pan rar agonist ch55 Search Results


ch 55  (Bio-Techne corporation)
99
Bio-Techne corporation ch 55
Ch 55, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pan+rar+agonist+ch55/Ch+55/custom%402020%4039427535
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pan rar agonist ch55  (Tocris)
96
Tocris pan rar agonist ch55
(A) Vitamin A-derived retinol is metabolized to RA, which activates retinoic acid receptors (RARs). RARs bind target gene promoters to drive RA-dependent transcription. (B) HT-29 cells (human intestinal epithelial cells) were treated with the RAR antagonist BMS493 or the RAR agonist <t>Ch55</t> and simultaneously stimulated overnight with RA and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=6 per group). (C) HCT-116, a transfection-competent human intestinal epithelial cell line expressing RARA and RARG , was treated for 24 hours with an siRNA targeting either gene and then stimulated overnight with retinol and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=4 per group). (D) IEC-specific disruption of RAR signaling using a dominant-negative RAR (dnRAR) knock-in allele. dnRAR mice harbor a loxP -flanked STOP cassette upstream of a dominant-negative RAR open reading frame. The dnRAR is derived from a mutant human RARα (RAR403) lacking the ligand-dependent transactivation domain and functions as a pan-RAR inhibitor. Crossing dnRAR mice with Villin-Cre transgenic mice excises the STOP cassette in IECs, resulting in IEC-selective expression of dnRAR and inhibition of RAR signaling. (E) qPCR analysis of Reg3g expression in small intestines of conventional dnRAR fl/fl (n=12) and dnRAR IEC (n=17) mice from five litters, and germ-free wild-type mice (n=21). (F) Immunofluorescence microscopy of REG3G in small intestines of dnRAR fl/fl and dnRAR IEC mice. Sections were stained for REG3G and counterstained with DAPI. Scale bar, 100 μ m. Images are representative of at least three fields per sample and two independent experiments (three littermates per group). (G) Mean fluorescence intensities of at least 150 villi from the images represented in (F) were quantified across at least two mice of each genotype. RAR, retinoic acid receptor; RA, retinoic acid; IEC, intestinal epithelial cell; REG3G, regenerating islet-derived protein 3γ; siRNA, small interfering RNA; dnRAR, dominant negative retinoic acid receptor; Conv, conventional; GF, germ-free. Means ± SEM are plotted; *p < 0.05; **p < 0.01; ***p<0.001; ns, not significant by Mann-Whitney test. See also .
Pan Rar Agonist Ch55, supplied by Tocris, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pan+rar+agonist+ch55/Ch+55/bio_rxiv__64898__2026__03__08__710399-208-19-22
Average 96 stars, based on 1 article reviews
pan rar agonist ch55 - by Bioz Stars, 2026-09
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ch55  (FUJIFILM)
90
FUJIFILM ch55
(A) Vitamin A-derived retinol is metabolized to RA, which activates retinoic acid receptors (RARs). RARs bind target gene promoters to drive RA-dependent transcription. (B) HT-29 cells (human intestinal epithelial cells) were treated with the RAR antagonist BMS493 or the RAR agonist <t>Ch55</t> and simultaneously stimulated overnight with RA and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=6 per group). (C) HCT-116, a transfection-competent human intestinal epithelial cell line expressing RARA and RARG , was treated for 24 hours with an siRNA targeting either gene and then stimulated overnight with retinol and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=4 per group). (D) IEC-specific disruption of RAR signaling using a dominant-negative RAR (dnRAR) knock-in allele. dnRAR mice harbor a loxP -flanked STOP cassette upstream of a dominant-negative RAR open reading frame. The dnRAR is derived from a mutant human RARα (RAR403) lacking the ligand-dependent transactivation domain and functions as a pan-RAR inhibitor. Crossing dnRAR mice with Villin-Cre transgenic mice excises the STOP cassette in IECs, resulting in IEC-selective expression of dnRAR and inhibition of RAR signaling. (E) qPCR analysis of Reg3g expression in small intestines of conventional dnRAR fl/fl (n=12) and dnRAR IEC (n=17) mice from five litters, and germ-free wild-type mice (n=21). (F) Immunofluorescence microscopy of REG3G in small intestines of dnRAR fl/fl and dnRAR IEC mice. Sections were stained for REG3G and counterstained with DAPI. Scale bar, 100 μ m. Images are representative of at least three fields per sample and two independent experiments (three littermates per group). (G) Mean fluorescence intensities of at least 150 villi from the images represented in (F) were quantified across at least two mice of each genotype. RAR, retinoic acid receptor; RA, retinoic acid; IEC, intestinal epithelial cell; REG3G, regenerating islet-derived protein 3γ; siRNA, small interfering RNA; dnRAR, dominant negative retinoic acid receptor; Conv, conventional; GF, germ-free. Means ± SEM are plotted; *p < 0.05; **p < 0.01; ***p<0.001; ns, not significant by Mann-Whitney test. See also .
Ch55, supplied by FUJIFILM, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pan+rar+agonist+ch55/ch55/pm17475839-50-13-17
Average 90 stars, based on 1 article reviews
ch55 - by Bioz Stars, 2026-09
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cholesterol (lot ch-55)  (Avanti Inc)
90
Avanti Inc cholesterol (lot ch-55)
(A) Vitamin A-derived retinol is metabolized to RA, which activates retinoic acid receptors (RARs). RARs bind target gene promoters to drive RA-dependent transcription. (B) HT-29 cells (human intestinal epithelial cells) were treated with the RAR antagonist BMS493 or the RAR agonist <t>Ch55</t> and simultaneously stimulated overnight with RA and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=6 per group). (C) HCT-116, a transfection-competent human intestinal epithelial cell line expressing RARA and RARG , was treated for 24 hours with an siRNA targeting either gene and then stimulated overnight with retinol and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=4 per group). (D) IEC-specific disruption of RAR signaling using a dominant-negative RAR (dnRAR) knock-in allele. dnRAR mice harbor a loxP -flanked STOP cassette upstream of a dominant-negative RAR open reading frame. The dnRAR is derived from a mutant human RARα (RAR403) lacking the ligand-dependent transactivation domain and functions as a pan-RAR inhibitor. Crossing dnRAR mice with Villin-Cre transgenic mice excises the STOP cassette in IECs, resulting in IEC-selective expression of dnRAR and inhibition of RAR