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  • 94
    New England Biolabs bcli
    Construction of rv3852 knockout Mtb and verification by Southern blot and PCR. (A) Upper panel displays the genetic organization of the rv3852 region in Mtb (WT), Lower panel displays the same region with replacement of rv3852 by hygromycin resistance gene in rv3852 knockout Mtb (KO). Filled rectangle indicates the location of probe used in the Southern blot. Sites of digestion by <t>BclI</t> on genomic <t>DNA</t> from WT and KO as well as the sizes of the generated DNA fragment (a and b) are demonstrated under each panel. PCR products from genomic DNA from WT (1 and 2) and KO (3 and 4) are denoted. (B) Left, Southern blot of BclI digested genomic DNA from WT and KO. Calculated sizes of the fragments hybridizing with the probe were 3714 bp (WT) and 2916 bp (KO) as indicated in A. Right, PCR products from genomic DNA from WT and KO. The calculated sizes of the PCR products were 902 (Lane 1), 860 (Lane 2) for WT and 1322 (Lane 3), 1560 bp (Lane 4) for KO as indicated in A.
    Bcli, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 94/100, based on 354 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bcli/product/New England Biolabs
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    94
    Thermo Fisher bcli
    RFLP profiling of hsa-miR-196a-2 rs11614913 C > T (a) and hsa-miR-499 rs 3746444 T > C (b). 1a - 146 bp DNA fragment was amplified using PCR and incubated with <t>MspI</t> at 37°C for 12–16 hrs. Hsa-miR-196a-2 rs11614913 C > T genotype were deduced from migration profile on 2% agarose gel electrophoresis. Lane M shows 50bp molecular marker, wild type DNA visible in lane CC, heterozygous mutant in lane CT and homozygous mutant in lane TT. 1b - 149 bp DNA fragment was amplified using PCR, incubated with <t>BclI</t> at 37°C for 12–16 hrs, hsa-miR-499 rs 3746444 T > C genotype were deduced from migration profile on 2% agarose gel electrophoresis. Lane M shows 50bp molecular marker, wild type DNA visible in lane TT, heterozygous mutant in lane TC and homozygous mutant in lane CC.
    Bcli, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bcli/product/Thermo Fisher
    Average 94 stars, based on 71 article reviews
    Price from $9.99 to $1999.99
    bcli - by Bioz Stars, 2020-08
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    92
    Promega bcli
    Generation of vinculin A-deficient zebrafish mutants using TALENs. (A) Schematic representation of the endogenous <t>vcla</t> locus targeted by TALEN gene editing technology at the exon4-intron4 boundary. The TALEN arms flank a <t>BclI</t> restriction enzyme recognition site (highlighted in red) used for screening mutant alleles through restriction fragment length polymorphism (RFLP) analysis. (B) RFLP analysis of embryos injected with increasing dosages of vcla TALEN mRNA. Uncleaved bands represent efficient TALEN activity. (C) Summary of the range of mutations found at the vcla TALEN target locus in the F1 offspring of vcla TALEN-injected fish. Arrow denotes the mutation of the vcla mutant used in further experiments. (D) Sequence chromatograms from cDNA of wild-type vinculin (top) and of the vcla Δ8B mutant allele (bottom).
    Bcli, supplied by Promega, used in various techniques. Bioz Stars score: 92/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Millipore bcli
    Effect of <t>Bcl-x</t> L Bh4 4–23 (BCL; 5 × 10 −2 μg/ml, n = 6; A ) or <t>carbenoxolone</t> (100 μM, n = 5; B ) on ATP release from human erythrocytes incubated with isoproterenol. Erythrocytes were incubated with either the inhibitor or its respective vehicle, DMF or saline, for 25 min before addition of isoproterenol (1 μM). Values are means ± SE. *Different from respective baseline ( P
    Bcli, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bcli/product/Millipore
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    bcli  (Roche)
    90
    Roche bcli
    Effect of <t>Bcl-x</t> L Bh4 4–23 (BCL; 5 × 10 −2 μg/ml, n = 6; A ) or <t>carbenoxolone</t> (100 μM, n = 5; B ) on ATP release from human erythrocytes incubated with isoproterenol. Erythrocytes were incubated with either the inhibitor or its respective vehicle, DMF or saline, for 25 min before addition of isoproterenol (1 μM). Values are means ± SE. *Different from respective baseline ( P
    Bcli, supplied by Roche, used in various techniques. Bioz Stars score: 90/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Roche bcli restriction enzymes
    Effect of <t>Bcl-x</t> L Bh4 4–23 (BCL; 5 × 10 −2 μg/ml, n = 6; A ) or <t>carbenoxolone</t> (100 μM, n = 5; B ) on ATP release from human erythrocytes incubated with isoproterenol. Erythrocytes were incubated with either the inhibitor or its respective vehicle, DMF or saline, for 25 min before addition of isoproterenol (1 μM). Values are means ± SE. *Different from respective baseline ( P
    Bcli Restriction Enzymes, supplied by Roche, used in various techniques. Bioz Stars score: 85/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    New England Biolabs bcli restriction endonuclease
    Effect of <t>Bcl-x</t> L Bh4 4–23 (BCL; 5 × 10 −2 μg/ml, n = 6; A ) or <t>carbenoxolone</t> (100 μM, n = 5; B ) on ATP release from human erythrocytes incubated with isoproterenol. Erythrocytes were incubated with either the inhibitor or its respective vehicle, DMF or saline, for 25 min before addition of isoproterenol (1 μM). Values are means ± SE. *Different from respective baseline ( P
    Bcli Restriction Endonuclease, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 99/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Construction of rv3852 knockout Mtb and verification by Southern blot and PCR. (A) Upper panel displays the genetic organization of the rv3852 region in Mtb (WT), Lower panel displays the same region with replacement of rv3852 by hygromycin resistance gene in rv3852 knockout Mtb (KO). Filled rectangle indicates the location of probe used in the Southern blot. Sites of digestion by BclI on genomic DNA from WT and KO as well as the sizes of the generated DNA fragment (a and b) are demonstrated under each panel. PCR products from genomic DNA from WT (1 and 2) and KO (3 and 4) are denoted. (B) Left, Southern blot of BclI digested genomic DNA from WT and KO. Calculated sizes of the fragments hybridizing with the probe were 3714 bp (WT) and 2916 bp (KO) as indicated in A. Right, PCR products from genomic DNA from WT and KO. The calculated sizes of the PCR products were 902 (Lane 1), 860 (Lane 2) for WT and 1322 (Lane 3), 1560 bp (Lane 4) for KO as indicated in A.

