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ck666 (Tocris)

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Tocris ck666
Ck666, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 106 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ck666/CK+666/pm42014922-421-32-33
Average 94 stars, based on 106 article reviews

ck666 - by Bioz Stars, 2026-09

94/100 stars

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Incubation:

Article Title: The cortical actin cytoskeleton and desmosomes act together in keratin filament network maintenance.
Article Snippet: .. Blastocysts were treated either with 100 nM jasplakinolide (Tocris Bioscience, Wiesbaden, Germany), 10 μM latrunculin B (Adipogen, Fuellinsdorf, Switzerland), 10 μM cytochalasin D (Sigma-Aldrich), 10 μM para-nitroblebbistatin (optopharma, Budapest, Hungary), 200 μM CK666 (Tocris Bioscience), 100 μM SMIFH2 (Tocris Bioscience) or dimethyl sulfoxide (DMSO) for 1 h. Incubation time and drug concentrations were optimized in living intestine of Krt8-YFP mice based on available literature. ..

Article Title: The Arp2/3 complex maintains genome integrity and survival of epidermal Langerhans cells
Article Snippet: Images were acquired with a digital 4k CCD camera Quemesa (EMSIS GmbH, Münster, Germany) mounted on a Tecnai Spirit transmission electron microscope (ThermoFisher, Eindhoven, Netherlands) operated at 80 kV. .. 2*10 6 cells were incubated with 25μM CK666 (Tocris, cat. #3950) or 1μM Etoposide (Sigma-Aldrich, cat. #E1383) diluted in DC media. ..

Article Title: Cell loss disrupts mechanical homeostasis to drive retinal pigment epithelium ageing-like phenotype in vitro.
Article Snippet: .. For phagocytosis studies, the monolayers were incubated for 30min with 500 nM CK666, followedby incubationwith the photoreceptor fragments and the bridging molecules in CK-666 containing medium for 4 h. For modulating formin activity, 20 μM SMIFH2 (Tocris Bioscience, #4401) was used instead keeping the same timing and procedure. ..

other:

Article Title: Rectification of planar orientation angle switches behavior and replenishes contractile junctions
Article Snippet: CK666 (Cat#3950; TOCRIS) , Arp2/3 inhibitor , DMSO diluted 1:20 in H 2 O , 250 μm.

Activity Assay:

Transfection:

Article Title: JMY powers dendritogenesis and is regulated by CaM revealing a general, critical principle in neuromorphogenesis
Article Snippet: .. About 30 h after transfection, neurons were fixed with 4% (w/v) PFA for 5 min. For inhibitor experiments, the cultured primary neurons were cultured with CK666 (stock solution 100 mM in DMSO) and the CaM inhibitor CGS9343B (1,3-dihydro-1-[1-[(4-methyl-4H,6H-pyrrolo[1,2-a][4,1]-benzoxazepin-4-yl)methyl]-4-iperidinyl]-2H-benzimidazol-2-one(1:1) maleate; Tocris) (stock solution 20 mM in DMSO), respectively, for 6 h before fixation at in total 30 h post-transfection. ..

Cell Culture:

Article Title: JMY powers dendritogenesis and is regulated by CaM revealing a general, critical principle in neuromorphogenesis.
Article Snippet: .. For inhibitor experiments, the cultured primary neurons were cultured with CK666 (stock solution 100mM in DMSO) and the CaM inhibitor CGS9343B (1,3-dihydro-1-[1-[(4-methyl-4H,6H-pyrrolo[1,2-a][4,1]-benzoxazepin-4-yl)methyl]-4-iperidinyl]-2H-benzimidazol-2-one(1:1) maleate; Tocris) (stock solution20mMinDMSO), respectively, for 6 hbeforefixation at in total 30 h post-transfection. ..

