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Croda International Plc t mas
MSMO1 modulates the relative content <t>of</t> <t>T-MAS</t> to regulate endoplasmic reticulum stress (A) Schematic diagram of cholesterol metabolic pathways, starting with squalene. (B) Heatmap showing the cholesterol metabolites with the most statistically significant differences between MSMO1-KD MDA-MB-231 and control cells. (C) Volcano plots showing differential metabolites between MSMO1-KD and control cells. T-MAS exhibited a significant increase (Log 2 (fold change) = 5.66 p < 0.001) in MSMO1-KD cells. (D) Representative images of thioflavin T (ThT) staining assay with or without the treatment of 1 mM 4-PBA for 3 h and 1 μg/mL T-MAS for 48 h. Scale bars, 10 μm. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MDA-MB-231 cells with or without the pretreatment of 1 μM PERKi for 3 h and the treatment of 1 μg/mL T-MAS for 48 h. (F and G) IC50 curves of MSMO1 overexpressing and MSMO1-KD cells and the corresponding control cells for Tg with or without the treatment of 1 μg/mL T-MAS. Data are represented as mean ± SEM.
T Mas, supplied by Croda International Plc, used in various techniques. Bioz Stars score: 94/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "MSMO1 promotes chemotherapy resistance through modulation of T-MAS metabolism via PERK/elF2α/ATF4/CHOP pathway"

Article Title: MSMO1 promotes chemotherapy resistance through modulation of T-MAS metabolism via PERK/elF2α/ATF4/CHOP pathway

Journal: iScience

doi: 10.1016/j.isci.2026.114790

MSMO1 modulates the relative content of T-MAS to regulate endoplasmic reticulum stress (A) Schematic diagram of cholesterol metabolic pathways, starting with squalene. (B) Heatmap showing the cholesterol metabolites with the most statistically significant differences between MSMO1-KD MDA-MB-231 and control cells. (C) Volcano plots showing differential metabolites between MSMO1-KD and control cells. T-MAS exhibited a significant increase (Log 2 (fold change) = 5.66 p < 0.001) in MSMO1-KD cells. (D) Representative images of thioflavin T (ThT) staining assay with or without the treatment of 1 mM 4-PBA for 3 h and 1 μg/mL T-MAS for 48 h. Scale bars, 10 μm. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MDA-MB-231 cells with or without the pretreatment of 1 μM PERKi for 3 h and the treatment of 1 μg/mL T-MAS for 48 h. (F and G) IC50 curves of MSMO1 overexpressing and MSMO1-KD cells and the corresponding control cells for Tg with or without the treatment of 1 μg/mL T-MAS. Data are represented as mean ± SEM.
Figure Legend Snippet: MSMO1 modulates the relative content of T-MAS to regulate endoplasmic reticulum stress (A) Schematic diagram of cholesterol metabolic pathways, starting with squalene. (B) Heatmap showing the cholesterol metabolites with the most statistically significant differences between MSMO1-KD MDA-MB-231 and control cells. (C) Volcano plots showing differential metabolites between MSMO1-KD and control cells. T-MAS exhibited a significant increase (Log 2 (fold change) = 5.66 p < 0.001) in MSMO1-KD cells. (D) Representative images of thioflavin T (ThT) staining assay with or without the treatment of 1 mM 4-PBA for 3 h and 1 μg/mL T-MAS for 48 h. Scale bars, 10 μm. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MDA-MB-231 cells with or without the pretreatment of 1 μM PERKi for 3 h and the treatment of 1 μg/mL T-MAS for 48 h. (F and G) IC50 curves of MSMO1 overexpressing and MSMO1-KD cells and the corresponding control cells for Tg with or without the treatment of 1 μg/mL T-MAS. Data are represented as mean ± SEM.

