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incucyte organoid analysis software module (Sartorius AG)

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Sartorius AG incucyte organoid analysis software module

Oxygen consumption rate (OCR) in the presence or absence of spheroids (A) <t>Incucyte</t> image of spheroid in the center of the microplate well at the end of the assay and (B) the corresponding OCR kinetic graph showing a response after drug injections as expected. (C) Image of a microplate well with no spheroid detected at the end of the assay and (D) corresponding OCR kinetic graph showing no response after drug injections.

Incucyte Organoid Analysis Software Module, supplied by Sartorius AG, used in various techniques. Bioz Stars score: 99/100, based on 15951 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/module/Live+Cell+Analysis+Instruments/pmc13127629-50-0-6
Average 99 stars, based on 15951 article reviews

incucyte organoid analysis software module - by Bioz Stars, 2026-10

99/100 stars

Images

1) Product Images from "Protocol for Seahorse 3D Mito Stress assay in patient-derived atypical teratoid rhabdoid tumor CHLA-05-ATRT single neurospheres"

Article Title: Protocol for Seahorse 3D Mito Stress assay in patient-derived atypical teratoid rhabdoid tumor CHLA-05-ATRT single neurospheres

Journal: STAR Protocols

doi: 10.1016/j.xpro.2026.104515

Oxygen consumption rate (OCR) in the presence or absence of spheroids (A) Incucyte image of spheroid in the center of the microplate well at the end of the assay and (B) the corresponding OCR kinetic graph showing a response after drug injections as expected. (C) Image of a microplate well with no spheroid detected at the end of the assay and (D) corresponding OCR kinetic graph showing no response after drug injections.

Figure Legend Snippet: Oxygen consumption rate (OCR) in the presence or absence of spheroids (A) Incucyte image of spheroid in the center of the microplate well at the end of the assay and (B) the corresponding OCR kinetic graph showing a response after drug injections as expected. (C) Image of a microplate well with no spheroid detected at the end of the assay and (D) corresponding OCR kinetic graph showing no response after drug injections.

Techniques Used:

Effect of coating timing on spheroid retention in microplate wells (A) Incucyte image of a poly-lysine coated microplate with spheroids transferred on the same day as the assay, taken before the assay. (B) Image of the same plate taken after the assay, showing that the spheroids were displaced and/or destroyed during the assay. (C) Image of a poly-lysine coated microplate with spheroids transferred the day before the assay, taken before the assay and (D) after the assay, showing that the spheroids were intact.

Figure Legend Snippet: Effect of coating timing on spheroid retention in microplate wells (A) Incucyte image of a poly-lysine coated microplate with spheroids transferred on the same day as the assay, taken before the assay. (B) Image of the same plate taken after the assay, showing that the spheroids were displaced and/or destroyed during the assay. (C) Image of a poly-lysine coated microplate with spheroids transferred the day before the assay, taken before the assay and (D) after the assay, showing that the spheroids were intact.

Techniques Used:

other:

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia
Article Snippet: Wound images were captured at identical locations at 0- and 24-h post-wounding using an Incucyte live-cell analysis system (ESSEN Bioscience, Incucyte S3).

Software:

Article Title: Nitric oxide-dependent stabilization of vimentin confers chemoresistance in ovarian cancer
Article Snippet: Real-time monitoring of wound closure was performed using the IncuCyte Live-Cell Analysis System (Sartorius, Essen Bioscience), with images captured every 6 h over 3 days. .. Wound closure was quantified using the automated analysis algorithms provided in the IncuCyte S3 2022B Rev2 software (Sartorius, Essen Bioscience). .. Total RNA was extracted using RNeasy mini kit from QIAGEN (Cat. #74104) according to the manufacturer’s protocol.

Article Title: Protocol for Seahorse 3D Mito Stress assay in patient-derived atypical teratoid rhabdoid tumor CHLA-05-ATRT single neurospheres
Article Snippet: Seahorse XFe96 Analyzer , Agilent , S7800B. .. Incucyte Organoid Analysis Software Module , Sartorius , 9600–0034. .. 96 well ultra-low attachment plates , Corning , 7007.

Migration:

Article Title: A MYC family switch: L-MYC drives and maintains neuroendocrine lineage programs in prostate cancer
Article Snippet: .. Cell migration was evaluated using a wound-healing assay performed with the IncuCyte® system following the manufacturer’s (Sartorius) protocol. ..

