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  • 90
    Cayman Chemical bml 111
    <t>BML-111</t> alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
    Bml 111, supplied by Cayman Chemical, 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/result/bml 111/product/Cayman Chemical
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bml 111 - by Bioz Stars, 2022-10
    90/100 stars
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    95
    Millipore β lactoglobulin
    Comparison of Δh ads values for the adsorption of BSA and <t>β‐lactoglobulin</t> to Butyl Sepharose 4 FF at 1.2 mol/kg (NH 4 ) 2 SO 4 . Adsorption of BSA (A) and β‐lactoglobulin (B) at 308 K. Adsorption of BSA (C) and β‐lactoglobulin (D) at 303 K. Adsorption of BSA (E) and β‐lactoglobulin (F) at 298 K
    β Lactoglobulin, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/β lactoglobulin/product/Millipore
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    β lactoglobulin - by Bioz Stars, 2022-10
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    93
    Enzo Biochem caspase 8
    Caspase 3 and <t>caspase</t> 8 activities following TNF treatment are enhanced in TNF-sensitive and repressed in TNF-resistant cells. A) Caspase 3 activity. U2OSE6AS (coding for the antisense version of HA-E6), U2OSE66 (E6-expressing, TNF-sensitive) and U2OSE612 (E6-expressing, TNF-resistant) cells were treated with TNF (5 ng/ml) in the presence of cycloheximide (5 μg/ml) for the times indicated and then lysed. Lysates were analyzed for caspase 3 activity using DEVD-AMC as the substrate in the presence and absence of the caspase 3 inhibitor DEVD-CHO. The activity in wells containing the inhibitor was subtracted from that in wells lacking the inhibitor. Activity is expressed as the percentage of caspase activity in untreated U2OSE6AS cells. Each time point was measured in triplicate, and error bars represent the standard deviation. The Student’s one-tailed t test was used to determine statistical significance of the differences between U2OSE6AS and U2OSE66 cells, with * representing a 0.95 level of confidence. C) U2OSE6AS, U2OSE66 and U2OSE612 cells were treated and lysed as described in A, then analyzed for caspase 8 activity using IETD-AMC as the substrate in the presence and absence of the caspase 8 inhibitor IETD-CHO. Data was analyzed as in (A), with the exception that values were normalized to the value of U2OSE6AS cells at 1.5 hrs rather than at 0 hrs. The Student’s one-tailed t test was used to determine statistical significance of the differences between U2OSE6AS and U2OSE66 cells, with * representing a 0.95 level of confidence.
    Caspase 8, supplied by Enzo Biochem, 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/result/caspase 8/product/Enzo Biochem
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    Image Search Results


    BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

    Article Snippet: As shown in Fig. a, LPS minimally affected, yet BML-111 alone potently elevated the LC3-II level and thus the LC3-II/LC3-I ratio (P < 0.05, when comparing LPS-treated or BML-111-trated cells with control cells).

    Techniques: In Vivo, Staining

    The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

    Article Snippet: As shown in Fig. a, LPS minimally affected, yet BML-111 alone potently elevated the LC3-II level and thus the LC3-II/LC3-I ratio (P < 0.05, when comparing LPS-treated or BML-111-trated cells with control cells).

    Techniques: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

    BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

    Article Snippet: As shown in Fig. a, LPS minimally affected, yet BML-111 alone potently elevated the LC3-II level and thus the LC3-II/LC3-I ratio (P < 0.05, when comparing LPS-treated or BML-111-trated cells with control cells).

    Techniques: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

    BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

    Article Snippet: As shown in Fig. a, LPS minimally affected, yet BML-111 alone potently elevated the LC3-II level and thus the LC3-II/LC3-I ratio (P < 0.05, when comparing LPS-treated or BML-111-trated cells with control cells).

    Techniques: Affinity Magnetic Separation, Expressing, Western Blot

    BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

    Article Snippet: As shown in Fig. a, LPS minimally affected, yet BML-111 alone potently elevated the LC3-II level and thus the LC3-II/LC3-I ratio (P < 0.05, when comparing LPS-treated or BML-111-trated cells with control cells).

    Techniques: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

    BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

    Article Snippet: As shown in Fig. a, LPS minimally affected, yet BML-111 alone potently elevated the LC3-II level and thus the LC3-II/LC3-I ratio (P < 0.05, when comparing LPS-treated or BML-111-trated cells with control cells).

    Techniques: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

    Comparison of Δh ads values for the adsorption of BSA and β‐lactoglobulin to Butyl Sepharose 4 FF at 1.2 mol/kg (NH 4 ) 2 SO 4 . Adsorption of BSA (A) and β‐lactoglobulin (B) at 308 K. Adsorption of BSA (C) and β‐lactoglobulin (D) at 303 K. Adsorption of BSA (E) and β‐lactoglobulin (F) at 298 K

    Journal: Journal of Separation Science

    Article Title: Hydrophobic interaction chromatography of proteins: Studies of unfolding upon adsorption by isothermal titration calorimetry. Hydrophobic interaction chromatography of proteins: Studies of unfolding upon adsorption by isothermal titration calorimetry

    doi: 10.1002/jssc.201800016

    Figure Lengend Snippet: Comparison of Δh ads values for the adsorption of BSA and β‐lactoglobulin to Butyl Sepharose 4 FF at 1.2 mol/kg (NH 4 ) 2 SO 4 . Adsorption of BSA (A) and β‐lactoglobulin (B) at 308 K. Adsorption of BSA (C) and β‐lactoglobulin (D) at 303 K. Adsorption of BSA (E) and β‐lactoglobulin (F) at 298 K

    Article Snippet: BSA (A6003; essentially fatty acid free) and β‐lactoglobulin (L3908) were purchased from Sigma–Aldrich (Vienna, Austria).