Techniques Used: Control, Staining, Western Blot, Expressing

T-MAS induces ER stress and activates PERK/eIF2α/ATF4/CHOP pathway (A) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit TM7SF2 to reduce the cellular levels of T-MAS. (B and C) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in MSMO1-KD and control cells with or without siRNA interfering with TM7SF2. (D) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit CYP51A1 to reduce the cellular levels of FF-MAS and downstream metabolites. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in wild-type SK-BR-3 cells with or without the pretreatment of 100 nM Tg for 3 h and siRNA interfering with CYP51A1. (F) Western blotting images showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MSMO1-KD and control MDA-MB-231 cells with or without siRNA interfering with CYP51A1. (G and I) Schematic view of silencing TM7SF2 through siRNA to inhibit the transformation of FF-MAS to T-MAS, followed by the administration of FF-MAS or T-MAS to the cells. (H and J) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP with or without siRNA interfering with TM7SF2 and 1 μg/mL FF-MAS(or 1 μg/mL T-MAS) treatment of 48 h.
Figure Legend Snippet: T-MAS induces ER stress and activates PERK/eIF2α/ATF4/CHOP pathway (A) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit TM7SF2 to reduce the cellular levels of T-MAS. (B and C) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in MSMO1-KD and control cells with or without siRNA interfering with TM7SF2. (D) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit CYP51A1 to reduce the cellular levels of FF-MAS and downstream metabolites. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in wild-type SK-BR-3 cells with or without the pretreatment of 100 nM Tg for 3 h and siRNA interfering with CYP51A1. (F) Western blotting images showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MSMO1-KD and control MDA-MB-231 cells with or without siRNA interfering with CYP51A1. (G and I) Schematic view of silencing TM7SF2 through siRNA to inhibit the transformation of FF-MAS to T-MAS, followed by the administration of FF-MAS or T-MAS to the cells. (H and J) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP with or without siRNA interfering with TM7SF2 and 1 μg/mL FF-MAS(or 1 μg/mL T-MAS) treatment of 48 h.

Techniques Used: Western Blot, Expressing, Control, Transformation Assay

T-MAS enhances the chemosensitivity of breast cancer organoids (A) Representative electron microscope (EM) images of untreated, 1 μg/mL T-MAS treated, 500 nM PTX treated, and 500 nM PTX plus 1 μg/mL T-MAS treated cells. Arrowheads indicate the ER. 120 ER widths were measured in each group. x5k scale bars, 5 μm. x25k scale bars, 1 μm. (B) Schematic view of sample collection ( n = 7). Tissue specimens from the primary tumor were collected by core needle biopsy and then induced into organoids for drug sensitivity testing. Plasma exosomes were further extracted from the blood sample. (C) Correlation analysis between primary tumor site and plasma exosome MSMO1 expression level (R = 0.86, p = 0.013). (D) Representative images of fluorescence microscopy show Live (AO = green)/dead (PI = red) analysis of breast cancer organoids following treatment of 500 nM PTX or 200 μM CBP or in combination with 1 μg/mL T-MAS. Scale bars, 20 μm. (E) Quantification results of organoid live/dead analysis. Data are represented as mean ± SEM. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗∗ p < 0.0001.
Figure Legend Snippet: T-MAS enhances the chemosensitivity of breast cancer organoids (A) Representative electron microscope (EM) images of untreated, 1 μg/mL T-MAS treated, 500 nM PTX treated, and 500 nM PTX plus 1 μg/mL T-MAS treated cells. Arrowheads indicate the ER. 120 ER widths were measured in each group. x5k scale bars, 5 μm. x25k scale bars, 1 μm. (B) Schematic view of sample collection ( n = 7). Tissue specimens from the primary tumor were collected by core needle biopsy and then induced into organoids for drug sensitivity testing. Plasma exosomes were further extracted from the blood sample. (C) Correlation analysis between primary tumor site and plasma exosome MSMO1 expression level (R = 0.86, p = 0.013). (D) Representative images of fluorescence microscopy show Live (AO = green)/dead (PI = red) analysis of breast cancer organoids following treatment of 500 nM PTX or 200 μM CBP or in combination with 1 μg/mL T-MAS. Scale bars, 20 μm. (E) Quantification results of organoid live/dead analysis. Data are represented as mean ± SEM. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗∗ p < 0.0001.