Wound Healing Assay:

Image Search Results

A Function of R352Q-, S549R-, S549N-, W1282X- (TGA stop-codon in position 1282) and N1303K-CFTR was determined by the halide-sensitive YFP-quenching assay upon treatment with single potentiators (VX-445 - 2 µM, VX-770 - 3 µM, bDMC and ABBV-974 - 10 µM, and apigenin - 50 µM, 37 ˚ C) or their combinations in CFBE41o- cells ( n = 3). The N1303K -CFTR conformational defects were partially rescued with VX-661 (3 µM, 24 hours, 37 ˚ C). CFTR activity was measured after maximal phosphorylation with forskolin and IBMX as described in Methods. Data are means ± SEM of three independent experiments. * P < 0.05, ** P < 0.01 by one-way ANOVA followed by Tukey’s post-hoc test. B Heat map of the combinatorial profiling was established by calculating the dual potentiator effects, determined by the halide-sensitive YFP quenching assay (A, n = 3), in relation to their theoretical additivity. Combinatorial profiles were subsequently used to cluster compounds by average linkage analysis, and the distance was determined by Spearman’s rank correlation.

Journal: npj Drug Discovery

Article Title: Triple potentiator combinations increase the functional correction of several CFTR gating mutants

doi: 10.1038/s44386-026-00061-6

Figure Lengend Snippet: A Function of R352Q-, S549R-, S549N-, W1282X- (TGA stop-codon in position 1282) and N1303K-CFTR was determined by the halide-sensitive YFP-quenching assay upon treatment with single potentiators (VX-445 - 2 µM, VX-770 - 3 µM, bDMC and ABBV-974 - 10 µM, and apigenin - 50 µM, 37 ˚ C) or their combinations in CFBE41o- cells ( n = 3). The N1303K -CFTR conformational defects were partially rescued with VX-661 (3 µM, 24 hours, 37 ˚ C). CFTR activity was measured after maximal phosphorylation with forskolin and IBMX as described in Methods. Data are means ± SEM of three independent experiments. * P < 0.05, ** P < 0.01 by one-way ANOVA followed by Tukey’s post-hoc test. B Heat map of the combinatorial profiling was established by calculating the dual potentiator effects, determined by the halide-sensitive YFP quenching assay (A, n = 3), in relation to their theoretical additivity. Combinatorial profiles were subsequently used to cluster compounds by average linkage analysis, and the distance was determined by Spearman’s rank correlation.

Article Snippet: CFTR modulators VX-445, VX-770 and ABBV-974 (former GLPG1837), as well as forskolin and CFTR Inh -172, were purchased from MedChemExpress.

