RET signaling interactions involved in kidney branching. B. Immunofluorescence of cleared E14 mouse kidney. Top left , ECAD and SIX2. Bottom left, RET and GFRA1. Top right , isolated RET. Bottom right , isolated GFRA1 signal. C. Air-liquid interface (ALI) culture of mouse embryonic kidney explants. D. Design of GDNF-RET signaling perturbation experiments in ALI culture. E. Immunofluorescence of E13 kidneys grown in ALI culture for 4 days in 100 nM Selpercatinib (+RETi), 100 ng ml -1 GDNF (+GDNF), or control media. Inset , close-up of tip domains. Explants are immunostained for EpCAM (epithelium), RET (tip cells), and JAG1 (early nephrons). F. Tip number on days 1-4 across all conditions, N = 4 kidneys per condition. P -values by one-way Kruskal-Wallis test with Dunn’s post hoc test. G. Differentiation of iUB organoids from hiPSCs H. Immunofluorescence of epithelial (ECAD) and tip (RET) markers in a day 12 iUB organoid. I. Design of GDNF-RET signaling perturbations for iUB organoids. J. Merged brightfield and GATA3:mCherry images of iUB organoids at days 9 and 12. Organoids were cultured in control (-GDNF) or complete branching medium (+GDNF, 50 ng ml -1 ), excess GDNF (++GDNF, 250 ng ml -1 ), or complete branching medium with 100 nM Selpercatinib (+RETi). See: Fig. S4F . K. Projected area (x10 4 µm 2 ) on days 9 and 12 for all conditions, n = 47, 56, 40, 46 iUB organoids (-GDNF, +RETi, +GDNF, ++GDNF) from 2 independent biological replicates. L. Circularity (a.u.) on days 9 and 12. M. Bud number on days 9 and 12. P -values in panels K, L, M by one-way ANOVA with Dunnett’s post hoc test using +GDNF as reference group.

    Article Snippet: MDCK cells were not starved and were treated with 50 ng ml -1 GDNF (#212-GD-050, R&D Systems) and 100 ng ml -1 recombinant human Gfrɑ1 (#714-GR-100, R&D Systems) at defined time points.

    Techniques: Immunofluorescence, Isolation, Control, Cell Culture

    Blue light stimulation of optoRET drives ERK signaling and ligand-independent budding in iUB organoids. C. Schematic of hiPSC-optoRET generation using piggyBac transposase and differentiation into iUB-optoRET organoids. D. Immunofluorescence of iUB-optoRET monolayers stimulated for 2 hr under the indicated conditions (±light). Blue light stimulation was provided by an optoPlate-96 (470 nm, 50 mW cm -2 , 1 s every 10 s) for 2 hrs. Top , optoRET (detected by anti-GFP) and nuclei (DAPI). Bottom , intensity-coded ppERK (a.u.). E. Violin plot of ppERK (a.u.) for iUB-optoRET cells under -light and +light conditions, n = 2458, 2030 cells (control, +light) pooled from 2 independent biological replicates. P -value by Welch’s t-test. F. Immunofluorescence density plot of ppERK (a.u.) as a function of optoRET(eGFP) intensity (a.u.) for cells shown in B. n = 2458, 2030 cells (control, +light) pooled from two independent biological replicates. G. Stimulation conditions for iUB-optoRET organoids: control (−light/−GDNF), +light, +GDNF, and combined (+light/+GDNF) treatments. H. Live fluorescence images of GATA3 mCherry iUB-optoRET organoids under optogenetic and ligand-based stimulation conditions. Blue light stimulation was provided by an optoPlate-96 (320 mW cm -2 , 0.5 s every 4 min) between days 7-11 and the +GDNF and +light/+GDNF groups received 50 ng ml -1 GDNF. I. Bud number on day 11 across all conditions, n = 50, 50, 51, 50 organoids (control, +light, +GDNF, +light/+GDNF) from 2 independent biological replicates. P -values by one-way Kruskal-Wallis test with Dunn’s post hoc test. J. Differential expression analysis from bulk RNA-seq of iUB-optoRET organoids grown in ±light stimulation conditions (see also: Fig. S14 ). Top , relative density of tip and trunk marker genes. Bottom , volcano plot of all genes organized by significance (-log 10 ( p )) and log 2 (fold-change) with tip and trunk-specific markers highlighted. Data are derived from 3 biological replicates. K. Gene Set Enrichment Analysis (GSEA) as a function of normalized enrichment score (NES). Hallmark gene sets are color coded by false discovery rate (FDR), size coded by the size of the gene set.

    Journal: bioRxiv

    Article Title: Synthetic budding morphogenesis by optogenetic receptor tyrosine kinase signaling