Techniques Used: Microscopy, Clinical Proteomics, Expressing, Fluorescence



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Image Search Results


MSMO1 modulates the relative content of T-MAS to regulate endoplasmic reticulum stress (A) Schematic diagram of cholesterol metabolic pathways, starting with squalene. (B) Heatmap showing the cholesterol metabolites with the most statistically significant differences between MSMO1-KD MDA-MB-231 and control cells. (C) Volcano plots showing differential metabolites between MSMO1-KD and control cells. T-MAS exhibited a significant increase (Log 2 (fold change) = 5.66 p < 0.001) in MSMO1-KD cells. (D) Representative images of thioflavin T (ThT) staining assay with or without the treatment of 1 mM 4-PBA for 3 h and 1 μg/mL T-MAS for 48 h. Scale bars, 10 μm. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MDA-MB-231 cells with or without the pretreatment of 1 μM PERKi for 3 h and the treatment of 1 μg/mL T-MAS for 48 h. (F and G) IC50 curves of MSMO1 overexpressing and MSMO1-KD cells and the corresponding control cells for Tg with or without the treatment of 1 μg/mL T-MAS. Data are represented as mean ± SEM.

Journal: iScience

Article Title: MSMO1 promotes chemotherapy resistance through modulation of T-MAS metabolism via PERK/elF2α/ATF4/CHOP pathway

doi: 10.1016/j.isci.2026.114790

Figure Lengend Snippet: MSMO1 modulates the relative content of T-MAS to regulate endoplasmic reticulum stress (A) Schematic diagram of cholesterol metabolic pathways, starting with squalene. (B) Heatmap showing the cholesterol metabolites with the most statistically significant differences between MSMO1-KD MDA-MB-231 and control cells. (C) Volcano plots showing differential metabolites between MSMO1-KD and control cells. T-MAS exhibited a significant increase (Log 2 (fold change) = 5.66 p < 0.001) in MSMO1-KD cells. (D) Representative images of thioflavin T (ThT) staining assay with or without the treatment of 1 mM 4-PBA for 3 h and 1 μg/mL T-MAS for 48 h. Scale bars, 10 μm. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MDA-MB-231 cells with or without the pretreatment of 1 μM PERKi for 3 h and the treatment of 1 μg/mL T-MAS for 48 h. (F and G) IC50 curves of MSMO1 overexpressing and MSMO1-KD cells and the corresponding control cells for Tg with or without the treatment of 1 μg/mL T-MAS. Data are represented as mean ± SEM.

Article Snippet: T-MAS , Avanti , Cat#: 700073P.

Techniques: Control, Staining, Western Blot, Expressing

T-MAS induces ER stress and activates PERK/eIF2α/ATF4/CHOP pathway (A) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit TM7SF2 to reduce the cellular levels of T-MAS. (B and C) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in MSMO1-KD and control cells with or without siRNA interfering with TM7SF2. (D) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit CYP51A1 to reduce the cellular levels of FF-MAS and downstream metabolites. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in wild-type SK-BR-3 cells with or without the pretreatment of 100 nM Tg for 3 h and siRNA interfering with CYP51A1. (F) Western blotting images showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MSMO1-KD and control MDA-MB-231 cells with or without siRNA interfering with CYP51A1. (G and I) Schematic view of silencing TM7SF2 through siRNA to inhibit the transformation of FF-MAS to T-MAS, followed by the administration of FF-MAS or T-MAS to the cells. (H and J) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP with or without siRNA interfering with TM7SF2 and 1 μg/mL FF-MAS(or 1 μg/mL T-MAS) treatment of 48 h.