Techniques: Activity Assay, Phospho-proteomics

A Representative traces (left) of the I sc of G551D-CFTR in gene-edited (ge) 16HBE cells activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and apigenin (50 µM) or in reverse order. At the end of the experiment, CFTR was inhibited with CFTR Inh -172 (20 μM). Measurements were performed in the presence of a basolateral-to-apical chloride gradient in the presence of 100 μM amiloride. Quantification of the I sc (right, n = 3) shows the contribution of Fsk, VX-770, VX-445, and apigenin to the maximal current, depending on the order of potentiator addition, expressed as a percentage of the forskolin-stimulated WT-CFTR current in 16HBE14o- cells. N.s. – not significant, * P < 0.05, ** P < 0.01, *** P < 0.001 by unpaired two-tailed t-test for the successive addition of potentiators. B Immunoblot (top panel) of parental 16HBE14o- or 16HBEge expressing endogenous WT- or G551D-CFTR, respectively. CFTR was visualized with 660 antibody, and anti–Na + /K + -ATPase antibody served as a loading control. The empty arrowheads indicate the mature, complex glycosylated CFTR (C-band), the filled arrowheads show the immature, core glycosylated protein (B-band). The relative abundance of the C-band was quantified by densitometry (lower panel, n = 4). C Representative traces (left) and quantification of the I sc (right) in HNE isolated from one patient homozygous for G551D-CFTR upon activation with forskolin (Fsk, 20 μM) and potentiation with VX-770 (3 μM), VX-445 (2 μM) and apigenin (50 μM) expressed as percentage of mean Fsk-induced WT-CFTR currents in HNE from 10 healthy donors. Measurements were performed as in panel A. N.s. – not significant, * P < 0.05, ** P < 0.01, *** P < 0.001 by unpaired two-tailed t-test for the successive addition of potentiators. D Inside-out patch clamp recording of G551D-CFTR in the presence of 2 mM ATP + 300 nM PKA (black), +50 nM Vx-770 (green), +1 µM VX-445 (blue), +1 µM apigenin (blue), and +50 µM P-dATP (orange, ’CCC’ (channel counting cocktail)). Membrane potential was -80 mV, scales of time and amplitude are shown, gray section illustrates channel closure upon simultaneous removal of ATP, PKA and compounds. E Calculated absolute values of P o for the four segments ( n = 7-8) obtained as described in Methods. * P < 0.05, ** P < 0.01 by one-way ANOVA followed by Tukey’s post-hoc test. F ) Effect of VX-770 (3 μM) or apigenin (50 μM) on the potency of VX-445 for the phosphorylated G551D-CFTR potentiation, measured by halide-sensitive YFP quenching assay in CFBE41o- cells ( n = 3). Values are expressed as a percentage of the response to 3 μM VX-770. G Effect of VX-770 (3 μM) or VX-445 (2 μM) on the potency of apigenin for the phosphorylated G551D-CFTR potentiation, determined by the YFP quenching assay in CFBE41o- cells ( n = 3). Data in ( A , B , E – G ) are means ± SEM of the indicated number of independent experiments. Data in ( C ) are means ± SD of three measurements.

Journal: npj Drug Discovery

Article Title: Triple potentiator combinations increase the functional correction of several CFTR gating mutants

doi: 10.1038/s44386-026-00061-6

Figure Lengend Snippet: A Representative traces (left) of the I sc of G551D-CFTR in gene-edited (ge) 16HBE cells activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and apigenin (50 µM) or in reverse order. At the end of the experiment, CFTR was inhibited with CFTR Inh -172 (20 μM). Measurements were performed in the presence of a basolateral-to-apical chloride gradient in the presence of 100 μM amiloride. Quantification of the I sc (right, n = 3) shows the contribution of Fsk, VX-770, VX-445, and apigenin to the maximal current, depending on the order of potentiator addition, expressed as a percentage of the forskolin-stimulated WT-CFTR current in 16HBE14o- cells. N.s. – not significant, * P < 0.05, ** P < 0.01, *** P < 0.001 by unpaired two-tailed t-test for the successive addition of potentiators. B Immunoblot (top panel) of parental 16HBE14o- or 16HBEge expressing endogenous WT- or G551D-CFTR, respectively. CFTR was visualized with 660 antibody, and anti–Na + /K + -ATPase antibody served as a loading control. The empty arrowheads indicate the mature, complex glycosylated CFTR (C-band), the filled arrowheads show the immature, core glycosylated protein (B-band). The relative abundance of the C-band was quantified by densitometry (lower panel, n = 4). C Representative traces (left) and quantification of the I sc (right) in HNE isolated from one patient homozygous for G551D-CFTR upon activation with forskolin (Fsk, 20 μM) and potentiation with VX-770 (3 μM), VX-445 (2 μM) and apigenin (50 μM) expressed as percentage of mean Fsk-induced WT-CFTR currents in HNE from 10 healthy donors. Measurements were performed as in panel A. N.s. – not significant, * P < 0.05, ** P < 0.01, *** P < 0.001 by unpaired two-tailed t-test for the successive addition of potentiators. D Inside-out patch clamp recording of G551D-CFTR in the presence of 2 mM ATP + 300 nM PKA (black), +50 nM Vx-770 (green), +1 µM VX-445 (blue), +1 µM apigenin (blue), and +50 µM P-dATP (orange, ’CCC’ (channel counting cocktail)). Membrane potential was -80 mV, scales of time and amplitude are shown, gray section illustrates channel closure upon simultaneous removal of ATP, PKA and compounds. E Calculated absolute values of P o for the four segments ( n = 7-8) obtained as described in Methods. * P < 0.05, ** P < 0.01 by one-way ANOVA followed by Tukey’s post-hoc test. F ) Effect of VX-770 (3 μM) or apigenin (50 μM) on the potency of VX-445 for the phosphorylated G551D-CFTR potentiation, measured by halide-sensitive YFP quenching assay in CFBE41o- cells ( n = 3). Values are expressed as a percentage of the response to 3 μM VX-770. G Effect of VX-770 (3 μM) or VX-445 (2 μM) on the potency of apigenin for the phosphorylated G551D-CFTR potentiation, determined by the YFP quenching assay in CFBE41o- cells ( n = 3). Data in ( A , B , E – G ) are means ± SEM of the indicated number of independent experiments. Data in ( C ) are means ± SD of three measurements.