Image Search Results

APOE in APPNEVs impairs synapses by downregulating F‐actin polymerization signaling. (A and B) DIV14 primary neurons are treated for 48 h with DMSO (Vehicle), 10 µM Rac1 inhibitor NSC23766, 5 µM N‐WASP inhibitor Wiskostatin, 30 µM Arp2/3 inhibitor CK666, or 10 µg/mL APPNEVs. Synaptic integrity is assessed by measuring PSD95 protein expression through western blot analysis (A) and immunofluorescence staining (B). (C and D) To further investigate the role of APOE in APPNEVs on actin cytoskeleton regulation, DIV14 primary neurons are treated for 48 h with DMSO (Vehicle), 1 µM EZ‐482, 10 µg/mL APPNEVs, or a combination of 10 µg/mL APPNEVs and 1 µM EZ‐482 (pre‐incubated for 1 h). (C) Rac1 activation is evaluated using a pull‐down assay to isolate Rac1‐GTP, followed by western blot analysis to quantify the levels of active GTP‐bound Rac1 and total Rac1. (D) To assess Arp2/3 complex activation, neurons are immunostained for phosphorylated Arp2 (p‐Arp2). The cytoskeletal structure is visualized using phalloidin staining, while nuclei are stained with DAPI. Phosphorylation levels and cytoskeletal organization are analyzed using confocal microscopy. (E) Neurons are treated for 6 h with 10 µg/mL APPNEVs, with or without 25 nM Rac1 activator ML‐099, and p‐Arp2 levels are detected by western blot. (F) Neurons are incubated with APPNEVs for 48 h, followed by treatment with or without 20 nM Jasplakinolide for the final 20 min. F‐actin in neurons is visualized using phalloidin staining and z‐stack confocal imaging, and the total number of dendritic spines is quantified. Data are presented as mean ± SEM from n = 3–5 independent experiments per condition. Statistical comparisons are performed using one‐way ANOVA followed by Tukey's post‐hoc test, with statistical significance indicates as * p < 0.05 and ** p < 0.01. “ns” indicates no significant change.

Journal: Journal of Extracellular Vesicles

Article Title: Neuronal Extracellular Vesicles Carrying APOE Downregulate Filament Actin Polymerization Signaling to Inhibit Synapse Formation in Alzheimer's Disease

doi: 10.1002/jev2.70248

Figure Lengend Snippet: APOE in APPNEVs impairs synapses by downregulating F‐actin polymerization signaling. (A and B) DIV14 primary neurons are treated for 48 h with DMSO (Vehicle), 10 µM Rac1 inhibitor NSC23766, 5 µM N‐WASP inhibitor Wiskostatin, 30 µM Arp2/3 inhibitor CK666, or 10 µg/mL APPNEVs. Synaptic integrity is assessed by measuring PSD95 protein expression through western blot analysis (A) and immunofluorescence staining (B). (C and D) To further investigate the role of APOE in APPNEVs on actin cytoskeleton regulation, DIV14 primary neurons are treated for 48 h with DMSO (Vehicle), 1 µM EZ‐482, 10 µg/mL APPNEVs, or a combination of 10 µg/mL APPNEVs and 1 µM EZ‐482 (pre‐incubated for 1 h). (C) Rac1 activation is evaluated using a pull‐down assay to isolate Rac1‐GTP, followed by western blot analysis to quantify the levels of active GTP‐bound Rac1 and total Rac1. (D) To assess Arp2/3 complex activation, neurons are immunostained for phosphorylated Arp2 (p‐Arp2). The cytoskeletal structure is visualized using phalloidin staining, while nuclei are stained with DAPI. Phosphorylation levels and cytoskeletal organization are analyzed using confocal microscopy. (E) Neurons are treated for 6 h with 10 µg/mL APPNEVs, with or without 25 nM Rac1 activator ML‐099, and p‐Arp2 levels are detected by western blot. (F) Neurons are incubated with APPNEVs for 48 h, followed by treatment with or without 20 nM Jasplakinolide for the final 20 min. F‐actin in neurons is visualized using phalloidin staining and z‐stack confocal imaging, and the total number of dendritic spines is quantified. Data are presented as mean ± SEM from n = 3–5 independent experiments per condition. Statistical comparisons are performed using one‐way ANOVA followed by Tukey's post‐hoc test, with statistical significance indicates as * p < 0.05 and ** p < 0.01. “ns” indicates no significant change.

Article Snippet: Neurons were cultured for 14 DIV (days in vitro) and treated with 10 μg/mL APPNEVs or WTNEVs, 1 μM of the APOE inhibitor EZ‐482 (HY‐103706, MCE), 10 μM of the Rac1 inhibitor NSC23766 (HY‐15723A, MCE), 5 μM of the N‐WASP inhibitor Wiskostatin (HY‐12534, MCE), 30 μM of the Arp2/3 inhibitor CK666 (HY‐16926, MCE), 25 nM Rac1 activator ML‐099 (HY‐124306; MedChemExpress), or vehicle control.