Journal: iScience

Article Title: MSMO1 promotes chemotherapy resistance through modulation of T-MAS metabolism via PERK/elF2α/ATF4/CHOP pathway

doi: 10.1016/j.isci.2026.114790

Figure Lengend Snippet: T-MAS induces ER stress and activates PERK/eIF2α/ATF4/CHOP pathway (A) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit TM7SF2 to reduce the cellular levels of T-MAS. (B and C) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in MSMO1-KD and control cells with or without siRNA interfering with TM7SF2. (D) Diagram of the cholesterol metabolism pathway, using siRNA to inhibit CYP51A1 to reduce the cellular levels of FF-MAS and downstream metabolites. (E) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, CHOP in wild-type SK-BR-3 cells with or without the pretreatment of 100 nM Tg for 3 h and siRNA interfering with CYP51A1. (F) Western blotting images showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP in MSMO1-KD and control MDA-MB-231 cells with or without siRNA interfering with CYP51A1. (G and I) Schematic view of silencing TM7SF2 through siRNA to inhibit the transformation of FF-MAS to T-MAS, followed by the administration of FF-MAS or T-MAS to the cells. (H and J) Western blotting analysis showing the expression of BIP, PERK, p -eIF2α, ATF4, and CHOP with or without siRNA interfering with TM7SF2 and 1 μg/mL FF-MAS(or 1 μg/mL T-MAS) treatment of 48 h.

Article Snippet: T-MAS , Avanti , Cat#: 700073P.

Techniques: Western Blot, Expressing, Control, Transformation Assay

T-MAS enhances the chemosensitivity of breast cancer organoids (A) Representative electron microscope (EM) images of untreated, 1 μg/mL T-MAS treated, 500 nM PTX treated, and 500 nM PTX plus 1 μg/mL T-MAS treated cells. Arrowheads indicate the ER. 120 ER widths were measured in each group. x5k scale bars, 5 μm. x25k scale bars, 1 μm. (B) Schematic view of sample collection ( n = 7). Tissue specimens from the primary tumor were collected by core needle biopsy and then induced into organoids for drug sensitivity testing. Plasma exosomes were further extracted from the blood sample. (C) Correlation analysis between primary tumor site and plasma exosome MSMO1 expression level (R = 0.86, p = 0.013). (D) Representative images of fluorescence microscopy show Live (AO = green)/dead (PI = red) analysis of breast cancer organoids following treatment of 500 nM PTX or 200 μM CBP or in combination with 1 μg/mL T-MAS. Scale bars, 20 μm. (E) Quantification results of organoid live/dead analysis. Data are represented as mean ± SEM. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗∗ p < 0.0001.

Journal: iScience

Article Title: MSMO1 promotes chemotherapy resistance through modulation of T-MAS metabolism via PERK/elF2α/ATF4/CHOP pathway

doi: 10.1016/j.isci.2026.114790

Figure Lengend Snippet: T-MAS enhances the chemosensitivity of breast cancer organoids (A) Representative electron microscope (EM) images of untreated, 1 μg/mL T-MAS treated, 500 nM PTX treated, and 500 nM PTX plus 1 μg/mL T-MAS treated cells. Arrowheads indicate the ER. 120 ER widths were measured in each group. x5k scale bars, 5 μm. x25k scale bars, 1 μm. (B) Schematic view of sample collection ( n = 7). Tissue specimens from the primary tumor were collected by core needle biopsy and then induced into organoids for drug sensitivity testing. Plasma exosomes were further extracted from the blood sample. (C) Correlation analysis between primary tumor site and plasma exosome MSMO1 expression level (R = 0.86, p = 0.013). (D) Representative images of fluorescence microscopy show Live (AO = green)/dead (PI = red) analysis of breast cancer organoids following treatment of 500 nM PTX or 200 μM CBP or in combination with 1 μg/mL T-MAS. Scale bars, 20 μm. (E) Quantification results of organoid live/dead analysis. Data are represented as mean ± SEM. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗∗ p < 0.0001.

Article Snippet: T-MAS , Avanti , Cat#: 700073P.

Techniques: Microscopy, Clinical Proteomics, Expressing, Fluorescence