functional protein domains Search Results


91
ProSci Incorporated bax
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
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Gilson Inc coiled-coil protein with a functional grip domain
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
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InterPro Inc protein families and functional domains by
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Protein Families And Functional Domains By, supplied by InterPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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InterPro Inc integrated resource of protein families, domains and functional sites database of uniprot consortium (interpro)
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Integrated Resource Of Protein Families, Domains And Functional Sites Database Of Uniprot Consortium (Interpro), supplied by InterPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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InterPro Inc functional and structural annotations for protein families, domains and functional sites
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Functional And Structural Annotations For Protein Families, Domains And Functional Sites, supplied by InterPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BioMimetic Therapeutics functionalized transmembrane domains of receptor proteins
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Functionalized Transmembrane Domains Of Receptor Proteins, supplied by BioMimetic Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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InterPro Inc protein of unknown function upf0089
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Protein Of Unknown Function Upf0089, supplied by InterPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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InterPro Inc motifs and functional domains conserved along the protein sequence
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Motifs And Functional Domains Conserved Along The Protein Sequence, supplied by InterPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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InterPro Inc predicted functional protein domains
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Predicted Functional Protein Domains, supplied by InterPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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InterPro Inc functional domain analysis of adam10 protein sequence
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
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InterPro Inc mapping of the detected protein domains and functional sites to go terms
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
Mapping Of The Detected Protein Domains And Functional Sites To Go Terms, supplied by InterPro Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Verlag GmbH protein structure and functional domains
Activation <t>of</t> <t>p53</t> and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, <t>Bax,</t> and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.
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Image Search Results


Activation of p53 and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, Bax, and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Journal: The Journal of Neuroscience

Article Title: Downregulation of miR-23a and miR-27a following Experimental Traumatic Brain Injury Induces Neuronal Cell Death through Activation of Proapoptotic Bcl-2 Proteins

doi: 10.1523/JNEUROSCI.1260-14.2014

Figure Lengend Snippet: Activation of p53 and increased protein expression of proapoptotic Bcl2 molecules after TBI. Western blot analysis of the level of proapoptotic proteins in mouse-injured cortex after TBI. Tissue lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against p53, phosphorylated p53 (Ser 15), PUMA, Noxa, Bax, and β-actin. Levels of p53, phosphorylated p53 (Ser 15), PUMA, Noxa, and Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus sham (N = 4). **p < 0.01 versus sham (N = 4). ***p < 0.001 versus sham (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Article Snippet: Abcam: V5 (ab27674); Histone H2A.X (ab11175); Santa Cruz Biotechnology: AIF (sc-13116); Apaf-1 (sc-65890); cytochrome c (sc-13560); FAS (sc-716); Bim (sc-11425); Cell Signaling Technology: Cleaved Caspase-3 (#9661); Cleaved PARP (#9545); Phospho-Histone H2A.X (Ser139) (#9718); Phospho-p53 (Ser15) (#9284); p53 (1C12) (#2524); Bax (#2772); XIAP (#2042); Enzo Life Sciences: GAPDH (ADI-CSA-335); Bax (active monomer) (ALX-804-224-C100); α-fodrin (BML-FG6090); ProSci: PUMA (#3041); Noxa (#2437); EMD Millipore: Bak (06-536); Sigma: β-actin (A1978).

Techniques: Activation Assay, Expressing, Western Blot

mRNA and protein levels of proapoptotic members of Bcl-2 family were increased in etoposide-treated primary cortical neurons. A, qPCR quantification of expression of proapoptotic genes: Noxa, Puma, and Bax in primary cortical neurons at different time points after etoposide treatment. Level of gene expression was normalized to GAPDH expression. Neuronal apoptosis were induced by etoposide as described above. Data are mean ± SD. *p < 0.05 versus control untreated RCNs (N = 4). **p < 0.01 versus control untreated RCNs (N = 4). ***p < 0.001 versus control untreated RCNs (N = 4). B, Western blot analysis of the level of proapoptotic proteins in primary cortical neurons at different time points after etoposide treatment. Cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against PUMA, Noxa, Bax, active Bax, and β-actin. Levels of PUMA, Noxa, Bax, and active Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus control untreated RCNs (N = 4). **p < 0.01 versus control untreated RCNs (N = 4). ***p < 0.001 versus control untreated RCNs (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Journal: The Journal of Neuroscience

