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torin2  (Tocris)


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    Tocris torin2
    Torin2, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 78 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/torin+2/Torin+2/10__1016_slash_j__isci__2026__115860-581-21-24
    Average 93 stars, based on 78 article reviews
    torin2 - by Bioz Stars, 2026-10
    93/100 stars

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    other:

    Article Title: HCN1 channels mediate mu opioid receptor long-term depression at insular cortex inputs to the dorsal striatum
    Article Snippet: We used the MOR agonist [D-Ala 2 , NMe-Phe 4 , Gly-ol 5 ]-enkephalin (DAMGO; H-2535, Bachem), GABA A receptor antagonist picrotoxin (PTX, P1675, Sigma-Aldrich), PKI (6221, Tocris), KT5720 (1288, Tocris), Forskolin (F3917, Sigma-Aldrich), Cyclo-heximide (0970, Tocris), ZD7288 (1000, Tocris), WIN55,212-2 (1038, Tocris) and Torin 2 (4248, Tocris).

    Article Title: HCN1 channels mediate mu opioid receptor long‐term depression at insular cortex inputs to the dorsal striatum
    Article Snippet: We used the MOR agonist [D-Ala2, NMe-Phe4, Gly-ol5]-enkephalin (DAMGO; H-2535, Bachem), GABAA receptor antagonist picrotoxin (PTX, P1675, Sigma-Aldrich), PKI (6221, Tocris), KT5720 (1288, Tocris), Forskolin (F3917, Sigma-Aldrich), Cycloheximide (0970, Tocris), ZD7288 (1000, Tocris), WIN55,212-2 (1038, Tocris) and Torin 2 (4248, Tocris).

    FACS:

    Article Title: REDD1 interacts with AIF and regulates mitochondrial reactive oxygen species generation in the keratinocyte response to UVB.
    Article Snippet: .. Rapamycin (50 nM, Developmental Therapeutics Program, National Cancer Institute), Torin 2 (50 nM, Tocris, Bristol, UK), Z-VAD-FMK (50 mM, Tocris) or DMSO vehicle was added to the tissue culture medium either overnight (FACS) or 1 h prior (Western) to UVB treatment. ..

    Western Blot:

    Article Title: REDD1 interacts with AIF and regulates mitochondrial reactive oxygen species generation in the keratinocyte response to UVB.
    Article Snippet: .. Rapamycin (50 nM, Developmental Therapeutics Program, National Cancer Institute), Torin 2 (50 nM, Tocris, Bristol, UK), Z-VAD-FMK (50 mM, Tocris) or DMSO vehicle was added to the tissue culture medium either overnight (FACS) or 1 h prior (Western) to UVB treatment. ..