Article Snippet: CFTR modulators VX-445, VX-770 and ABBV-974 (former GLPG1837), as well as forskolin and CFTR Inh -172, were purchased from MedChemExpress.

Techniques: Two Tailed Test, Western Blot, Expressing, Control, Isolation, Activation Assay, Patch Clamp, Membrane

A Representative traces (left) and quantification (right, n = 3) of the I sc of VX-661-corrected (3 µM, 24 hours, 37˚C) W1282X-CFTR in 16HBEge activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and apigenin (50 µM) or in reverse order. B Quantification ( n = 3) of the I sc of VX-661 + VX-445 corrected W1282X-CFTR in 16HBEge. C Representative traces (left) and quantification of the I sc (right) in 1 µM SMG1i + 3 µM VX-661 + 2 µM VX-445 treated (24 hours, 37˚C) HNE isolated from one patient homozygous for W1282X-CFTR upon activation with forskolin (Fsk, 20 μM) and potentiation with VX-770 (3 μM) and apigenin (50 μM) expressed as percentage of mean Fsk-induced WT-CFTR currents in HNE from 10 healthy donors. D Representative traces (left) and quantification (right, n = 3) of the I sc of VX-661-corrected (3 µM, 24 hours, 37˚C) N1303K-CFTR in 16HBEge activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and apigenin (50 µM) or in reverse order. E Representative traces (left) and quantification of the I sc (right) in 3 µM VX-661 treated (24 hours, 37 °C) HNE isolated from one patient homozygous for N1303K-CFTR upon activation with forskolin (Fsk, 20 μM) and potentiation with VX-770 (3 μM), VX-445 (2 μM) and apigenin (50 μM) expressed as percentage of mean Fsk-induced WT-CFTR currents in HNE from 10 healthy donors. Data in ( A ) and ( C ) are means ± SEM of three independent experiments. Data in ( B ) and ( D ) are means ± SD of three measurements. N.s. – not significant, * P < 0.05, ** P < 0.01, *** P < 0.001 by unpaired two-tailed t-test for the successive addition of potentiators.

Journal: npj Drug Discovery

Article Title: Triple potentiator combinations increase the functional correction of several CFTR gating mutants

doi: 10.1038/s44386-026-00061-6

Figure Lengend Snippet: A Representative traces (left) and quantification (right, n = 3) of the I sc of VX-661-corrected (3 µM, 24 hours, 37˚C) W1282X-CFTR in 16HBEge activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and apigenin (50 µM) or in reverse order. B Quantification ( n = 3) of the I sc of VX-661 + VX-445 corrected W1282X-CFTR in 16HBEge. C Representative traces (left) and quantification of the I sc (right) in 1 µM SMG1i + 3 µM VX-661 + 2 µM VX-445 treated (24 hours, 37˚C) HNE isolated from one patient homozygous for W1282X-CFTR upon activation with forskolin (Fsk, 20 μM) and potentiation with VX-770 (3 μM) and apigenin (50 μM) expressed as percentage of mean Fsk-induced WT-CFTR currents in HNE from 10 healthy donors. D Representative traces (left) and quantification (right, n = 3) of the I sc of VX-661-corrected (3 µM, 24 hours, 37˚C) N1303K-CFTR in 16HBEge activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and apigenin (50 µM) or in reverse order. E Representative traces (left) and quantification of the I sc (right) in 3 µM VX-661 treated (24 hours, 37 °C) HNE isolated from one patient homozygous for N1303K-CFTR upon activation with forskolin (Fsk, 20 μM) and potentiation with VX-770 (3 μM), VX-445 (2 μM) and apigenin (50 μM) expressed as percentage of mean Fsk-induced WT-CFTR currents in HNE from 10 healthy donors. Data in ( A ) and ( C ) are means ± SEM of three independent experiments. Data in ( B ) and ( D ) are means ± SD of three measurements. N.s. – not significant, * P < 0.05, ** P < 0.01, *** P < 0.001 by unpaired two-tailed t-test for the successive addition of potentiators.