    doi: 10.64898/2026.03.31.715459

    Figure Lengend Snippet: Blue light stimulation of optoRET drives ERK signaling and ligand-independent budding in iUB organoids. C. Schematic of hiPSC-optoRET generation using piggyBac transposase and differentiation into iUB-optoRET organoids. D. Immunofluorescence of iUB-optoRET monolayers stimulated for 2 hr under the indicated conditions (±light). Blue light stimulation was provided by an optoPlate-96 (470 nm, 50 mW cm -2 , 1 s every 10 s) for 2 hrs. Top , optoRET (detected by anti-GFP) and nuclei (DAPI). Bottom , intensity-coded ppERK (a.u.). E. Violin plot of ppERK (a.u.) for iUB-optoRET cells under -light and +light conditions, n = 2458, 2030 cells (control, +light) pooled from 2 independent biological replicates. P -value by Welch’s t-test. F. Immunofluorescence density plot of ppERK (a.u.) as a function of optoRET(eGFP) intensity (a.u.) for cells shown in B. n = 2458, 2030 cells (control, +light) pooled from two independent biological replicates. G. Stimulation conditions for iUB-optoRET organoids: control (−light/−GDNF), +light, +GDNF, and combined (+light/+GDNF) treatments. H. Live fluorescence images of GATA3 mCherry iUB-optoRET organoids under optogenetic and ligand-based stimulation conditions. Blue light stimulation was provided by an optoPlate-96 (320 mW cm -2 , 0.5 s every 4 min) between days 7-11 and the +GDNF and +light/+GDNF groups received 50 ng ml -1 GDNF. I. Bud number on day 11 across all conditions, n = 50, 50, 51, 50 organoids (control, +light, +GDNF, +light/+GDNF) from 2 independent biological replicates. P -values by one-way Kruskal-Wallis test with Dunn’s post hoc test. J. Differential expression analysis from bulk RNA-seq of iUB-optoRET organoids grown in ±light stimulation conditions (see also: Fig. S14 ). Top , relative density of tip and trunk marker genes. Bottom , volcano plot of all genes organized by significance (-log 10 ( p )) and log 2 (fold-change) with tip and trunk-specific markers highlighted. Data are derived from 3 biological replicates. K. Gene Set Enrichment Analysis (GSEA) as a function of normalized enrichment score (NES). Hallmark gene sets are color coded by false discovery rate (FDR), size coded by the size of the gene set.

    Article Snippet: MDCK cells were not starved and were treated with 50 ng ml -1 GDNF (#212-GD-050, R&D Systems) and 100 ng ml -1 recombinant human Gfrɑ1 (#714-GR-100, R&D Systems) at defined time points.

    Techniques: Immunofluorescence, Control, Fluorescence, Quantitative Proteomics, RNA Sequencing, Marker, Derivative Assay

    Spatially patterned optoRET stimulation drives asymmetric budding in iUB organoids. A. Strategy for targeted optogenetic stimulation of iUB-optoRET organoids. B. Average projections of GATA3:mCherry for small ( top panels ) and large ( bottom panels ) iUB-optoRET organoids under control, +GDNF, +light whole, and +light half conditions. Light stimulation was provided by 488 nm DMD-based light projection (0.5 s every 4 mins) for 4 days. Organoids in the +GDNF group received 50 ng ml -1 GDNF. Top row , average projections across individual organoids at day 7. Middle row , average projections across individual organoids at day 11. Bottom row , normalized average projections for individual organoids at day 11. C. Representative average projections of individual small ( top ) and large ( bottom ) iUB-optoRET organoids on day 11. The cyan dashed line divides the non-illuminated side ( left , -light half) from the illuminated side ( right , +light half). Magenta dots indicate bud locations. D. Confocal immunofluorescence images of optoRET+ and RET+ cells within iUB-optoRET bud tips in +light whole condition. Endogenous RET was visualized with an antibody against the extracellular domain (ECD). Left , ECAD, optoRET, and RET(ECD). Middle , optoRET and tip outline. Right , RET(ECD) and tip outline. E. Radial histograms of bud orientation angle (°) for small organoids across all conditions, n = 19, 20, 19, 20 organoids (control, +GDNF, +light whole, and +light half) pooled from 2 biological replicates. P -values by Kolmogorov-Smirnov test against a uniform reference distribution.

    Journal: bioRxiv

    Article Title: Synthetic budding morphogenesis by optogenetic receptor tyrosine kinase signaling

    doi: 10.64898/2026.03.31.715459

    Figure Lengend Snippet: Spatially patterned optoRET stimulation drives asymmetric budding in iUB organoids. A. Strategy for targeted optogenetic stimulation of iUB-optoRET organoids. B. Average projections of GATA3:mCherry for small ( top panels ) and large ( bottom panels ) iUB-optoRET organoids under control, +GDNF, +light whole, and +light half conditions. Light stimulation was provided by 488 nm DMD-based light projection (0.5 s every 4 mins) for 4 days. Organoids in the +GDNF group received 50 ng ml -1 GDNF. Top row , average projections across individual organoids at day 7. Middle row , average projections across individual organoids at day 11. Bottom row , normalized average projections for individual organoids at day 11. C. Representative average projections of individual small ( top ) and large ( bottom ) iUB-optoRET organoids on day 11. The cyan dashed line divides the non-illuminated side ( left , -light half) from the illuminated side ( right , +light half). Magenta dots indicate bud locations. D. Confocal immunofluorescence images of optoRET+ and RET+ cells within iUB-optoRET bud tips in +light whole condition. Endogenous RET was visualized with an antibody against the extracellular domain (ECD). Left , ECAD, optoRET, and RET(ECD). Middle , optoRET and tip outline. Right , RET(ECD) and tip outline. E. Radial histograms of bud orientation angle (°) for small organoids across all conditions, n = 19, 20, 19, 20 organoids (control, +GDNF, +light whole, and +light half) pooled from 2 biological replicates. P -values by Kolmogorov-Smirnov test against a uniform reference distribution.

    Article Snippet: MDCK cells were not starved and were treated with 50 ng ml -1 GDNF (#212-GD-050, R&D Systems) and 100 ng ml -1 recombinant human Gfrɑ1 (#714-GR-100, R&D Systems) at defined time points.

    Techniques: Control, Immunofluorescence