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    PFD combined with OS/AF promotes autophagic flux to enhance the cytotoxicity of EGFR-TKIs in NSCLC cells. (A-D) Western blot analysis of autophagy-related proteins (P62, Beclin-1, ATG5, LC3B) in PC9 (A,C) and HCC827 (B,D) cells treated with PFD alone, OS/AF alone, or their combination, with or without the autolysosome inhibitor bafilomycin A1. GAPDH was used as the loading control. (E,F) Immunofluorescence staining of LC3B (green) with DAPI nuclear counterstain (blue) in PC9 cells treated with AF (E) or OS (F) in the presence or absence of PFD. (G,H) Autophagic flux detection in PC9 cells via mCherry-GFP-LC3 tandem fluorescent reporter system, after treatment with OS (G) or AF (H) combined with PFD, with or without bafilomycin A1. (I) Quantitative analysis of autophagosomes (GFP + mCherry + dots) and autolysosomes (mCherry + only dots) per cell from the images in (G,H). (J,K) Relative survival rate of PC9 (J) and HCC827 (K) cells treated with gradient concentrations of autophagy activator <t>Torin</t> <t>2</t> combined with OS or AF, detected by CCK-8 assay. AF, afatinib; CCK-8, Cell Counting Kit-8; DAPI, 4',6-diamidino-2-phenylindole; EGFR, epidermal growth factor receptor; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; NSCLC, non-small cell lung cancer; OS, osimertinib; PFD, pirfenidone; TKI, tyrosine kinase inhibitors.
    Torin 2, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/torin+2/Torin+2/pmc13657879-85-19-21
    Average 94 stars, based on 1 article reviews
    torin 2 - by Bioz Stars, 2026-10
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    torin2  (TargetMol)
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    (A) IFA of infected HeLa cells reveals that PI4K2A-HA is recruited to the PVM throughout liver stage development independent of CASM. For the quantifications, means ± SD of three independent experiments are shown. WT, wildtype; KO, knockout. (B) Live-cell microscopy of fluorescent phosphoinositide reporters in infected HeLa cells at 24-29 hpi reveals that liver stage parasites are associated with PI(4)P. (C) The PI(4)P reporter co-localizes with the PVM marker UIS4 in IFA. PI(4)P levels at the PVM are significantly reduced in PI4K2A-KO cells and this effect is rescued by PI4K2A complementation. For the percentage of PI(4)P-labelled parasites means ± SD are shown, while for the mean fluorescence intensity analysis of the PI(4)P reporter, data points derived from individual parasites with means indicated in red are displayed. Data are derived from two independent experiments. Statistical significance was assessed by Welch’s ANOVA followed by Dunnett’s T3 multiple-comparison test. ***p < 0.001, ****p < 0.0001. AB, PI4K2A-HA addback. See also Figure S1. (D, E) 10 nM <t>Torin2</t> treatment from 2 to 8 hpi blocks export of UIS4 to the PVM and impairs recruitment of host PI4K2A to the PVM. Shown are pooled data of four independent experiments with means indicated in red. Statistical significance was assessed by Welch’s t-test. ****p < 0.0001. See also Figure S2. Scale bars, 10 µm.
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    mtorc1 2 complexes medchem  (MedChemExpress)
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    (A) IFA of infected HeLa cells reveals that PI4K2A-HA is recruited to the PVM throughout liver stage development independent of CASM. For the quantifications, means ± SD of three independent experiments are shown. WT, wildtype; KO, knockout. (B) Live-cell microscopy of fluorescent phosphoinositide reporters in infected HeLa cells at 24-29 hpi reveals that liver stage parasites are associated with PI(4)P. (C) The PI(4)P reporter co-localizes with the PVM marker UIS4 in IFA. PI(4)P levels at the PVM are significantly reduced in PI4K2A-KO cells and this effect is rescued by PI4K2A complementation. For the percentage of PI(4)P-labelled parasites means ± SD are shown, while for the mean fluorescence intensity analysis of the PI(4)P reporter, data points derived from individual parasites with means indicated in red are displayed. Data are derived from two independent experiments. Statistical significance was assessed by Welch’s ANOVA followed by Dunnett’s T3 multiple-comparison test. ***p < 0.001, ****p < 0.0001. AB, PI4K2A-HA addback. See also Figure S1. (D, E) 10 nM <t>Torin2</t> treatment from 2 to 8 hpi blocks export of UIS4 to the PVM and impairs recruitment of host PI4K2A to the PVM. Shown are pooled data of four independent experiments with means indicated in red. Statistical significance was assessed by Welch’s t-test. ****p < 0.0001. See also Figure S2. Scale bars, 10 µm.
    Mtorc1 2 Complexes Medchem, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/torin+2/Torin+2/us12630523-101-7-29
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    mtorc1 2 complexes medchem - by Bioz Stars, 2026-10
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    torin 2  (Thermo Fisher)
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    (A) IFA of infected HeLa cells reveals that PI4K2A-HA is recruited to the PVM throughout liver stage development independent of CASM. For the quantifications, means ± SD of three independent experiments are shown. WT, wildtype; KO, knockout. (B) Live-cell microscopy of fluorescent phosphoinositide reporters in infected HeLa cells at 24-29 hpi reveals that liver stage parasites are associated with PI(4)P. (C) The PI(4)P reporter co-localizes with the PVM marker UIS4 in IFA. PI(4)P levels at the PVM are significantly reduced in PI4K2A-KO cells and this effect is rescued by PI4K2A complementation. For the percentage of PI(4)P-labelled parasites means ± SD are shown, while for the mean fluorescence intensity analysis of the PI(4)P reporter, data points derived from individual parasites with means indicated in red are displayed. Data are derived from two independent experiments. Statistical significance was assessed by Welch’s ANOVA followed by Dunnett’s T3 multiple-comparison test. ***p < 0.001, ****p < 0.0001. AB, PI4K2A-HA addback. See also Figure S1. (D, E) 10 nM <t>Torin2</t> treatment from 2 to 8 hpi blocks export of UIS4 to the PVM and impairs recruitment of host PI4K2A to the PVM. Shown are pooled data of four independent experiments with means indicated in red. Statistical significance was assessed by Welch’s t-test. ****p < 0.0001. See also Figure S2. Scale bars, 10 µm.
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    Average 99 stars, based on 1 article reviews
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    torin2  (Tocris)
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    (A) IFA of infected HeLa cells reveals that PI4K2A-HA is recruited to the PVM throughout liver stage development independent of CASM. For the quantifications, means ± SD of three independent experiments are shown. WT, wildtype; KO, knockout. (B) Live-cell microscopy of fluorescent phosphoinositide reporters in infected HeLa cells at 24-29 hpi reveals that liver stage parasites are associated with PI(4)P. (C) The PI(4)P reporter co-localizes with the PVM marker UIS4 in IFA. PI(4)P levels at the PVM are significantly reduced in PI4K2A-KO cells and this effect is rescued by PI4K2A complementation. For the percentage of PI(4)P-labelled parasites means ± SD are shown, while for the mean fluorescence intensity analysis of the PI(4)P reporter, data points derived from individual parasites with means indicated in red are displayed. Data are derived from two independent experiments. Statistical significance was assessed by Welch’s ANOVA followed by Dunnett’s T3 multiple-comparison test. ***p < 0.001, ****p < 0.0001. AB, PI4K2A-HA addback. See also Figure S1. (D, E) 10 nM <t>Torin2</t> treatment from 2 to 8 hpi blocks export of UIS4 to the PVM and impairs recruitment of host PI4K2A to the PVM. Shown are pooled data of four independent experiments with means indicated in red. Statistical significance was assessed by Welch’s t-test. ****p < 0.0001. See also Figure S2. Scale bars, 10 µm.
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    torin2  (Selleck Chemicals)
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    (A) IFA of infected HeLa cells reveals that PI4K2A-HA is recruited to the PVM throughout liver stage development independent of CASM. For the quantifications, means ± SD of three independent experiments are shown. WT, wildtype; KO, knockout. (B) Live-cell microscopy of fluorescent phosphoinositide reporters in infected HeLa cells at 24-29 hpi reveals that liver stage parasites are associated with PI(4)P. (C) The PI(4)P reporter co-localizes with the PVM marker UIS4 in IFA. PI(4)P levels at the PVM are significantly reduced in PI4K2A-KO cells and this effect is rescued by PI4K2A complementation. For the percentage of PI(4)P-labelled parasites means ± SD are shown, while for the mean fluorescence intensity analysis of the PI(4)P reporter, data points derived from individual parasites with means indicated in red are displayed. Data are derived from two independent experiments. Statistical significance was assessed by Welch’s ANOVA followed by Dunnett’s T3 multiple-comparison test. ***p < 0.001, ****p < 0.0001. AB, PI4K2A-HA addback. See also Figure S1. (D, E) 10 nM <t>Torin2</t> treatment from 2 to 8 hpi blocks export of UIS4 to the PVM and impairs recruitment of host PI4K2A to the PVM. Shown are pooled data of four independent experiments with means indicated in red. Statistical significance was assessed by Welch’s t-test. ****p < 0.0001. See also Figure S2. Scale bars, 10 µm.
    Torin2, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    PFD combined with OS/AF promotes autophagic flux to enhance the cytotoxicity of EGFR-TKIs in NSCLC cells. (A-D) Western blot analysis of autophagy-related proteins (P62, Beclin-1, ATG5, LC3B) in PC9 (A,C) and HCC827 (B,D) cells treated with PFD alone, OS/AF alone, or their combination, with or without the autolysosome inhibitor bafilomycin A1. GAPDH was used as the loading control. (E,F) Immunofluorescence staining of LC3B (green) with DAPI nuclear counterstain (blue) in PC9 cells treated with AF (E) or OS (F) in the presence or absence of PFD. (G,H) Autophagic flux detection in PC9 cells via mCherry-GFP-LC3 tandem fluorescent reporter system, after treatment with OS (G) or AF (H) combined with PFD, with or without bafilomycin A1. (I) Quantitative analysis of autophagosomes (GFP + mCherry + dots) and autolysosomes (mCherry + only dots) per cell from the images in (G,H). (J,K) Relative survival rate of PC9 (J) and HCC827 (K) cells treated with gradient concentrations of autophagy activator Torin 2 combined with OS or AF, detected by CCK-8 assay. AF, afatinib; CCK-8, Cell Counting Kit-8; DAPI, 4',6-diamidino-2-phenylindole; EGFR, epidermal growth factor receptor; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; NSCLC, non-small cell lung cancer; OS, osimertinib; PFD, pirfenidone; TKI, tyrosine kinase inhibitors.