Article Snippet: CFTR modulators VX-445, VX-770 and ABBV-974 (former GLPG1837), as well as forskolin and CFTR Inh -172, were purchased from MedChemExpress.

Techniques: Isolation, Activation Assay, Two Tailed Test

A Chemical sites that were subjected to modification in the medicinal chemistry optimization of ML-014. B, C Primary screen of ML-014 analogs as co-potentiator in combination with either VX-770 or VX-445 for potentiation of G551D- ( B ) or N1303K-CFTR ( C ) expressed in CFBE41o- cells. The relative transport activity of CFTR variants was measured by the halide-sensitive YFP-quenching assay and is expressed as percentage of the triple potentiator combination VX-770 + VX-445+apigenin (3P). Data are means of 4 technical replicates ± SD. D Main Structure-Activity Relationships derived from modification of ML-014. E Structure and activity of the most representative analogs (see text for the description of the compounds).

Journal: npj Drug Discovery

Article Title: Triple potentiator combinations increase the functional correction of several CFTR gating mutants

doi: 10.1038/s44386-026-00061-6

Figure Lengend Snippet: A Chemical sites that were subjected to modification in the medicinal chemistry optimization of ML-014. B, C Primary screen of ML-014 analogs as co-potentiator in combination with either VX-770 or VX-445 for potentiation of G551D- ( B ) or N1303K-CFTR ( C ) expressed in CFBE41o- cells. The relative transport activity of CFTR variants was measured by the halide-sensitive YFP-quenching assay and is expressed as percentage of the triple potentiator combination VX-770 + VX-445+apigenin (3P). Data are means of 4 technical replicates ± SD. D Main Structure-Activity Relationships derived from modification of ML-014. E Structure and activity of the most representative analogs (see text for the description of the compounds).

Article Snippet: CFTR modulators VX-445, VX-770 and ABBV-974 (former GLPG1837), as well as forskolin and CFTR Inh -172, were purchased from MedChemExpress.

Techniques: Modification, Activity Assay, Derivative Assay

A Representative trace (left) and quantification (right, n = 3) of the dose-response of ML-014 analogs added as third potentiators (1st 3 µM VX-770, 2nd 2 µM VX-445, in the presence of 20 µM forskolin) to potentiate VX-661 corrected (3 µM, 24 hours, 37˚C) N1303K-CFTR in 16HBEge. Data are means ± SEM of three independent experiments. B Efficacy of triple potentiator combinations for the functional correction of N1303K-CFTR in HNE epithelia. Representative traces (left) and quantification (right, n = 3) of the I sc of VX-661 corrected (3 µM, 24 hours, 37˚C) N1303K-CFTR in homozygous HNE activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and ML-014 analogs (14 µM). Data are means ± SD of three measurements. * P < 0.05, ** P < 0.01 by unpaired two-tailed t-test in comparison to DMSO control. C, D Efficacy of ML-051 and apigenin for the potentiation of S549R-CFTR ( C ) and I507del-CFTR ( D ) in the presence of the Trikafta modulator combination. Representative traces (left) and quantification (right, n = 3–7) of the I sc of 3 µM VX-661 + 2 µM VX-445 corrected (24 hours, 37 °C) S549R-CFTR and I507del-CFTR in CFBE41o- activated with forskolin (Fsk, 20 M) and potentiated with VX-770 (3 μM) followed by apigenin (50 µM) or ML-51 (10 µM). Data are means ± SEM of 3–7 independent experiments.