Techniques: Expressing, Western Blot, Immunofluorescence, Staining, Incubation, Activation Assay, Pull Down Assay, Phospho-proteomics, Confocal Microscopy, Imaging

Schematic model of APPNEVs carrying APOE downregulate F‐actin polymerization signaling to inhibit synapse formation in AD. During AD progression, EVs derived from APP/PS1 neurons transport APOE into healthy neurons, potentially interacting with neuronal APOE receptors (LRP1, LDLR, VLDLR) to transduction the signaling. This signaling inhibits Rac1‐GTP activation and subsequently downregulates F‐actin polymerization through the Rac1–N‐WASP–Arp2/3 pathway. Disruption of this pathway impairs mature synapse formation, ultimately converting healthy neurons into synaptically damaged neurons and exacerbating AD progression.

Journal: Journal of Extracellular Vesicles

Article Title: Neuronal Extracellular Vesicles Carrying APOE Downregulate Filament Actin Polymerization Signaling to Inhibit Synapse Formation in Alzheimer's Disease

doi: 10.1002/jev2.70248

Figure Lengend Snippet: Schematic model of APPNEVs carrying APOE downregulate F‐actin polymerization signaling to inhibit synapse formation in AD. During AD progression, EVs derived from APP/PS1 neurons transport APOE into healthy neurons, potentially interacting with neuronal APOE receptors (LRP1, LDLR, VLDLR) to transduction the signaling. This signaling inhibits Rac1‐GTP activation and subsequently downregulates F‐actin polymerization through the Rac1–N‐WASP–Arp2/3 pathway. Disruption of this pathway impairs mature synapse formation, ultimately converting healthy neurons into synaptically damaged neurons and exacerbating AD progression.

Techniques: Derivative Assay, Transduction, Activation Assay, Disruption

A) ECAD internalization was monitored by IF in MCF10A-EPN3 cells treated with AP2µ KD or mock. Top, representative images; internalized ECAD (green), DAPI (blue). Bar, 20 µm. Bottom, quantification of relative internalized ECAD fluorescence intensity/cell in individual field of views, normalized to mock control. N (fields of view): Mock=4, AP2µ=35; n=3. B) ECAD internalization in MCF10A-EPN3 cells subjected to single or double Eps15/Eps15L1 KDs. Representative images and quantification as in (A). Bar, 20 µm. N (fields of view): Mock=42, Eps15 KD=39, Eps15L1 KD=40, Double KD=35, n=3. C) Left panels: PM, representative immuno-EM images showing PM-ECAD-positive (gold-labeled) tubular invaginations (indicated by arrows) in MCF10A-EV and MCF10A-EPN3 cells; scale bar, 200 nm; Int, representative immuno-EM images showing internalized ECAD-positive (gold-labeled) structures (indicated by arrows and enlarged in the insets) in MCF10A-EV and MCF10A-EPN3 cells; scale bar, 250 nm. Right upper panel: quantification of internalized ECAD expressed as a percentage of PM-ECAD. N (cells): EV=24, EPN3=27. Right-lower panel: gold-labelled ECAD-positive clathrin-coated pits (CCPs) and tubular invaginations (TIs) expressed as percentage of total number of structures in 100 µm PM length/cell. N (cells): EV=27, EPN3=25. D) Effects of inhibitors on ECAD internalization in MCF10A-EPN3 cells. Cells were pre-treated with the indicated compounds or vehicle (DMSO) before measuring ECAD internalization as in (A): CK666 (50 µM, 1 h), Genz-123346 (4 µM, 6 days), Lactose (100 mM, 1h), I3 (20 µM, 10 min). Representative images and quantification as in (A). Bar, 20 µm. N (fields of view): CK666=42 (DMSO control=44) (n=5); Genz=20 (DMSO control=20) (n=3); Lactose=33 (mock=40) (n=3); I3=40 (DMSO control=53) (n=6). E) ECAD internalization in MCF10A-EPN3 cells subjected to I3 treatment as in (D), Gal3 KD or Gal3 KD/I3 treatment. Representative images and quantification as in (A). Bar, 20 µm. N (fields of view): Mock=34, I3=23, Gal3 KD=26, Gal3 KD/I3=28, n=2. F) Co-internalization of Gal3–ECAD was monitored for 10 min in MCF10A-EV and -EPN3 cells. Left: representative confocal images, Gal3-Alexa488 (green), anti-ECAD (red), DAPI (blue). Bar: 20 µm. Right: Manders overlap coefficient of internalized Gal3-ECAD. N (cells): EV/EPN3=69; n=2. In all panels, results are shown as mean±SD, except panel for E in which median ± max/min values are shown. p-values (unpaired Student’s t-test, two-tailed): **** <0.0001; *** <0.001; ** <0.01; * <0.05, ns, not significant.

