mrk 560 Search Results


mrk 560  (MedChemExpress)
93
MedChemExpress mrk 560
(A) Cell survival assay of indicated T-ALL cell lines stably expressing Vec, UVRAG WT, or ΔCCD3 mutant after 7-day treatment with indicated concentrations <t>of</t> <t>MRK-560</t> (n = 3 replicates for each condition per cell line). Immunoblots show Flag-UVRAG expression, with actin as loading control. (B) IB of indicated proteins in CUTLL1 cells from (A), with or without MRK-560 treatment (10 mM, 7 days). (C) Schematic overview of experiment design. NSG mice bearing primary T-ALL PDX 332x ( via tail vein injection) were treated with or without Dox to induce Flag-UVRAG expression after disease establishment, followed by daily i.p. injections of MRK-560 (30 mmol kg -1 ) for 14 days. Immunoblots show Flag-UVRAG and NICD expression in PDX 332x cells (top). (D-G) Percentages of human CD45 + cells in peripheral blood (D), bone marrow (E), and spleen (F), and overall spleen weight (G) from Dox-treated (On_Dox) or untreated (No_Dox) mice transplanted with patient sample 332x and treated with DMSO or MRK-560 for 14 days. Fold changes comparing MRK-560 vs . vehicle within each group are shown (n = 5 per group). Representative spleen images shown (right). (H) Kaplan-Meier survival curves for xenotransplanted mice ± Dox treatment, administered Vehicle or MRK-560 as described in (C). (I) Proposed working model illustrating K27-linked ubiquitination checkpoint controlling membrane-bound NOTCH1ΔE via the UVRAG-ITCH-ESCRT pathway. UVRAG, together with ITCH E3 ligase, promotes K27-linked ubiquitination of NOTCH1ΔE, directing its lysosomal degradation and reducing NOTCH1 signaling upstream of γ-secretase cleavage. Dysregulation of this checkpoint enhances NOTCH1 signaling, promoting T-ALL progression and dampening therapeutic responsiveness. Data in (B) are representative of three independent experiments. Data in (A) and (D-G) represent mean ± s.e.m. analyzed by Student’s two-tailed t test for two-group comparisons or one-way ANOVA followed by Tukey’s post hoc test. **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant. See also Figure S10.
Mrk 560, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mrk+560/MRK-560/bio_rxiv__64898__2025__12__18__695023-247-46-47
Average 93 stars, based on 1 article reviews
mrk 560 - by Bioz Stars, 2026-10
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mrk-560  (MuseChem Chemicals)
N/A
MRK-560（Cat No.:I008017）is a potent and selective γ-secretase inhibitor that targets presenilin-1–containing complexes while sparing presenilin-2. This selectivity reduces unwanted side effects commonly associated with broad γ-secretase inhibition. MRK-560 effectively blocks amyloid-β (Aβ) peptide formation, making
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mrk560  (Tocris)
92
Tocris mrk560
(A) Cell survival assay of indicated T-ALL cell lines stably expressing Vec, UVRAG WT, or ΔCCD3 mutant after 7-day treatment with indicated concentrations <t>of</t> <t>MRK-560</t> (n = 3 replicates for each condition per cell line). Immunoblots show Flag-UVRAG expression, with actin as loading control. (B) IB of indicated proteins in CUTLL1 cells from (A), with or without MRK-560 treatment (10 mM, 7 days). (C) Schematic overview of experiment design. NSG mice bearing primary T-ALL PDX 332x ( via tail vein injection) were treated with or without Dox to induce Flag-UVRAG expression after disease establishment, followed by daily i.p. injections of MRK-560 (30 mmol kg -1 ) for 14 days. Immunoblots show Flag-UVRAG and NICD expression in PDX 332x cells (top). (D-G) Percentages of human CD45 + cells in peripheral blood (D), bone marrow (E), and spleen (F), and overall spleen weight (G) from Dox-treated (On_Dox) or untreated (No_Dox) mice transplanted with patient sample 332x and treated with DMSO or MRK-560 for 14 days. Fold changes comparing MRK-560 vs . vehicle within each group are shown (n = 5 per group). Representative spleen images shown (right). (H) Kaplan-Meier survival curves for xenotransplanted mice ± Dox treatment, administered Vehicle or MRK-560 as described in (C). (I) Proposed working model illustrating K27-linked ubiquitination checkpoint controlling membrane-bound NOTCH1ΔE via the UVRAG-ITCH-ESCRT pathway. UVRAG, together with ITCH E3 ligase, promotes K27-linked ubiquitination of NOTCH1ΔE, directing its lysosomal degradation and reducing NOTCH1 signaling upstream of γ-secretase cleavage. Dysregulation of this checkpoint enhances NOTCH1 signaling, promoting T-ALL progression and dampening therapeutic responsiveness. Data in (B) are representative of three independent experiments. Data in (A) and (D-G) represent mean ± s.e.m. analyzed by Student’s two-tailed t test for two-group comparisons or one-way ANOVA followed by Tukey’s post hoc test. **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant. See also Figure S10.
Mrk560, supplied by Tocris, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mrk+560/MRK+560/pmc04840960-294-18-22
Average 92 stars, based on 1 article reviews
mrk560 - by Bioz Stars, 2026-10
92/100 stars
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mrk 560  (Tocris)
93
Tocris mrk 560