signaling. (E) qPCR analysis of Reg3g expression in small intestines of conventional dnRAR fl/fl (n=12) and dnRAR IEC (n=17) mice from five litters, and germ-free wild-type mice (n=21). (F) Immunofluorescence microscopy of REG3G in small intestines of dnRAR fl/fl and dnRAR IEC mice. Sections were stained for REG3G and counterstained with DAPI. Scale bar, 100 μ m. Images are representative of at least three fields per sample and two independent experiments (three littermates per group). (G) Mean fluorescence intensities of at least 150 villi from the images represented in (F) were quantified across at least two mice of each genotype. RAR, retinoic acid receptor; RA, retinoic acid; IEC, intestinal epithelial cell; REG3G, regenerating islet-derived protein 3γ; siRNA, small interfering RNA; dnRAR, dominant negative retinoic acid receptor; Conv, conventional; GF, germ-free. Means ± SEM are plotted; *p < 0.05; **p < 0.01; ***p<0.001; ns, not significant by Mann-Whitney test. See also .
Cholesterol (Lot Ch 55), supplied by Avanti Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pan+rar+agonist+ch55/cholesterol/pmc02940274-357-27-8
Average 90 stars, based on 1 article reviews
cholesterol (lot ch-55) - by Bioz Stars, 2026-09
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cultrex pathclear 3 d culture matrix rgf bme  (Bio-Techne corporation)
96
Bio-Techne corporation cultrex pathclear 3 d culture matrix rgf bme
(A) Vitamin A-derived retinol is metabolized to RA, which activates retinoic acid receptors (RARs). RARs bind target gene promoters to drive RA-dependent transcription. (B) HT-29 cells (human intestinal epithelial cells) were treated with the RAR antagonist BMS493 or the RAR agonist <t>Ch55</t> and simultaneously stimulated overnight with RA and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=6 per group). (C) HCT-116, a transfection-competent human intestinal epithelial cell line expressing RARA and RARG , was treated for 24 hours with an siRNA targeting either gene and then stimulated overnight with retinol and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=4 per group). (D) IEC-specific disruption of RAR signaling using a dominant-negative RAR (dnRAR) knock-in allele. dnRAR mice harbor a loxP -flanked STOP cassette upstream of a dominant-negative RAR open reading frame. The dnRAR is derived from a mutant human RARα (RAR403) lacking the ligand-dependent transactivation domain and functions as a pan-RAR inhibitor. Crossing dnRAR mice with Villin-Cre transgenic mice excises the STOP cassette in IECs, resulting in IEC-selective expression of dnRAR and inhibition of RAR signaling. (E) qPCR analysis of Reg3g expression in small intestines of conventional dnRAR fl/fl (n=12) and dnRAR IEC (n=17) mice from five litters, and germ-free wild-type mice (n=21). (F) Immunofluorescence microscopy of REG3G in small intestines of dnRAR fl/fl and dnRAR IEC mice. Sections were stained for REG3G and counterstained with DAPI. Scale bar, 100 μ m. Images are representative of at least three fields per sample and two independent experiments (three littermates per group). (G) Mean fluorescence intensities of at least 150 villi from the images represented in (F) were quantified across at least two mice of each genotype. RAR, retinoic acid receptor; RA, retinoic acid; IEC, intestinal epithelial cell; REG3G, regenerating islet-derived protein 3γ; siRNA, small interfering RNA; dnRAR, dominant negative retinoic acid receptor; Conv, conventional; GF, germ-free. Means ± SEM are plotted; *p < 0.05; **p < 0.01; ***p<0.001; ns, not significant by Mann-Whitney test. See also .
Cultrex Pathclear 3 D Culture Matrix Rgf Bme, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pan+rar+agonist+ch55/Cultrex+3-D+Culture+Matrix+RGF+Basement+Membrane+Extract/pmc08282848-304-15-22
Average 96 stars, based on 1 article reviews
cultrex pathclear 3 d culture matrix rgf bme - by Bioz Stars, 2026-09
96/100 stars
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cholesterol  (Croda International Plc)
99
Croda International Plc cholesterol
(A) Vitamin A-derived retinol is metabolized to RA, which activates retinoic acid receptors (RARs). RARs bind target gene promoters to drive RA-dependent transcription. (B) HT-29 cells (human intestinal epithelial cells) were treated with the RAR antagonist BMS493 or the RAR agonist <t>Ch55</t> and simultaneously stimulated overnight with RA and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=6 per group). (C) HCT-116, a transfection-competent human intestinal epithelial cell line expressing RARA and RARG , was treated for 24 hours with an siRNA targeting either gene and then stimulated overnight with retinol and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=4 per group). (D) IEC-specific disruption of RAR signaling using a dominant-negative RAR (dnRAR) knock-in allele. dnRAR mice harbor a loxP -flanked STOP cassette upstream of a dominant-negative RAR open reading frame. The dnRAR is derived from a mutant human RARα (RAR403) lacking the ligand-dependent transactivation domain and functions as a pan-RAR inhibitor. Crossing dnRAR mice with Villin-Cre transgenic mice excises the STOP cassette in IECs, resulting in IEC-selective expression of dnRAR and inhibition of RAR signaling. (E) qPCR analysis of Reg3g expression in small intestines of conventional dnRAR fl/fl (n=12) and dnRAR IEC (n=17) mice from five litters, and germ-free wild-type mice (n=21). (F) Immunofluorescence microscopy of REG3G in small intestines of dnRAR fl/fl and dnRAR IEC mice. Sections were stained for REG3G and counterstained with DAPI. Scale bar, 100 μ m. Images are representative of at least three fields per sample and two independent experiments (three littermates per group). (G) Mean fluorescence intensities of at least 150 villi from the images represented in (F) were quantified across at least two mice of each genotype. RAR, retinoic acid receptor; RA, retinoic acid; IEC, intestinal epithelial cell; REG3G, regenerating islet-derived protein 3γ; siRNA, small interfering RNA; dnRAR, dominant negative retinoic acid receptor; Conv, conventional; GF, germ-free. Means ± SEM are plotted; *p < 0.05; **p < 0.01; ***p<0.001; ns, not significant by Mann-Whitney test. See also .
Cholesterol, supplied by Croda International Plc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pan+rar+agonist+ch55/cholesterol/pmc02695672-51-31-37
Average 99 stars, based on 1 article reviews
cholesterol - by Bioz Stars, 2026-09
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Image Search Results