Journal: bioRxiv

Article Title: Targeting GL-Lect driven endocytosis to suppress cell plasticity in breast cancer

doi: 10.64898/2026.01.08.698324

Figure Lengend Snippet: A) ECAD internalization was monitored by IF in MCF10A-EPN3 cells treated with AP2µ KD or mock. Top, representative images; internalized ECAD (green), DAPI (blue). Bar, 20 µm. Bottom, quantification of relative internalized ECAD fluorescence intensity/cell in individual field of views, normalized to mock control. N (fields of view): Mock=4, AP2µ=35; n=3. B) ECAD internalization in MCF10A-EPN3 cells subjected to single or double Eps15/Eps15L1 KDs. Representative images and quantification as in (A). Bar, 20 µm. N (fields of view): Mock=42, Eps15 KD=39, Eps15L1 KD=40, Double KD=35, n=3. C) Left panels: PM, representative immuno-EM images showing PM-ECAD-positive (gold-labeled) tubular invaginations (indicated by arrows) in MCF10A-EV and MCF10A-EPN3 cells; scale bar, 200 nm; Int, representative immuno-EM images showing internalized ECAD-positive (gold-labeled) structures (indicated by arrows and enlarged in the insets) in MCF10A-EV and MCF10A-EPN3 cells; scale bar, 250 nm. Right upper panel: quantification of internalized ECAD expressed as a percentage of PM-ECAD. N (cells): EV=24, EPN3=27. Right-lower panel: gold-labelled ECAD-positive clathrin-coated pits (CCPs) and tubular invaginations (TIs) expressed as percentage of total number of structures in 100 µm PM length/cell. N (cells): EV=27, EPN3=25. D) Effects of inhibitors on ECAD internalization in MCF10A-EPN3 cells. Cells were pre-treated with the indicated compounds or vehicle (DMSO) before measuring ECAD internalization as in (A): CK666 (50 µM, 1 h), Genz-123346 (4 µM, 6 days), Lactose (100 mM, 1h), I3 (20 µM, 10 min). Representative images and quantification as in (A). Bar, 20 µm. N (fields of view): CK666=42 (DMSO control=44) (n=5); Genz=20 (DMSO control=20) (n=3); Lactose=33 (mock=40) (n=3); I3=40 (DMSO control=53) (n=6). E) ECAD internalization in MCF10A-EPN3 cells subjected to I3 treatment as in (D), Gal3 KD or Gal3 KD/I3 treatment. Representative images and quantification as in (A). Bar, 20 µm. N (fields of view): Mock=34, I3=23, Gal3 KD=26, Gal3 KD/I3=28, n=2. F) Co-internalization of Gal3–ECAD was monitored for 10 min in MCF10A-EV and -EPN3 cells. Left: representative confocal images, Gal3-Alexa488 (green), anti-ECAD (red), DAPI (blue). Bar: 20 µm. Right: Manders overlap coefficient of internalized Gal3-ECAD. N (cells): EV/EPN3=69; n=2. In all panels, results are shown as mean±SD, except panel for E in which median ± max/min values are shown. p-values (unpaired Student’s t-test, two-tailed): **** <0.0001; *** <0.001; ** <0.01; * <0.05, ns, not significant.

Article Snippet: The following inhibitors of endocytic players were used in this study: CK666 (Arp2/3 complex inhibitor, 50 μM, SML0006 Merck), EIPA (NHE inhibitor, 50 μM; used as macropinocytosis inhibitor, A3085 Merck), I3 (non-permeable Galectin-3 inhibitor, 20 μM, GalectoBiotech), Genz-123346 (ceramide synthase inhibitor, 4 μM, 5.38285 Merck), and (+)-Lactose (pan-galectin inhibitor, 100 mM, L3750 Merck).