(A) Cell survival assay of indicated T-ALL cell lines stably expressing Vec, UVRAG WT, or ΔCCD3 mutant after 7-day treatment with indicated concentrations <t>of</t> <t>MRK-560</t> (n = 3 replicates for each condition per cell line). Immunoblots show Flag-UVRAG expression, with actin as loading control. (B) IB of indicated proteins in CUTLL1 cells from (A), with or without MRK-560 treatment (10 mM, 7 days). (C) Schematic overview of experiment design. NSG mice bearing primary T-ALL PDX 332x ( via tail vein injection) were treated with or without Dox to induce Flag-UVRAG expression after disease establishment, followed by daily i.p. injections of MRK-560 (30 mmol kg -1 ) for 14 days. Immunoblots show Flag-UVRAG and NICD expression in PDX 332x cells (top). (D-G) Percentages of human CD45 + cells in peripheral blood (D), bone marrow (E), and spleen (F), and overall spleen weight (G) from Dox-treated (On_Dox) or untreated (No_Dox) mice transplanted with patient sample 332x and treated with DMSO or MRK-560 for 14 days. Fold changes comparing MRK-560 vs . vehicle within each group are shown (n = 5 per group). Representative spleen images shown (right). (H) Kaplan-Meier survival curves for xenotransplanted mice ± Dox treatment, administered Vehicle or MRK-560 as described in (C). (I) Proposed working model illustrating K27-linked ubiquitination checkpoint controlling membrane-bound NOTCH1ΔE via the UVRAG-ITCH-ESCRT pathway. UVRAG, together with ITCH E3 ligase, promotes K27-linked ubiquitination of NOTCH1ΔE, directing its lysosomal degradation and reducing NOTCH1 signaling upstream of γ-secretase cleavage. Dysregulation of this checkpoint enhances NOTCH1 signaling, promoting T-ALL progression and dampening therapeutic responsiveness. Data in (B) are representative of three independent experiments. Data in (A) and (D-G) represent mean ± s.e.m. analyzed by Student’s two-tailed t test for two-group comparisons or one-way ANOVA followed by Tukey’s post hoc test. **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant. See also Figure S10.
Mrk 560, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mrk+560/MRK+560/pmc12641031-251-3-31
Average 93 stars, based on 1 article reviews
mrk 560 - by Bioz Stars, 2026-10
93/100 stars
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transgenic βapp mice tg2576 mice  (AstraZeneca ltd)
90
AstraZeneca ltd transgenic βapp mice tg2576 mice
(A) Cell survival assay of indicated T-ALL cell lines stably expressing Vec, UVRAG WT, or ΔCCD3 mutant after 7-day treatment with indicated concentrations <t>of</t> <t>MRK-560</t> (n = 3 replicates for each condition per cell line). Immunoblots show Flag-UVRAG expression, with actin as loading control. (B) IB of indicated proteins in CUTLL1 cells from (A), with or without MRK-560 treatment (10 mM, 7 days). (C) Schematic overview of experiment design. NSG mice bearing primary T-ALL PDX 332x ( via tail vein injection) were treated with or without Dox to induce Flag-UVRAG expression after disease establishment, followed by daily i.p. injections of MRK-560 (30 mmol kg -1 ) for 14 days. Immunoblots show Flag-UVRAG and NICD expression in PDX 332x cells (top). (D-G) Percentages of human CD45 + cells in peripheral blood (D), bone marrow (E), and spleen (F), and overall spleen weight (G) from Dox-treated (On_Dox) or untreated (No_Dox) mice transplanted with patient sample 332x and treated with DMSO or MRK-560 for 14 days. Fold changes comparing MRK-560 vs . vehicle within each group are shown (n = 5 per group). Representative spleen images shown (right). (H) Kaplan-Meier survival curves for xenotransplanted mice ± Dox treatment, administered Vehicle or MRK-560 as described in (C). (I) Proposed working model illustrating K27-linked ubiquitination checkpoint controlling membrane-bound NOTCH1ΔE via the UVRAG-ITCH-ESCRT pathway. UVRAG, together with ITCH E3 ligase, promotes K27-linked ubiquitination of NOTCH1ΔE, directing its lysosomal degradation and reducing NOTCH1 signaling upstream of γ-secretase cleavage. Dysregulation of this checkpoint enhances NOTCH1 signaling, promoting T-ALL progression and dampening therapeutic responsiveness. Data in (B) are representative of three independent experiments. Data in (A) and (D-G) represent mean ± s.e.m. analyzed by Student’s two-tailed t test for two-group comparisons or one-way ANOVA followed by Tukey’s post hoc test. **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant. See also Figure S10.
Transgenic βapp Mice Tg2576 Mice, supplied by AstraZeneca ltd, 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/mrk+560/mrk+560/pmc02856073-74-3-14
Average 90 stars, based on 1 article reviews
transgenic βapp mice tg2576 mice - by Bioz Stars, 2026-10
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mrk 560  (BOC Sciences)
N/A
MRK 560, under the IUPAC name N-((1r,4r)-4-((4-chlorophenyl)sulfonyl)-4-(2,5-difluorophenyl)cyclohexyl)-1,1,1-trifluoromethanesulfonamide, is a novel orally bioavailable γ-secretase inhibitor and inhibites the production of Aβ40 and Aβ42 (in vitro: IC50= 0.65 nM).in vivo: Reduces Aβ in the brain (ED50s= 6
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mrk 560  (Biosynth Carbosynth)
N/A
γ-secretase inhibitor; reduces amyloid-β in brain . γ-secretase inhibitor; reduces amyloid-β in brain .
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mrk 560  (Toronto Research Chemicals)
N/A
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mrk 560  (Aladdin Scientific Corporation)
N/A
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mrk 560  (1PlusChem LLC)
N/A
MRK 560
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mrk 560  (Cayman Chemical)
N/A
MRK 560
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Image Search Results