Article Title: Downregulation of miR-23a and miR-27a following Experimental Traumatic Brain Injury Induces Neuronal Cell Death through Activation of Proapoptotic Bcl-2 Proteins

doi: 10.1523/JNEUROSCI.1260-14.2014

Figure Lengend Snippet: mRNA and protein levels of proapoptotic members of Bcl-2 family were increased in etoposide-treated primary cortical neurons. A, qPCR quantification of expression of proapoptotic genes: Noxa, Puma, and Bax in primary cortical neurons at different time points after etoposide treatment. Level of gene expression was normalized to GAPDH expression. Neuronal apoptosis were induced by etoposide as described above. Data are mean ± SD. *p < 0.05 versus control untreated RCNs (N = 4). **p < 0.01 versus control untreated RCNs (N = 4). ***p < 0.001 versus control untreated RCNs (N = 4). B, Western blot analysis of the level of proapoptotic proteins in primary cortical neurons at different time points after etoposide treatment. Cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against PUMA, Noxa, Bax, active Bax, and β-actin. Levels of PUMA, Noxa, Bax, and active Bax were quantified as fold change to control levels after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus control untreated RCNs (N = 4). **p < 0.01 versus control untreated RCNs (N = 4). ***p < 0.001 versus control untreated RCNs (N = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Article Snippet: Abcam: V5 (ab27674); Histone H2A.X (ab11175); Santa Cruz Biotechnology: AIF (sc-13116); Apaf-1 (sc-65890); cytochrome c (sc-13560); FAS (sc-716); Bim (sc-11425); Cell Signaling Technology: Cleaved Caspase-3 (#9661); Cleaved PARP (#9545); Phospho-Histone H2A.X (Ser139) (#9718); Phospho-p53 (Ser15) (#9284); p53 (1C12) (#2524); Bax (#2772); XIAP (#2042); Enzo Life Sciences: GAPDH (ADI-CSA-335); Bax (active monomer) (ALX-804-224-C100); α-fodrin (BML-FG6090); ProSci: PUMA (#3041); Noxa (#2437); EMD Millipore: Bak (06-536); Sigma: β-actin (A1978).

Techniques: Expressing, Western Blot

miR-23a and miR-27a mimics attenuate etoposide-induced expression of proapoptotic Bcl-2 family members. Neurons were transfected with miR-23a-3p and miR-27a-3p mimics and 4 h later treated with etoposide as described above. Whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against PUMA, Noxa, Bax, active Bax, and β-actin (A). Levels of PUMA (B), Noxa (C), Bax (D), and active Bax (E) were quantified as fold change to control RCN level after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus mock untreated RCNs. **p < 0.01 versus mock untreated RCNs. ***p < 0.001 versus mock untreated RCNs. +p < 0.05 versus etoposide-treated mock (n = 4). ++p < 0.01 versus etoposide-treated mock (n = 4). +++p < 0.001 versus etoposide-treated mock (n = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Journal: The Journal of Neuroscience

Article Title: Downregulation of miR-23a and miR-27a following Experimental Traumatic Brain Injury Induces Neuronal Cell Death through Activation of Proapoptotic Bcl-2 Proteins