    Journal: PLoS ONE

    Article Title: Identification of Rv3852 as an Agrimophol-Binding Protein in Mycobacterium tuberculosis

    doi: 10.1371/journal.pone.0126211

    Figure Lengend Snippet: Construction of rv3852 knockout Mtb and verification by Southern blot and PCR. (A) Upper panel displays the genetic organization of the rv3852 region in Mtb (WT), Lower panel displays the same region with replacement of rv3852 by hygromycin resistance gene in rv3852 knockout Mtb (KO). Filled rectangle indicates the location of probe used in the Southern blot. Sites of digestion by BclI on genomic DNA from WT and KO as well as the sizes of the generated DNA fragment (a and b) are demonstrated under each panel. PCR products from genomic DNA from WT (1 and 2) and KO (3 and 4) are denoted. (B) Left, Southern blot of BclI digested genomic DNA from WT and KO. Calculated sizes of the fragments hybridizing with the probe were 3714 bp (WT) and 2916 bp (KO) as indicated in A. Right, PCR products from genomic DNA from WT and KO. The calculated sizes of the PCR products were 902 (Lane 1), 860 (Lane 2) for WT and 1322 (Lane 3), 1560 bp (Lane 4) for KO as indicated in A.

    Article Snippet: For Southern blot analysis, genomic DNA from wild type Mtb and hygromycin resistant Mtb were digested by BclI (New England BioLabs) at 50°C overnight, run on the 1% agarose gel, transferred to the membrane (Amersham) and blotted by a designed probe.

    Techniques: Knock-Out, Southern Blot, Polymerase Chain Reaction, Generated

    DNase I hypersensitive sites of GFP transgenes. (A) Southern blot of two C-GFP and two A-GFP subclones. DNA from DNase I–digested cells was digested with Pst I and Bcl I and hybridized with a GFP probe. 0, 10, and 50 U DNase I are indicated by the filled horizontal arrows. (B) Ethidium bromide–stained gel of DNA fragments before hybridization for A. (C) An ovalbumin probe was used to reprobe the blot in A. (D) Vertical arrows indicate DNase I hypersensitive sites observed with GFP for C-GFP and A-GFP clones. The horizontal blue box indicates the probe. The experiment was repeated with DNase I digestion of different C-GFP and A-GFP cell clones showing no difference in DNase hypersensitivity.

    Journal: The Journal of Experimental Medicine

    Article Title: Attracting AID to targets of somatic hypermutation

    doi: 10.1084/jem.20090821

    Figure Lengend Snippet: DNase I hypersensitive sites of GFP transgenes. (A) Southern blot of two C-GFP and two A-GFP subclones. DNA from DNase I–digested cells was digested with Pst I and Bcl I and hybridized with a GFP probe. 0, 10, and 50 U DNase I are indicated by the filled horizontal arrows. (B) Ethidium bromide–stained gel of DNA fragments before hybridization for A. (C) An ovalbumin probe was used to reprobe the blot in A. (D) Vertical arrows indicate DNase I hypersensitive sites observed with GFP for C-GFP and A-GFP clones. The horizontal blue box indicates the probe. The experiment was repeated with DNase I digestion of different C-GFP and A-GFP cell clones showing no difference in DNase hypersensitivity.