(A) Cell survival assay of indicated T-ALL cell lines stably expressing Vec, UVRAG WT, or ΔCCD3 mutant after 7-day treatment with indicated concentrations of MRK-560 (n = 3 replicates for each condition per cell line). Immunoblots show Flag-UVRAG expression, with actin as loading control. (B) IB of indicated proteins in CUTLL1 cells from (A), with or without MRK-560 treatment (10 mM, 7 days). (C) Schematic overview of experiment design. NSG mice bearing primary T-ALL PDX 332x ( via tail vein injection) were treated with or without Dox to induce Flag-UVRAG expression after disease establishment, followed by daily i.p. injections of MRK-560 (30 mmol kg -1 ) for 14 days. Immunoblots show Flag-UVRAG and NICD expression in PDX 332x cells (top). (D-G) Percentages of human CD45 + cells in peripheral blood (D), bone marrow (E), and spleen (F), and overall spleen weight (G) from Dox-treated (On_Dox) or untreated (No_Dox) mice transplanted with patient sample 332x and treated with DMSO or MRK-560 for 14 days. Fold changes comparing MRK-560 vs . vehicle within each group are shown (n = 5 per group). Representative spleen images shown (right). (H) Kaplan-Meier survival curves for xenotransplanted mice ± Dox treatment, administered Vehicle or MRK-560 as described in (C). (I) Proposed working model illustrating K27-linked ubiquitination checkpoint controlling membrane-bound NOTCH1ΔE via the UVRAG-ITCH-ESCRT pathway. UVRAG, together with ITCH E3 ligase, promotes K27-linked ubiquitination of NOTCH1ΔE, directing its lysosomal degradation and reducing NOTCH1 signaling upstream of γ-secretase cleavage. Dysregulation of this checkpoint enhances NOTCH1 signaling, promoting T-ALL progression and dampening therapeutic responsiveness. Data in (B) are representative of three independent experiments. Data in (A) and (D-G) represent mean ± s.e.m. analyzed by Student’s two-tailed t test for two-group comparisons or one-way ANOVA followed by Tukey’s post hoc test. **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant. See also Figure S10.