doi: 10.1523/JNEUROSCI.1260-14.2014

Figure Lengend Snippet: miR-23a and miR-27a mimics attenuate etoposide-induced expression of proapoptotic Bcl-2 family members. Neurons were transfected with miR-23a-3p and miR-27a-3p mimics and 4 h later treated with etoposide as described above. Whole-cell lysates were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against PUMA, Noxa, Bax, active Bax, and β-actin (A). Levels of PUMA (B), Noxa (C), Bax (D), and active Bax (E) were quantified as fold change to control RCN level after measurement of band intensity by densitometry and normalization to levels of β-actin. Data are mean ± SD. *p < 0.05 versus mock untreated RCNs. **p < 0.01 versus mock untreated RCNs. ***p < 0.001 versus mock untreated RCNs. +p < 0.05 versus etoposide-treated mock (n = 4). ++p < 0.01 versus etoposide-treated mock (n = 4). +++p < 0.001 versus etoposide-treated mock (n = 4). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Article Snippet: Abcam: V5 (ab27674); Histone H2A.X (ab11175); Santa Cruz Biotechnology: AIF (sc-13116); Apaf-1 (sc-65890); cytochrome c (sc-13560); FAS (sc-716); Bim (sc-11425); Cell Signaling Technology: Cleaved Caspase-3 (#9661); Cleaved PARP (#9545); Phospho-Histone H2A.X (Ser139) (#9718); Phospho-p53 (Ser15) (#9284); p53 (1C12) (#2524); Bax (#2772); XIAP (#2042); Enzo Life Sciences: GAPDH (ADI-CSA-335); Bax (active monomer) (ALX-804-224-C100); α-fodrin (BML-FG6090); ProSci: PUMA (#3041); Noxa (#2437); EMD Millipore: Bak (06-536); Sigma: β-actin (A1978).

Techniques: Expressing, Transfection

miR-23a and miR-27a target PUMA, Noxa, and Bax. SH-SY5Y cells were transfected with either negative control miR (-ve cnt) or miR-23a-3p or miR-27a-3p mimics. Cells were also cotransfected with reporter plasmids with inserted 3′ UTRs of mouse PUMA (A), Noxa (B), and Bax (C). Twenty-four hours after transfection, cells were analyzed for Luciferase activity. Normalized Luciferase activities were shown as the percentage relative to the cells transfected with reporter plasmid and -ve Con miR mimic, which was set as 1. Experiments were performed in triplicate. Data are mean ± SD. **p < 0.01 (n = 3). ***p < 0.001 (n = 3). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Journal: The Journal of Neuroscience

Article Title: Downregulation of miR-23a and miR-27a following Experimental Traumatic Brain Injury Induces Neuronal Cell Death through Activation of Proapoptotic Bcl-2 Proteins

doi: 10.1523/JNEUROSCI.1260-14.2014

Figure Lengend Snippet: miR-23a and miR-27a target PUMA, Noxa, and Bax. SH-SY5Y cells were transfected with either negative control miR (-ve cnt) or miR-23a-3p or miR-27a-3p mimics. Cells were also cotransfected with reporter plasmids with inserted 3′ UTRs of mouse PUMA (A), Noxa (B), and Bax (C). Twenty-four hours after transfection, cells were analyzed for Luciferase activity. Normalized Luciferase activities were shown as the percentage relative to the cells transfected with reporter plasmid and -ve Con miR mimic, which was set as 1. Experiments were performed in triplicate. Data are mean ± SD. **p < 0.01 (n = 3). ***p < 0.001 (n = 3). Analysis by one-way ANOVA followed by multiple pairwise comparisons using Student-Newman-Keuls post hoc test.

Article Snippet: Abcam: V5 (ab27674); Histone H2A.X (ab11175); Santa Cruz Biotechnology: AIF (sc-13116); Apaf-1 (sc-65890); cytochrome c (sc-13560); FAS (sc-716); Bim (sc-11425); Cell Signaling Technology: Cleaved Caspase-3 (#9661); Cleaved PARP (#9545); Phospho-Histone H2A.X (Ser139) (#9718); Phospho-p53 (Ser15) (#9284); p53 (1C12) (#2524); Bax (#2772); XIAP (#2042); Enzo Life Sciences: GAPDH (ADI-CSA-335); Bax (active monomer) (ALX-804-224-C100); α-fodrin (BML-FG6090); ProSci: PUMA (#3041); Noxa (#2437); EMD Millipore: Bak (06-536); Sigma: β-actin (A1978).