    Article Snippet: Isolated DNA was digested with Pst I and Bcl I (New England Biolabs, Inc.), and a Sac I/BsrG I fragment from eGFP was used to make a probe using a random-priming synthesis kit (Roche) for Southern blot analysis.

    Techniques: Southern Blot, Staining, Hybridization, Clone Assay

    RFLP profiling of hsa-miR-196a-2 rs11614913 C > T (a) and hsa-miR-499 rs 3746444 T > C (b). 1a - 146 bp DNA fragment was amplified using PCR and incubated with MspI at 37°C for 12–16 hrs. Hsa-miR-196a-2 rs11614913 C > T genotype were deduced from migration profile on 2% agarose gel electrophoresis. Lane M shows 50bp molecular marker, wild type DNA visible in lane CC, heterozygous mutant in lane CT and homozygous mutant in lane TT. 1b - 149 bp DNA fragment was amplified using PCR, incubated with BclI at 37°C for 12–16 hrs, hsa-miR-499 rs 3746444 T > C genotype were deduced from migration profile on 2% agarose gel electrophoresis. Lane M shows 50bp molecular marker, wild type DNA visible in lane TT, heterozygous mutant in lane TC and homozygous mutant in lane CC.

    Journal: PLoS ONE

    Article Title: Association of miR-196a-2 and miR-499 variants with ulcerative colitis and their correlation with expression of respective miRNAs

    doi: 10.1371/journal.pone.0173447

    Figure Lengend Snippet: RFLP profiling of hsa-miR-196a-2 rs11614913 C > T (a) and hsa-miR-499 rs 3746444 T > C (b). 1a - 146 bp DNA fragment was amplified using PCR and incubated with MspI at 37°C for 12–16 hrs. Hsa-miR-196a-2 rs11614913 C > T genotype were deduced from migration profile on 2% agarose gel electrophoresis. Lane M shows 50bp molecular marker, wild type DNA visible in lane CC, heterozygous mutant in lane CT and homozygous mutant in lane TT. 1b - 149 bp DNA fragment was amplified using PCR, incubated with BclI at 37°C for 12–16 hrs, hsa-miR-499 rs 3746444 T > C genotype were deduced from migration profile on 2% agarose gel electrophoresis. Lane M shows 50bp molecular marker, wild type DNA visible in lane TT, heterozygous mutant in lane TC and homozygous mutant in lane CC.

    Article Snippet: Restriction digestion was carried out with 10U of MspI and BclI (Thermo Fisher Scientific, USA) restriction enzymes respectively at 37°C for 12–16 hr as per manufacturer’s instructions.

    Techniques: Amplification, Polymerase Chain Reaction, Incubation, Migration, Agarose Gel Electrophoresis, Marker, Mutagenesis

    2% Agarose gel electrophoresis of the BclI digested PCR product of Sarcocystis sp . M: 100-bp DNA ladder. Lane 1, 2, 5 – 7, 9 : S. cruzi , lane 3 – 4 : S. cruzi mixed with S. hirsuta , lane 8 : S. cruzi mixed with S. hominis

    Journal: Journal of Parasitic Diseases: Official Organ of the Indian Society for Parasitology

    Article Title: Molecular identification of Sarcocystis species in raw hamburgers using PCR–RFLP method in Kashan, central Iran

    doi: 10.1007/s12639-017-0925-3

    Figure Lengend Snippet: 2% Agarose gel electrophoresis of the BclI digested PCR product of Sarcocystis sp . M: 100-bp DNA ladder. Lane 1, 2, 5 – 7, 9 : S. cruzi , lane 3 – 4 : S. cruzi mixed with S. hirsuta , lane 8 : S. cruzi mixed with S. hominis

    Article Snippet: PCR products were digested with the restriction endonucleases BclI (Fermentas, Lithuania) to distinguish between species.

    Techniques: Agarose Gel Electrophoresis, Polymerase Chain Reaction

    Generation of vinculin A-deficient zebrafish mutants using TALENs. (A) Schematic representation of the endogenous vcla locus targeted by TALEN gene editing technology at the exon4-intron4 boundary. The TALEN arms flank a BclI restriction enzyme recognition site (highlighted in red) used for screening mutant alleles through restriction fragment length polymorphism (RFLP) analysis. (B) RFLP analysis of embryos injected with increasing dosages of vcla TALEN mRNA. Uncleaved bands represent efficient TALEN activity. (C) Summary of the range of mutations found at the vcla TALEN target locus in the F1 offspring of vcla TALEN-injected fish. Arrow denotes the mutation of the vcla mutant used in further experiments. (D) Sequence chromatograms from cDNA of wild-type vinculin (top) and of the vcla Δ8B mutant allele (bottom).