Techniques: Fluorescence, Control, Labeling, Two Tailed Test

A) Internalization of Tf-488 was monitored in MCF10A-EV and -EPN3 cells with or without AP2µ KD. Results are shown normalized to mock control. N (fields of view): EV, Mock=56, AP2µ KD=28 (n=3); EPN3, Mock=44, AP2µ KD=28 (n=3). B) Quantification of Tf-488 internalization in MCF10A-EV and - EPN3 cells subjected to single or double Eps15/Eps15L1 KDs. N (fields of view): EV, Mock=35, Eps15 KD=35, Eps15L1 KD=35, Double KD=35 (n=3); EPN3, Mock=36, Eps15 KD=35, Eps15L1 KD=35, Double KD=35 (n=3). C) Negative controls for inhibitor screening (supporting ). Quantification of Tf-488 internalization in MCF10A-EV and -EPN3 cells pre-treated with the following compounds or vehicle control: CK666 (50 µM, 1 h), Genz (4 µM, 6 days), I3 (20 µM, 10 min). N (fields of view): EV, DMSO=15, CK666=15, Genz=15, I3=15 (n=3); EPN3, DMSO=15, CK666=15, Genz=15, I3=14 (n=3). D-E) Positive controls for inhibitor screening (supporting ). (D) CD44 internalization was monitored in vivo by IF using an anti-CD44 antibody in MCF10A-EV and -EPN3 cells pre-treated with I3 (20 µM, 10 min) or vehicle control. Quantification of relative CD44 fluorescence intensity is shown normalized to control. N (fields of view): EV, DMSO=18, I3=16; EPN3, DMSO=18, I3=16 (n=3). (E) Shiga-toxin (STXB) endocytosis and binding was monitored by continuous incubation of STXB-488 conjugated ligand in MCF10A-EV and- EPN3 cells pre-treated with Genz (4 µM, 6 days). Quantification of relative STXB fluorescence intensity is shown normalized to control. N (fields of view): EV, DMSO=12, Genz=12; EPN3, DMSO=12, Genz=12 (n=3). F) Quantification of Transferrin internalization in MCF10A-EV and -EPN3 cells subjected to I3 (20 µM, 10 min) treatment, Gal3 KD or Gal3 KD/I3 treatment. N (fields of view): EV, mock=20, I3=20, Gal3 KD=20, Gal3 KD/I3=20 (n=2); EPN3, mock=21, I3=20, Gal3 KD=21, Gal3 KD/I3=21 (n=2). G) Quantification of CD44 internalization in MCF10A-EV and -EPN3 cells subjected to I3 (20 µM, 10 min) treatment, Gal3 KD or Gal3 KD/I3 treatment. N (fields of view): EV, mock=20, I3=20, Gal3 KD=21, Gal3 KD/I3=20 (n=2); EPN3, mock=20, I3=19, Gal3 KD=20, Gal3 KD/I3=20 (n=2). H) ECAD internalization was monitored in MCF10A-EV cells subjected to Eps15/Eps15L1 single or double KD. Quantification of relative ECAD fluorescence intensity/cell normalized to mock control. N (fields of view): Mock=42, Eps15 KD=39, Eps15L1 KD=37 and Double KD=40 (n=3). I-M) ECAD internalization was monitored in MCF10A-EV cells pre-treated as in panel C. Top, representative images showing internalized ECAD (green) and DAPI staining (blue). Bar, 20 µm. Bottom, quantification of relative ECAD fluorescence intensity is shown normalized to control. N (fields of view): (I) DMSO=18, CK666=18; (L) DMSO=15, Genz=15; (M) DMSO=19, I3=17 (n=3). N) ECAD internalization was monitored in MCF10A-EV cells subjected to I3 (20 µM, 10 min) treatment, Gal3 KD or Gal3 KD/I3 treatment. N (fields of view): EV, mock=26, I3=27, Gal3 KD=26, Gal3 KD/I3=28 (n=2). p-values in the relevant panels (Unpaired Student’s t-test, two-tailed): ****, <0.0001; ** <0.001, * <0.05