Journal: npj Drug Discovery

Article Title: Triple potentiator combinations increase the functional correction of several CFTR gating mutants

doi: 10.1038/s44386-026-00061-6

Figure Lengend Snippet: A Representative trace (left) and quantification (right, n = 3) of the dose-response of ML-014 analogs added as third potentiators (1st 3 µM VX-770, 2nd 2 µM VX-445, in the presence of 20 µM forskolin) to potentiate VX-661 corrected (3 µM, 24 hours, 37˚C) N1303K-CFTR in 16HBEge. Data are means ± SEM of three independent experiments. B Efficacy of triple potentiator combinations for the functional correction of N1303K-CFTR in HNE epithelia. Representative traces (left) and quantification (right, n = 3) of the I sc of VX-661 corrected (3 µM, 24 hours, 37˚C) N1303K-CFTR in homozygous HNE activated with forskolin (Fsk, 20 μM) and potentiated with VX-770 (3 μM) followed by VX-445 (2 μM) and ML-014 analogs (14 µM). Data are means ± SD of three measurements. * P < 0.05, ** P < 0.01 by unpaired two-tailed t-test in comparison to DMSO control. C, D Efficacy of ML-051 and apigenin for the potentiation of S549R-CFTR ( C ) and I507del-CFTR ( D ) in the presence of the Trikafta modulator combination. Representative traces (left) and quantification (right, n = 3–7) of the I sc of 3 µM VX-661 + 2 µM VX-445 corrected (24 hours, 37 °C) S549R-CFTR and I507del-CFTR in CFBE41o- activated with forskolin (Fsk, 20 M) and potentiated with VX-770 (3 μM) followed by apigenin (50 µM) or ML-51 (10 µM). Data are means ± SEM of 3–7 independent experiments.

Article Snippet: CFTR modulators VX-445, VX-770 and ABBV-974 (former GLPG1837), as well as forskolin and CFTR Inh -172, were purchased from MedChemExpress.

Techniques: Functional Assay, Two Tailed Test, Comparison, Control

D-limonene reduces lipid accumulation in hepatocytes by targeting the PPARγ/SCD-1 axis. (A) Representative Oil Red O-stained images of rat BRL-3A hepatocytes treated as indicated (scale bar = 50 μm). (B) Quantification of lipid-droplet area in BRL-3A cells (n = 3). (C) Representative Oil Red O-stained images of human HepG2 hepatocytes under different treatments (scale bar = 100 μm). (D) Quantification of lipid-droplet area in HepG2 cells (n = 3). (E–G) Protein levels of PPARγ and SCD-1 assessed by Western blot. Compared with the FFA model group, * P < 0.05, *** P < 0.001, **** P < 0.0001, and ns: not significant; # P < 0.05, ### P < 0.001, #### P < 0.0001 (A939: A939572, SCD-1antagonist; T007: T0070907, PPARγ antagonist; Rosi: rosiglitazone, PPARγ agonist). See for detailed concentrations.

Journal: Frontiers in Pharmacology

Article Title: D-limonene ameliorates metabolic dysfunction-associated steatotic liver disease by inhibiting the PPARγ/SCD-1 pathway and improving lipid metabolism disorders

doi: 10.3389/fphar.2026.1843336

Figure Lengend Snippet: D-limonene reduces lipid accumulation in hepatocytes by targeting the PPARγ/SCD-1 axis. (A) Representative Oil Red O-stained images of rat BRL-3A hepatocytes treated as indicated (scale bar = 50 μm). (B) Quantification of lipid-droplet area in BRL-3A cells (n = 3). (C) Representative Oil Red O-stained images of human HepG2 hepatocytes under different treatments (scale bar = 100 μm). (D) Quantification of lipid-droplet area in HepG2 cells (n = 3). (E–G) Protein levels of PPARγ and SCD-1 assessed by Western blot. Compared with the FFA model group, * P < 0.05, *** P < 0.001, **** P < 0.0001, and ns: not significant; # P < 0.05, ### P < 0.001, #### P < 0.0001 (A939: A939572, SCD-1antagonist; T007: T0070907, PPARγ antagonist; Rosi: rosiglitazone, PPARγ agonist). See for detailed concentrations.

Article Snippet: The pharmacological modulators T0070907 (Cat. No. HY-13202 ), A939572 (Cat. No. HY-50709 ), and rosiglitazone (Cat. No. 122320-73-4) were procured from MedChemExpress (South Brunswick, United States).

Techniques: Staining, Western Blot

Review

incucyte organoid analysis software module (Sartorius AG)

Structured Review

Images

1) Product Images from "Protocol for Seahorse 3D Mito Stress assay in patient-derived atypical teratoid rhabdoid tumor CHLA-05-ATRT single neurospheres"

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Wound Healing Assay:

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