    Journal: PLoS ONE

    Article Title: Zygotic vinculin is not essential for embryonic development in zebrafish

    doi: 10.1371/journal.pone.0182278

    Figure Lengend Snippet: Generation of vinculin A-deficient zebrafish mutants using TALENs. (A) Schematic representation of the endogenous vcla locus targeted by TALEN gene editing technology at the exon4-intron4 boundary. The TALEN arms flank a BclI restriction enzyme recognition site (highlighted in red) used for screening mutant alleles through restriction fragment length polymorphism (RFLP) analysis. (B) RFLP analysis of embryos injected with increasing dosages of vcla TALEN mRNA. Uncleaved bands represent efficient TALEN activity. (C) Summary of the range of mutations found at the vcla TALEN target locus in the F1 offspring of vcla TALEN-injected fish. Arrow denotes the mutation of the vcla mutant used in further experiments. (D) Sequence chromatograms from cDNA of wild-type vinculin (top) and of the vcla Δ8B mutant allele (bottom).

    Article Snippet: To assess vcla mutant alleles, the PCR amplicons were incubated with BclI (Promega) at 50°C for 2 hrs, resulting in the generation of 504 bp and 179 bp fragments.

    Techniques: TALENs, Mutagenesis, Injection, Activity Assay, Fluorescence In Situ Hybridization, Sequencing

    Effect of Bcl-x L Bh4 4–23 (BCL; 5 × 10 −2 μg/ml, n = 6; A ) or carbenoxolone (100 μM, n = 5; B ) on ATP release from human erythrocytes incubated with isoproterenol. Erythrocytes were incubated with either the inhibitor or its respective vehicle, DMF or saline, for 25 min before addition of isoproterenol (1 μM). Values are means ± SE. *Different from respective baseline ( P

    Journal: American Journal of Physiology - Heart and Circulatory Physiology

    Article Title: Prostacyclin receptor-mediated ATP release from erythrocytes requires the voltage-dependent anion channel

    doi: 10.1152/ajpheart.00998.2011

    Figure Lengend Snippet: Effect of Bcl-x L Bh4 4–23 (BCL; 5 × 10 −2 μg/ml, n = 6; A ) or carbenoxolone (100 μM, n = 5; B ) on ATP release from human erythrocytes incubated with isoproterenol. Erythrocytes were incubated with either the inhibitor or its respective vehicle, DMF or saline, for 25 min before addition of isoproterenol (1 μM). Values are means ± SE. *Different from respective baseline ( P

    Article Snippet: Isolated human erythrocytes diluted to a 20% hematocrit were incubated with isoproterenol (1 μM) or its vehicle (saline) in the presence of a 25-min pretreatment with either BCL (5 × 10−2 μg/ml) or carbenoxolone (Carb; 100 μM; Sigma) or their respective vehicles (DMF or saline).

    Techniques: Incubation

    Inducible deletion of Bcl-x L enhances β-cell glucose signaling. A : Quantification of Bcl-x L and Bcl-2 mRNA levels by quantitative PCR (qPCR) ( n = 3) and Bcl-x L protein by Western blot ( n = 6) in islets from tamoxifen-injected Bcl-x flox/flox :Pdx1-CreER (Bcl-x βKO) mice relative to islets from tamoxifen-injected littermate Bcl-x flox/flox (Bcl-x WT) mice (data are mean ± SEM; * P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Inducible deletion of Bcl-x L enhances β-cell glucose signaling. A : Quantification of Bcl-x L and Bcl-2 mRNA levels by quantitative PCR (qPCR) ( n = 3) and Bcl-x L protein by Western blot ( n = 6) in islets from tamoxifen-injected Bcl-x flox/flox :Pdx1-CreER (Bcl-x βKO) mice relative to islets from tamoxifen-injected littermate Bcl-x flox/flox (Bcl-x WT) mice (data are mean ± SEM; * P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Real-time Polymerase Chain Reaction, Western Blot, Injection, Mouse Assay

    Loss of Bcl-2 enhances β-cell glucose responses. A : Quantitative PCR (qPCR) quantification of Bcl-2 and Bcl-x L mRNA levels in islets from Bcl-2 +/− and Bcl-2 −/− mice relative to Bcl-2 +/+ littermates ( n = 3 mice of each genotype). All data are mean ± SEM. B : Average cytosolic Ca 2+ levels of dispersed islet cells from littermate Bcl-2 +/+ , Bcl-2 +/− , and Bcl-2 −/− mice. Shaded hanging bars represent SEM. C : Incremental area under the curve of Ca 2+ responses ( n = 98 Bcl-2 +/+ cells, n = 144 Bcl-2 +/− cells, and n = 147 Bcl-2 −/− cells from three mice of each genotype; * P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Loss of Bcl-2 enhances β-cell glucose responses. A : Quantitative PCR (qPCR) quantification of Bcl-2 and Bcl-x L mRNA levels in islets from Bcl-2 +/− and Bcl-2 −/− mice relative to Bcl-2 +/+ littermates ( n = 3 mice of each genotype). All data are mean ± SEM. B : Average cytosolic Ca 2+ levels of dispersed islet cells from littermate Bcl-2 +/+ , Bcl-2 +/− , and Bcl-2 −/− mice. Shaded hanging bars represent SEM. C : Incremental area under the curve of Ca 2+ responses ( n = 98 Bcl-2 +/+ cells, n = 144 Bcl-2 +/− cells, and n = 147 Bcl-2 −/− cells from three mice of each genotype; * P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Real-time Polymerase Chain Reaction, Mouse Assay