Journal: bioRxiv

Article Title: A K27-linked Ubiquitin Checkpoint Controls NOTCH Homeostasis

doi: 10.64898/2025.12.18.695023

Figure Lengend Snippet: (A) Cell survival assay of indicated T-ALL cell lines stably expressing Vec, UVRAG WT, or ΔCCD3 mutant after 7-day treatment with indicated concentrations of MRK-560 (n = 3 replicates for each condition per cell line). Immunoblots show Flag-UVRAG expression, with actin as loading control. (B) IB of indicated proteins in CUTLL1 cells from (A), with or without MRK-560 treatment (10 mM, 7 days). (C) Schematic overview of experiment design. NSG mice bearing primary T-ALL PDX 332x ( via tail vein injection) were treated with or without Dox to induce Flag-UVRAG expression after disease establishment, followed by daily i.p. injections of MRK-560 (30 mmol kg -1 ) for 14 days. Immunoblots show Flag-UVRAG and NICD expression in PDX 332x cells (top). (D-G) Percentages of human CD45 + cells in peripheral blood (D), bone marrow (E), and spleen (F), and overall spleen weight (G) from Dox-treated (On_Dox) or untreated (No_Dox) mice transplanted with patient sample 332x and treated with DMSO or MRK-560 for 14 days. Fold changes comparing MRK-560 vs . vehicle within each group are shown (n = 5 per group). Representative spleen images shown (right). (H) Kaplan-Meier survival curves for xenotransplanted mice ± Dox treatment, administered Vehicle or MRK-560 as described in (C). (I) Proposed working model illustrating K27-linked ubiquitination checkpoint controlling membrane-bound NOTCH1ΔE via the UVRAG-ITCH-ESCRT pathway. UVRAG, together with ITCH E3 ligase, promotes K27-linked ubiquitination of NOTCH1ΔE, directing its lysosomal degradation and reducing NOTCH1 signaling upstream of γ-secretase cleavage. Dysregulation of this checkpoint enhances NOTCH1 signaling, promoting T-ALL progression and dampening therapeutic responsiveness. Data in (B) are representative of three independent experiments. Data in (A) and (D-G) represent mean ± s.e.m. analyzed by Student’s two-tailed t test for two-group comparisons or one-way ANOVA followed by Tukey’s post hoc test. **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant. See also Figure S10.

Article Snippet: Where indicated, cells were treated with 20 mM chloroquine (CQ; Sigma-Aldrich), 10 mM NH4Cl (Sigma-Aldrich), 10 mM MG132 (Sigma-Aldrich), 1 mg ml -1 doxycycline (Sigma-Aldrich), 1 mM Torin 1 (Selleckchem), 30 mM Batimastat (Calbiochem), 10 mM DAPT (Millipore Sigma), 1 mM compound E (Millipore Sigma), and MRK-560 (MedChemExpress) for the indicated time points before collection.

Techniques: Clonogenic Cell Survival Assay, Stable Transfection, Expressing, Mutagenesis, Western Blot, Control, Injection, Ubiquitin Proteomics, Membrane, Two Tailed Test