    Journal: Translational Lung Cancer Research

    Article Title: Synergistic effects and molecular mechanisms of pirfenidone combined with EGFR-TKIs in non-small cell lung cancer

    doi: 10.21037/tlcr-2026-0900

    Figure Lengend Snippet: PFD combined with OS/AF promotes autophagic flux to enhance the cytotoxicity of EGFR-TKIs in NSCLC cells. (A-D) Western blot analysis of autophagy-related proteins (P62, Beclin-1, ATG5, LC3B) in PC9 (A,C) and HCC827 (B,D) cells treated with PFD alone, OS/AF alone, or their combination, with or without the autolysosome inhibitor bafilomycin A1. GAPDH was used as the loading control. (E,F) Immunofluorescence staining of LC3B (green) with DAPI nuclear counterstain (blue) in PC9 cells treated with AF (E) or OS (F) in the presence or absence of PFD. (G,H) Autophagic flux detection in PC9 cells via mCherry-GFP-LC3 tandem fluorescent reporter system, after treatment with OS (G) or AF (H) combined with PFD, with or without bafilomycin A1. (I) Quantitative analysis of autophagosomes (GFP + mCherry + dots) and autolysosomes (mCherry + only dots) per cell from the images in (G,H). (J,K) Relative survival rate of PC9 (J) and HCC827 (K) cells treated with gradient concentrations of autophagy activator Torin 2 combined with OS or AF, detected by CCK-8 assay. AF, afatinib; CCK-8, Cell Counting Kit-8; DAPI, 4',6-diamidino-2-phenylindole; EGFR, epidermal growth factor receptor; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; NSCLC, non-small cell lung cancer; OS, osimertinib; PFD, pirfenidone; TKI, tyrosine kinase inhibitors.