    Bcl-2/Bcl-x L inhibition triggers cytosolic Ca 2+ fluctuations. A and B : Cytosolic Ca 2+ responses of groups of mouse islet cells exposed to Bcl-2/Bcl-x L inhibitors C6 and YC137 in the presence of 3 mmol/L glucose. C and D : Representative cytosolic Ca 2+ responses to C6 in human islet cells ( n = 66 cells from three islet preparations) and MIN6 β-cells ( n = 34 cells). E : Quantification of the percentage of baseline quiescent mouse islet cells that responded within 30 min to various doses of C6 in the presence of either 3 or 0 mmol/L glucose ( n = 3–6 for each condition; * P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Bcl-2/Bcl-x L inhibition triggers cytosolic Ca 2+ fluctuations. A and B : Cytosolic Ca 2+ responses of groups of mouse islet cells exposed to Bcl-2/Bcl-x L inhibitors C6 and YC137 in the presence of 3 mmol/L glucose. C and D : Representative cytosolic Ca 2+ responses to C6 in human islet cells ( n = 66 cells from three islet preparations) and MIN6 β-cells ( n = 34 cells). E : Quantification of the percentage of baseline quiescent mouse islet cells that responded within 30 min to various doses of C6 in the presence of either 3 or 0 mmol/L glucose ( n = 3–6 for each condition; * P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Inhibition

    Effect of Bcl antagonism in Bax, Bak, and Bcl-x L –deficient islet cells. A : Percentage of islet cells responding to Bcl antagonism in preparations from Bax −/− ( left ), Bak −/− ( right ), and their wild-type control mice ( n = 3 mice). Data are mean ± SEM. Basal glucose was 3 mmol/L in all experiments. B : Western blot demonstrating global Bak deficiency and islet specific Bax knockout in tamoxifen-injected Bak −/− :Bax flox/flox :Pdx1-CreER (Bax-Bak βDKO) mice relative to tamoxifen-injected Bak −/− :Bax flox/flox and C57BL6/J (C57) mice. C : Bax protein levels were reduced by 85% in Bax-Bak βDKO islets ( n = 6; ** P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Effect of Bcl antagonism in Bax, Bak, and Bcl-x L –deficient islet cells. A : Percentage of islet cells responding to Bcl antagonism in preparations from Bax −/− ( left ), Bak −/− ( right ), and their wild-type control mice ( n = 3 mice). Data are mean ± SEM. Basal glucose was 3 mmol/L in all experiments. B : Western blot demonstrating global Bak deficiency and islet specific Bax knockout in tamoxifen-injected Bak −/− :Bax flox/flox :Pdx1-CreER (Bax-Bak βDKO) mice relative to tamoxifen-injected Bak −/− :Bax flox/flox and C57BL6/J (C57) mice. C : Bax protein levels were reduced by 85% in Bax-Bak βDKO islets ( n = 6; ** P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Mouse Assay, Western Blot, Knock-Out, Injection

    Small-molecule inhibition of Bcl-2/Bcl-x L rapidly displaces Bad and eventually induces mitochondrial apoptosis. A : Top : Western blot illustrating the loss of Bcl-x L coimmunoprecipitation with Bad in MIN6 β-cells treated with C6. Bottom : Densitometric quantification of the ratio of Bcl-x L to Bad protein in Bad immunoprecipitates after various durations of C6 exposure. Data (mean ± SEM) are normalized to control ( n = 3–5; * P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Small-molecule inhibition of Bcl-2/Bcl-x L rapidly displaces Bad and eventually induces mitochondrial apoptosis. A : Top : Western blot illustrating the loss of Bcl-x L coimmunoprecipitation with Bad in MIN6 β-cells treated with C6. Bottom : Densitometric quantification of the ratio of Bcl-x L to Bad protein in Bad immunoprecipitates after various durations of C6 exposure. Data (mean ± SEM) are normalized to control ( n = 3–5; * P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Inhibition, Western Blot