(A) Vitamin A-derived retinol is metabolized to RA, which activates retinoic acid receptors (RARs). RARs bind target gene promoters to drive RA-dependent transcription. (B) HT-29 cells (human intestinal epithelial cells) were treated with the RAR antagonist BMS493 or the RAR agonist Ch55 and simultaneously stimulated overnight with RA and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=6 per group). (C) HCT-116, a transfection-competent human intestinal epithelial cell line expressing RARA and RARG , was treated for 24 hours with an siRNA targeting either gene and then stimulated overnight with retinol and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=4 per group). (D) IEC-specific disruption of RAR signaling using a dominant-negative RAR (dnRAR) knock-in allele. dnRAR mice harbor a loxP -flanked STOP cassette upstream of a dominant-negative RAR open reading frame. The dnRAR is derived from a mutant human RARα (RAR403) lacking the ligand-dependent transactivation domain and functions as a pan-RAR inhibitor. Crossing dnRAR mice with Villin-Cre transgenic mice excises the STOP cassette in IECs, resulting in IEC-selective expression of dnRAR and inhibition of RAR signaling. (E) qPCR analysis of Reg3g expression in small intestines of conventional dnRAR fl/fl (n=12) and dnRAR IEC (n=17) mice from five litters, and germ-free wild-type mice (n=21). (F) Immunofluorescence microscopy of REG3G in small intestines of dnRAR fl/fl and dnRAR IEC mice. Sections were stained for REG3G and counterstained with DAPI. Scale bar, 100 μ m. Images are representative of at least three fields per sample and two independent experiments (three littermates per group). (G) Mean fluorescence intensities of at least 150 villi from the images represented in (F) were quantified across at least two mice of each genotype. RAR, retinoic acid receptor; RA, retinoic acid; IEC, intestinal epithelial cell; REG3G, regenerating islet-derived protein 3γ; siRNA, small interfering RNA; dnRAR, dominant negative retinoic acid receptor; Conv, conventional; GF, germ-free. Means ± SEM are plotted; *p < 0.05; **p < 0.01; ***p<0.001; ns, not significant by Mann-Whitney test. See also .