    Article Snippet: OS (MCE, HY-15787), PFD (MCE, HY-B0673), AF (MCE, HY-10261), A83-01 (MCE, HY-10432), rapamycin (MCE, HY-10219), bafilomycin A1 (MCE, HY-100558), torin 2 (MCE, HY-13002), temsirolimus (MCE, HY-50910), SP600125 (MCE, HY-12041), ferrostatin-1 (MCE, HY-100579), birinapant (MCE, HY-16591), and belnacasan (MCE, HY-13205).

    Techniques: Western Blot, Analysis, Control, Immunofluorescence, Staining, CCK-8 Assay, Cell Counting

    (A) IFA of infected HeLa cells reveals that PI4K2A-HA is recruited to the PVM throughout liver stage development independent of CASM. For the quantifications, means ± SD of three independent experiments are shown. WT, wildtype; KO, knockout. (B) Live-cell microscopy of fluorescent phosphoinositide reporters in infected HeLa cells at 24-29 hpi reveals that liver stage parasites are associated with PI(4)P. (C) The PI(4)P reporter co-localizes with the PVM marker UIS4 in IFA. PI(4)P levels at the PVM are significantly reduced in PI4K2A-KO cells and this effect is rescued by PI4K2A complementation. For the percentage of PI(4)P-labelled parasites means ± SD are shown, while for the mean fluorescence intensity analysis of the PI(4)P reporter, data points derived from individual parasites with means indicated in red are displayed. Data are derived from two independent experiments. Statistical significance was assessed by Welch’s ANOVA followed by Dunnett’s T3 multiple-comparison test. ***p < 0.001, ****p < 0.0001. AB, PI4K2A-HA addback. See also Figure S1. (D, E) 10 nM Torin2 treatment from 2 to 8 hpi blocks export of UIS4 to the PVM and impairs recruitment of host PI4K2A to the PVM. Shown are pooled data of four independent experiments with means indicated in red. Statistical significance was assessed by Welch’s t-test. ****p < 0.0001. See also Figure S2. Scale bars, 10 µm.

    Journal: bioRxiv

    Article Title: Plasmodium berghei liver stages establish a damage-mimicking vacuole to hijack host ER membrane contact site machinery for lipid uptake

    doi: 10.64898/2026.06.30.735545

    Figure Lengend Snippet: (A) IFA of infected HeLa cells reveals that PI4K2A-HA is recruited to the PVM throughout liver stage development independent of CASM. For the quantifications, means ± SD of three independent experiments are shown. WT, wildtype; KO, knockout. (B) Live-cell microscopy of fluorescent phosphoinositide reporters in infected HeLa cells at 24-29 hpi reveals that liver stage parasites are associated with PI(4)P. (C) The PI(4)P reporter co-localizes with the PVM marker UIS4 in IFA. PI(4)P levels at the PVM are significantly reduced in PI4K2A-KO cells and this effect is rescued by PI4K2A complementation. For the percentage of PI(4)P-labelled parasites means ± SD are shown, while for the mean fluorescence intensity analysis of the PI(4)P reporter, data points derived from individual parasites with means indicated in red are displayed. Data are derived from two independent experiments. Statistical significance was assessed by Welch’s ANOVA followed by Dunnett’s T3 multiple-comparison test. ***p < 0.001, ****p < 0.0001. AB, PI4K2A-HA addback. See also Figure S1. (D, E) 10 nM Torin2 treatment from 2 to 8 hpi blocks export of UIS4 to the PVM and impairs recruitment of host PI4K2A to the PVM. Shown are pooled data of four independent experiments with means indicated in red. Statistical significance was assessed by Welch’s t-test. ****p < 0.0001. See also Figure S2. Scale bars, 10 µm.

    Article Snippet: Cells were treated with DMSO, 20 μM nocodazole (Sigma-Aldrich, M1404), 250 μM LLOMe (Merck, L7393) or 10 nM Torin2 (TargetMol, T6100) as indicated.

    Techniques: Infection, Knock-Out, Microscopy, Marker, Fluorescence, Derivative Assay, Comparison