    Differential subcellular distribution of Bcl-2 and Bcl-x L in β-cells. A and B : Representative images of MIN6 cells expressing GFP-tagged Bcl-2 and YFP-tagged Bcl-x L and loaded with 100 nmol/L MitoTracker Red. C : MIN6 cell coexpressing Bcl-x L :YFP and ER-targeted monomeric red fluorescent protein (mRFP). D : Pearson correlation coefficient (coeff.) quantifying colocalization of Bcl-x L :YFP with mitochondrial dsRed ( n = 6) or ER mRFP ( n = 5) and Bcl-2:GFP with ER mRFP ( n = 5) in MIN6 β-cells (* P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Differential subcellular distribution of Bcl-2 and Bcl-x L in β-cells. A and B : Representative images of MIN6 cells expressing GFP-tagged Bcl-2 and YFP-tagged Bcl-x L and loaded with 100 nmol/L MitoTracker Red. C : MIN6 cell coexpressing Bcl-x L :YFP and ER-targeted monomeric red fluorescent protein (mRFP). D : Pearson correlation coefficient (coeff.) quantifying colocalization of Bcl-x L :YFP with mitochondrial dsRed ( n = 6) or ER mRFP ( n = 5) and Bcl-2:GFP with ER mRFP ( n = 5) in MIN6 β-cells (* P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Expressing

    Bcl-2/Bcl-x L antagonism stimulates β-cell mitochondrial metabolism, K ATP -dependent Ca 2+ entry, and insulin secretion. A : Representative recording of ER Ca 2+ changes in MIN6 β-cells exposed to C6 and carbachol (Cch) ( n = 6 cells). Inset: MIN6 cell expressing the ER-targeted D1ER Ca 2+ sensor. B : Lack of C6-induced Ca 2+ influx in the absence of extracellular Ca 2+ . The basally active cell illustrates the rapid loss of Ca 2+ entry upon Ca 2+ removal. C : Nifedipine blocks ongoing C6-induced Ca 2+ influx ( n = 14 cells). D : Quantification of nifedipine, diazoxide (Dz), and CCCP-mediated suppression of cytosolic Ca 2+ responses in mouse islet cells exposed to C6 or YC137 ( n = 3). E : Insulin secretion from dispersed islet-cells treated with C6, diazoxide, and/or tolbutamide (Tolb) ( n = 5). * P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Bcl-2/Bcl-x L antagonism stimulates β-cell mitochondrial metabolism, K ATP -dependent Ca 2+ entry, and insulin secretion. A : Representative recording of ER Ca 2+ changes in MIN6 β-cells exposed to C6 and carbachol (Cch) ( n = 6 cells). Inset: MIN6 cell expressing the ER-targeted D1ER Ca 2+ sensor. B : Lack of C6-induced Ca 2+ influx in the absence of extracellular Ca 2+ . The basally active cell illustrates the rapid loss of Ca 2+ entry upon Ca 2+ removal. C : Nifedipine blocks ongoing C6-induced Ca 2+ influx ( n = 14 cells). D : Quantification of nifedipine, diazoxide (Dz), and CCCP-mediated suppression of cytosolic Ca 2+ responses in mouse islet cells exposed to C6 or YC137 ( n = 3). E : Insulin secretion from dispersed islet-cells treated with C6, diazoxide, and/or tolbutamide (Tolb) ( n = 5). * P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Expressing

    Improved glucose tolerance in Bcl-x βKO mice. A : In vivo insulin secretion following intraperitoneal injection of 2 g/kg glucose in 10–12-week-old Bcl-x WT and βKO littermate mice ( n = 5). B and C : Intraperitoneal glucose tolerance tests of Bcl-x βKO and WT mice using 2 and 0.5 g/kg glucose doses ( n = 7 and n = 8, respectively; * P

    Journal: Diabetes

    Article Title: Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic ?-Cells

    doi: 10.2337/db11-1464

    Figure Lengend Snippet: Improved glucose tolerance in Bcl-x βKO mice. A : In vivo insulin secretion following intraperitoneal injection of 2 g/kg glucose in 10–12-week-old Bcl-x WT and βKO littermate mice ( n = 5). B and C : Intraperitoneal glucose tolerance tests of Bcl-x βKO and WT mice using 2 and 0.5 g/kg glucose doses ( n = 7 and n = 8, respectively; * P

    Article Snippet: Ablation of Bcl-x and Bax was achieved by injecting Pdx1-CreER–positive animals and littermate controls with 3 mg/40 g of tamoxifen (Sigma-Aldrich) on 5 consecutive days.