Journal: bioRxiv

Article Title: Targeting GL-Lect driven endocytosis to suppress cell plasticity in breast cancer

doi: 10.64898/2026.01.08.698324

Figure Lengend Snippet: A) Internalization of Tf-488 was monitored in MCF10A-EV and -EPN3 cells with or without AP2µ KD. Results are shown normalized to mock control. N (fields of view): EV, Mock=56, AP2µ KD=28 (n=3); EPN3, Mock=44, AP2µ KD=28 (n=3). B) Quantification of Tf-488 internalization in MCF10A-EV and - EPN3 cells subjected to single or double Eps15/Eps15L1 KDs. N (fields of view): EV, Mock=35, Eps15 KD=35, Eps15L1 KD=35, Double KD=35 (n=3); EPN3, Mock=36, Eps15 KD=35, Eps15L1 KD=35, Double KD=35 (n=3). C) Negative controls for inhibitor screening (supporting ). Quantification of Tf-488 internalization in MCF10A-EV and -EPN3 cells pre-treated with the following compounds or vehicle control: CK666 (50 µM, 1 h), Genz (4 µM, 6 days), I3 (20 µM, 10 min). N (fields of view): EV, DMSO=15, CK666=15, Genz=15, I3=15 (n=3); EPN3, DMSO=15, CK666=15, Genz=15, I3=14 (n=3). D-E) Positive controls for inhibitor screening (supporting ). (D) CD44 internalization was monitored in vivo by IF using an anti-CD44 antibody in MCF10A-EV and -EPN3 cells pre-treated with I3 (20 µM, 10 min) or vehicle control. Quantification of relative CD44 fluorescence intensity is shown normalized to control. N (fields of view): EV, DMSO=18, I3=16; EPN3, DMSO=18, I3=16 (n=3). (E) Shiga-toxin (STXB) endocytosis and binding was monitored by continuous incubation of STXB-488 conjugated ligand in MCF10A-EV and- EPN3 cells pre-treated with Genz (4 µM, 6 days). Quantification of relative STXB fluorescence intensity is shown normalized to control. N (fields of view): EV, DMSO=12, Genz=12; EPN3, DMSO=12, Genz=12 (n=3). F) Quantification of Transferrin internalization in MCF10A-EV and -EPN3 cells subjected to I3 (20 µM, 10 min) treatment, Gal3 KD or Gal3 KD/I3 treatment. N (fields of view): EV, mock=20, I3=20, Gal3 KD=20, Gal3 KD/I3=20 (n=2); EPN3, mock=21, I3=20, Gal3 KD=21, Gal3 KD/I3=21 (n=2). G) Quantification of CD44 internalization in MCF10A-EV and -EPN3 cells subjected to I3 (20 µM, 10 min) treatment, Gal3 KD or Gal3 KD/I3 treatment. N (fields of view): EV, mock=20, I3=20, Gal3 KD=21, Gal3 KD/I3=20 (n=2); EPN3, mock=20, I3=19, Gal3 KD=20, Gal3 KD/I3=20 (n=2). H) ECAD internalization was monitored in MCF10A-EV cells subjected to Eps15/Eps15L1 single or double KD. Quantification of relative ECAD fluorescence intensity/cell normalized to mock control. N (fields of view): Mock=42, Eps15 KD=39, Eps15L1 KD=37 and Double KD=40 (n=3). I-M) ECAD internalization was monitored in MCF10A-EV cells pre-treated as in panel C. Top, representative images showing internalized ECAD (green) and DAPI staining (blue). Bar, 20 µm. Bottom, quantification of relative ECAD fluorescence intensity is shown normalized to control. N (fields of view): (I) DMSO=18, CK666=18; (L) DMSO=15, Genz=15; (M) DMSO=19, I3=17 (n=3). N) ECAD internalization was monitored in MCF10A-EV cells subjected to I3 (20 µM, 10 min) treatment, Gal3 KD or Gal3 KD/I3 treatment. N (fields of view): EV, mock=26, I3=27, Gal3 KD=26, Gal3 KD/I3=28 (n=2). p-values in the relevant panels (Unpaired Student’s t-test, two-tailed): ****, <0.0001; ** <0.001, * <0.05

Techniques: Control, In Vivo, Fluorescence, Binding Assay, Incubation, Staining, Two Tailed Test

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ck666 (Tocris)

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