Techniques: Transfection, Negative Control, Luciferase, Activity Assay, Plasmid Preparation

Intracerebroventricular injection of miR-23a and miR-27a mimics attenuate expression of PUMA, Noxa, and Bax in injured cortex after TBI. qPCR quantification of miR-23a-3p, miR-27a-3p (A) and PUMA, Noxa, and Bax (B) expressions in mouse cortex 6 h after TBI and intracerebroventricular injection of miR-23a-3p or miR-27a-3p or negative control miR (-ve Con) mimics. Levels of miRs were normalized to U6 snRNA; levels of PUMA, Noxa, and Bax were normalized to GAPDH. Data are mean ± SD. *p < 0.05 versus sham animals. **p < 0.01 versus sham animals. ***p < 0.001 versus sham animals. +p < 0.05 versus injured -ve Con injected group (N = 4–6). ++p < 0.01 versus injured -ve Con injected group (N = 4–6). C, Whole-tissue lysates from mouse cortex 24 h after TBI and intracerebroventricular injection of miR-23a-3p or miR-27a-3p or -ve cnt mimics were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against PUMA, Noxa, Bax, active Bax, and β-actin. Levels of PUMA, Noxa, Bax, and active Bax in total lysates were quantified as fold change to the levels of sham after measurement of band intensity by densitometry. Data are mean ± SD. *p < 0.05 versus sham animals. **p < 0.01 versus sham animals. ***p < 0.001 versus sham animals. +p < 0.05 versus injured -ve cnt-injected group (N = 4–6). ++p < 0.01 versus injured -ve cnt-injected group (N = 4–6).

Journal: The Journal of Neuroscience

Article Title: Downregulation of miR-23a and miR-27a following Experimental Traumatic Brain Injury Induces Neuronal Cell Death through Activation of Proapoptotic Bcl-2 Proteins

doi: 10.1523/JNEUROSCI.1260-14.2014

Figure Lengend Snippet: Intracerebroventricular injection of miR-23a and miR-27a mimics attenuate expression of PUMA, Noxa, and Bax in injured cortex after TBI. qPCR quantification of miR-23a-3p, miR-27a-3p (A) and PUMA, Noxa, and Bax (B) expressions in mouse cortex 6 h after TBI and intracerebroventricular injection of miR-23a-3p or miR-27a-3p or negative control miR (-ve Con) mimics. Levels of miRs were normalized to U6 snRNA; levels of PUMA, Noxa, and Bax were normalized to GAPDH. Data are mean ± SD. *p < 0.05 versus sham animals. **p < 0.01 versus sham animals. ***p < 0.001 versus sham animals. +p < 0.05 versus injured -ve Con injected group (N = 4–6). ++p < 0.01 versus injured -ve Con injected group (N = 4–6). C, Whole-tissue lysates from mouse cortex 24 h after TBI and intracerebroventricular injection of miR-23a-3p or miR-27a-3p or -ve cnt mimics were fractioned on SDS-polyacrylamide gel and immunoblotted with antibodies against PUMA, Noxa, Bax, active Bax, and β-actin. Levels of PUMA, Noxa, Bax, and active Bax in total lysates were quantified as fold change to the levels of sham after measurement of band intensity by densitometry. Data are mean ± SD. *p < 0.05 versus sham animals. **p < 0.01 versus sham animals. ***p < 0.001 versus sham animals. +p < 0.05 versus injured -ve cnt-injected group (N = 4–6). ++p < 0.01 versus injured -ve cnt-injected group (N = 4–6).

Article Snippet: Abcam: V5 (ab27674); Histone H2A.X (ab11175); Santa Cruz Biotechnology: AIF (sc-13116); Apaf-1 (sc-65890); cytochrome c (sc-13560); FAS (sc-716); Bim (sc-11425); Cell Signaling Technology: Cleaved Caspase-3 (#9661); Cleaved PARP (#9545); Phospho-Histone H2A.X (Ser139) (#9718); Phospho-p53 (Ser15) (#9284); p53 (1C12) (#2524); Bax (#2772); XIAP (#2042); Enzo Life Sciences: GAPDH (ADI-CSA-335); Bax (active monomer) (ALX-804-224-C100); α-fodrin (BML-FG6090); ProSci: PUMA (#3041); Noxa (#2437); EMD Millipore: Bak (06-536); Sigma: β-actin (A1978).

Techniques: Injection, Expressing, Negative Control