    Techniques: Mouse Assay, In Vivo, Injection

    Effect of melatonin pre-treatment on anti and pro-apoptotic proteins expression of testes in mice exposed to whole-body 60 Co γ-irradiation. Western blot was performed to measured both the anti (ATM, p53, p21, Bax, Bcl-x, cytochrome C, active caspases-3 and caspases-9 proteins) and pro (Bcl-xL)-apoptotic proteins expression after 2h, 4h and 8h post-irradiation. The β-actin protein was used as loading control. * p

    Journal: Journal of Biomedical Science

    Article Title: Radioprotective potential of melatonin against 60Co γ-ray-induced testicular injury in male C57BL/6 mice

    doi: 10.1186/s12929-015-0156-9

    Figure Lengend Snippet: Effect of melatonin pre-treatment on anti and pro-apoptotic proteins expression of testes in mice exposed to whole-body 60 Co γ-irradiation. Western blot was performed to measured both the anti (ATM, p53, p21, Bax, Bcl-x, cytochrome C, active caspases-3 and caspases-9 proteins) and pro (Bcl-xL)-apoptotic proteins expression after 2h, 4h and 8h post-irradiation. The β-actin protein was used as loading control. * p

    Article Snippet: Antioxidants and chemicals Melatonin (N-acetyl-5-methoxytryptamine), soybean oil, Bradford reagent, PMSF, BSA, propidium iodide, protease inhibitor cocktail, anti-p53, anti-Bax, anti-Bcl-x, HRP-conjugate and formalin were procured from Sigma-Aldrich Chemical Co., St. Louis, MO, USA.

    Techniques: Expressing, Mouse Assay, Irradiation, Western Blot

    Kaplan-Meier chart showing event-free survival for the Bcl I genotype (A) , the N363S genotype (B) , and the α/β isoform expression ratio (C) .

    Journal: Blood research

    Article Title: The prognostic value of glucocorticoid receptors for adult acute lymphoblastic leukemia

    doi: 10.5045/br.2015.50.4.235

    Figure Lengend Snippet: Kaplan-Meier chart showing event-free survival for the Bcl I genotype (A) , the N363S genotype (B) , and the α/β isoform expression ratio (C) .

    Article Snippet: To determine Bcl I polymorphism genotypes, 20 µL of relevant PCR product (335 bp) was digested by 20 units of Bcl I restriction endonuclease (Sigma-Aldrich, UK) for 1.5 hours at 50℃.

    Techniques: Expressing

    (A) Lanes 1-4 represent polymerase chain reaction (PCR) products for Bcl I polymorphism from 4 acute lymphoblastic leukemia (ALL) patients (335 base pairs (bp)). (B) Restriction fragment length polymorphism-digested PCR products for Bcl I polymorphism from ALL patients. Lanes 1 and 2 represent restriction fragments of PCR products for ALL patients with the CC genotype (222, 117 bp). Lanes 3 and 4 represent restriction PCR products for ALL patients with the CG genotype (335, 222, 117 bp). (C) Lanes 1-4 represent PCR products for N363S polymorphism from ALL patients (248 bp). Lane M represents the 100 bp ladder marker.

    Journal: Blood research

    Article Title: The prognostic value of glucocorticoid receptors for adult acute lymphoblastic leukemia

    doi: 10.5045/br.2015.50.4.235

    Figure Lengend Snippet: (A) Lanes 1-4 represent polymerase chain reaction (PCR) products for Bcl I polymorphism from 4 acute lymphoblastic leukemia (ALL) patients (335 base pairs (bp)). (B) Restriction fragment length polymorphism-digested PCR products for Bcl I polymorphism from ALL patients. Lanes 1 and 2 represent restriction fragments of PCR products for ALL patients with the CC genotype (222, 117 bp). Lanes 3 and 4 represent restriction PCR products for ALL patients with the CG genotype (335, 222, 117 bp). (C) Lanes 1-4 represent PCR products for N363S polymorphism from ALL patients (248 bp). Lane M represents the 100 bp ladder marker.

    Article Snippet: To determine Bcl I polymorphism genotypes, 20 µL of relevant PCR product (335 bp) was digested by 20 units of Bcl I restriction endonuclease (Sigma-Aldrich, UK) for 1.5 hours at 50℃.

    Techniques: Polymerase Chain Reaction, Marker

    ( a) Human MM cell lines demonstrate differential expression of Bcl-2 prosurvival proteins. JJN3, OPM-2, RPMI-8226 and U266 were assessed for the expression of antiapoptotic Bcl-2 proteins by western blot: Bcl-2, Bcl-X L , Bcl-W, Mcl-1 and A1. ( b ) Differential sensitivities of human MM cell lines to ABT-737. Single-agent dose–response curves were constructed in human MM cell lines (JJN3, OPM-2, RPMI-8226 and U266) treated with ABT-737 for 24 and 48 h. ( c ) Synergistic induction of apoptosis in human MM cell lines JJN3, OPM-2, RPMI-8226 and U266 following 48 h treatment with panobinostat in combination with ABT-737 after 48 h incubation. * P