Journal: bioRxiv

Article Title: Epithelial sensing of vitamin A shapes intestinal antimicrobial defense

doi: 10.64898/2026.03.08.710399

Figure Lengend Snippet: (A) Vitamin A-derived retinol is metabolized to RA, which activates retinoic acid receptors (RARs). RARs bind target gene promoters to drive RA-dependent transcription. (B) HT-29 cells (human intestinal epithelial cells) were treated with the RAR antagonist BMS493 or the RAR agonist Ch55 and simultaneously stimulated overnight with RA and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=6 per group). (C) HCT-116, a transfection-competent human intestinal epithelial cell line expressing RARA and RARG , was treated for 24 hours with an siRNA targeting either gene and then stimulated overnight with retinol and IL-22. REG3G transcripts were quantified by qPCR. Each data point represents an independent experimental replicate (n=4 per group). (D) IEC-specific disruption of RAR signaling using a dominant-negative RAR (dnRAR) knock-in allele. dnRAR mice harbor a loxP -flanked STOP cassette upstream of a dominant-negative RAR open reading frame. The dnRAR is derived from a mutant human RARα (RAR403) lacking the ligand-dependent transactivation domain and functions as a pan-RAR inhibitor. Crossing dnRAR mice with Villin-Cre transgenic mice excises the STOP cassette in IECs, resulting in IEC-selective expression of dnRAR and inhibition of RAR signaling. (E) qPCR analysis of Reg3g expression in small intestines of conventional dnRAR fl/fl (n=12) and dnRAR IEC (n=17) mice from five litters, and germ-free wild-type mice (n=21). (F) Immunofluorescence microscopy of REG3G in small intestines of dnRAR fl/fl and dnRAR IEC mice. Sections were stained for REG3G and counterstained with DAPI. Scale bar, 100 μ m. Images are representative of at least three fields per sample and two independent experiments (three littermates per group). (G) Mean fluorescence intensities of at least 150 villi from the images represented in (F) were quantified across at least two mice of each genotype. RAR, retinoic acid receptor; RA, retinoic acid; IEC, intestinal epithelial cell; REG3G, regenerating islet-derived protein 3γ; siRNA, small interfering RNA; dnRAR, dominant negative retinoic acid receptor; Conv, conventional; GF, germ-free. Means ± SEM are plotted; *p < 0.05; **p < 0.01; ***p<0.001; ns, not significant by Mann-Whitney test. See also .

Article Snippet: Pharmacologic modulation of retinoic acid receptor (RAR) activity was performed using the pan-RAR antagonist BMS493 (Fisher Scientific) or the pan-RAR agonist Ch55 (Tocris).

Techniques: Derivative Assay, Transfection, Expressing, Disruption, Dominant Negative Mutation, Knock-In, Mutagenesis, Transgenic Assay, Inhibition, Immunofluorescence, Microscopy, Staining, Fluorescence, Small Interfering RNA, MANN-WHITNEY