    Techniques: Adsorption

    Values of Δh ads for the adsorption of BSA and β‐lactoglobulin to Toyopearl Butyl‐650 M at an (NH 4 ) 2 SO 4 concentration of 1.2 mol/kg (A and C) and at 0.7 mol/kg (NH 4 ) 2 SO 4 (B and D)

    Journal: Journal of Separation Science

    Article Title: Hydrophobic interaction chromatography of proteins: Studies of unfolding upon adsorption by isothermal titration calorimetry. Hydrophobic interaction chromatography of proteins: Studies of unfolding upon adsorption by isothermal titration calorimetry

    doi: 10.1002/jssc.201800016

    Figure Lengend Snippet: Values of Δh ads for the adsorption of BSA and β‐lactoglobulin to Toyopearl Butyl‐650 M at an (NH 4 ) 2 SO 4 concentration of 1.2 mol/kg (A and C) and at 0.7 mol/kg (NH 4 ) 2 SO 4 (B and D)

    Article Snippet: BSA (A6003; essentially fatty acid free) and β‐lactoglobulin (L3908) were purchased from Sigma–Aldrich (Vienna, Austria).

    Techniques: Adsorption, Concentration Assay

    Caspase 3 and caspase 8 activities following TNF treatment are enhanced in TNF-sensitive and repressed in TNF-resistant cells. A) Caspase 3 activity. U2OSE6AS (coding for the antisense version of HA-E6), U2OSE66 (E6-expressing, TNF-sensitive) and U2OSE612 (E6-expressing, TNF-resistant) cells were treated with TNF (5 ng/ml) in the presence of cycloheximide (5 μg/ml) for the times indicated and then lysed. Lysates were analyzed for caspase 3 activity using DEVD-AMC as the substrate in the presence and absence of the caspase 3 inhibitor DEVD-CHO. The activity in wells containing the inhibitor was subtracted from that in wells lacking the inhibitor. Activity is expressed as the percentage of caspase activity in untreated U2OSE6AS cells. Each time point was measured in triplicate, and error bars represent the standard deviation. The Student’s one-tailed t test was used to determine statistical significance of the differences between U2OSE6AS and U2OSE66 cells, with * representing a 0.95 level of confidence. C) U2OSE6AS, U2OSE66 and U2OSE612 cells were treated and lysed as described in A, then analyzed for caspase 8 activity using IETD-AMC as the substrate in the presence and absence of the caspase 8 inhibitor IETD-CHO. Data was analyzed as in (A), with the exception that values were normalized to the value of U2OSE6AS cells at 1.5 hrs rather than at 0 hrs. The Student’s one-tailed t test was used to determine statistical significance of the differences between U2OSE6AS and U2OSE66 cells, with * representing a 0.95 level of confidence.

    Journal: Cell death and differentiation

    Article Title: The Human Papillomavirus 16 E6 Protein Can Either Protect or Further Sensitize Cells to TNF: Effect of Dose (HPV E6 Sensitizes and Protects Cells from TNF)

    doi: 10.1038/sj.cdd.4401678

    Figure Lengend Snippet: Caspase 3 and caspase 8 activities following TNF treatment are enhanced in TNF-sensitive and repressed in TNF-resistant cells. A) Caspase 3 activity. U2OSE6AS (coding for the antisense version of HA-E6), U2OSE66 (E6-expressing, TNF-sensitive) and U2OSE612 (E6-expressing, TNF-resistant) cells were treated with TNF (5 ng/ml) in the presence of cycloheximide (5 μg/ml) for the times indicated and then lysed. Lysates were analyzed for caspase 3 activity using DEVD-AMC as the substrate in the presence and absence of the caspase 3 inhibitor DEVD-CHO. The activity in wells containing the inhibitor was subtracted from that in wells lacking the inhibitor. Activity is expressed as the percentage of caspase activity in untreated U2OSE6AS cells. Each time point was measured in triplicate, and error bars represent the standard deviation. The Student’s one-tailed t test was used to determine statistical significance of the differences between U2OSE6AS and U2OSE66 cells, with * representing a 0.95 level of confidence. C) U2OSE6AS, U2OSE66 and U2OSE612 cells were treated and lysed as described in A, then analyzed for caspase 8 activity using IETD-AMC as the substrate in the presence and absence of the caspase 8 inhibitor IETD-CHO. Data was analyzed as in (A), with the exception that values were normalized to the value of U2OSE6AS cells at 1.5 hrs rather than at 0 hrs. The Student’s one-tailed t test was used to determine statistical significance of the differences between U2OSE6AS and U2OSE66 cells, with * representing a 0.95 level of confidence.

    Article Snippet: Caspase activity was then measured using the fluorogenic substrate DEVD-AMC for caspase 3 and IETD-AMC for caspase 8 (Alexis Biochemicals) as described ( ).

    Techniques: Activity Assay, Expressing, Standard Deviation, One-tailed Test