    Journal: Cell Death & Disease

    Article Title: Preclinical screening of histone deacetylase inhibitors combined with ABT-737, rhTRAIL/MD5-1 or 5-azacytidine using syngeneic Vk*MYC multiple myeloma

    doi: 10.1038/cddis.2013.306

    Figure Lengend Snippet: ( a) Human MM cell lines demonstrate differential expression of Bcl-2 prosurvival proteins. JJN3, OPM-2, RPMI-8226 and U266 were assessed for the expression of antiapoptotic Bcl-2 proteins by western blot: Bcl-2, Bcl-X L , Bcl-W, Mcl-1 and A1. ( b ) Differential sensitivities of human MM cell lines to ABT-737. Single-agent dose–response curves were constructed in human MM cell lines (JJN3, OPM-2, RPMI-8226 and U266) treated with ABT-737 for 24 and 48 h. ( c ) Synergistic induction of apoptosis in human MM cell lines JJN3, OPM-2, RPMI-8226 and U266 following 48 h treatment with panobinostat in combination with ABT-737 after 48 h incubation. * P

    Article Snippet: Western blotting antibodies included: anti-acetylated histone H3 (Millipore, Billerica, MA, USA); anti-hBcl-2 (SantaCruz Biotechnology, SantaCruz, CA, USA); anti-mBcl-2 (BD Pharmingen, North Ryde, NSW, Australia), anti-hBcl-xL (BD Pharmingen); anti-Mcl-1 (BD Pharmingen); anti-Bcl2-A1 (J Borst, The Netherlands Cancer Institute, Amsterdam, The Netherlands); anti-Bcl-w (16H12, Millipore); anti-hDR-4 and -hDR-5 (Imgenex, San Diego, CA, USA); anti-mDR-5 (BD Pharmingen); and anti-cFLIPL NF6 (Alexis, Sapphire Biosciences, Waterloo, NSW, Australia).

    Techniques: Expressing, Western Blot, Construct, Incubation

    Bcl-w is a pericyte-induced antiapoptotic protein in ECs. (A-B) Expression of Bcl-w in ECs (A) or OCs (B) comprising cancer cells, pericytes, macrophages, and infrequent cancer-associated fibroblastic cells fractionated from PNET tumors excised from RIP1-Tag2

    Journal: Blood

    Article Title: Pericytes promote endothelial cell survival through induction of autocrine VEGF-A signaling and Bcl-w expression

    doi: 10.1182/blood-2011-01-331694

    Figure Lengend Snippet: Bcl-w is a pericyte-induced antiapoptotic protein in ECs. (A-B) Expression of Bcl-w in ECs (A) or OCs (B) comprising cancer cells, pericytes, macrophages, and infrequent cancer-associated fibroblastic cells fractionated from PNET tumors excised from RIP1-Tag2

    Article Snippet: Western blotting was performed using antibodies against Bcl-w (AB1723, 5μg/mL; Chemicon) and VEGF-A (MAB493, 1 μg/mL; R & D Systems) with β-actin (GTX26276, 1:5000; GeneTex) serving as loading control.

    Techniques: Expressing

    A coculture system reveals the functional significance of crosstalk between ECs and pericytes. (A,B) Quantitative RT-PCR analysis of Bcl-w (A) and VEGF-A (B) expression in MS1 endothelial cells cultured alone or together with HBVPs for 96 hours, either

    Journal: Blood

    Article Title: Pericytes promote endothelial cell survival through induction of autocrine VEGF-A signaling and Bcl-w expression

    doi: 10.1182/blood-2011-01-331694

    Figure Lengend Snippet: A coculture system reveals the functional significance of crosstalk between ECs and pericytes. (A,B) Quantitative RT-PCR analysis of Bcl-w (A) and VEGF-A (B) expression in MS1 endothelial cells cultured alone or together with HBVPs for 96 hours, either

    Article Snippet: Western blotting was performed using antibodies against Bcl-w (AB1723, 5μg/mL; Chemicon) and VEGF-A (MAB493, 1 μg/mL; R & D Systems) with β-actin (GTX26276, 1:5000; GeneTex) serving as loading control.

    Techniques: Functional Assay, Quantitative RT-PCR, Expressing, Cell Culture

    The crosstalk between pericytes and ECs is mediated by integrin α v activity. (A,B) Quantitative RT-PCR analysis of Bcl-w (A) and VEGF-A (B) expression in MS1 endothelial cells cultured alone or together with HBVPs for 96 hours in the presence

    Journal: Blood

    Article Title: Pericytes promote endothelial cell survival through induction of autocrine VEGF-A signaling and Bcl-w expression

    doi: 10.1182/blood-2011-01-331694

    Figure Lengend Snippet: The crosstalk between pericytes and ECs is mediated by integrin α v activity. (A,B) Quantitative RT-PCR analysis of Bcl-w (A) and VEGF-A (B) expression in MS1 endothelial cells cultured alone or together with HBVPs for 96 hours in the presence

    Article Snippet: Western blotting was performed using antibodies against Bcl-w (AB1723, 5μg/mL; Chemicon) and VEGF-A (MAB493, 1 μg/mL; R & D Systems) with β-actin (GTX26276, 1:5000; GeneTex) serving as loading control.

    Techniques: Activity Assay, Quantitative RT-PCR, Expressing, Cell Culture