ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ddb2
    Ddb2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ddb2
    Protection against UV-induced cytotoxicity by forced expression of <t>DDB2</t> . (A, B, C) Sensitivity to UV is presented for stable cell lines indicated or for (D, E, F) HR18 cells which express DDB2. The protein levels of DDB2, DDB1, and β-actin are shown in the insets. The plotted values represent means ± S.D. of experiments performed in triplicates. IC 50 values were also indicated in A and D.
    Ddb2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Damaged DNA-binding protein 2 (DDB2) protects against UV irradiation in human cells and Drosophila"

    Article Title: Damaged DNA-binding protein 2 (DDB2) protects against UV irradiation in human cells and Drosophila

    Journal: Journal of Biomedical Science

    doi: 10.1186/1423-0127-17-27

    Protection against UV-induced cytotoxicity by forced expression of DDB2 . (A, B, C) Sensitivity to UV is presented for stable cell lines indicated or for (D, E, F) HR18 cells which express DDB2. The protein levels of DDB2, DDB1, and β-actin are shown in the insets. The plotted values represent means ± S.D. of experiments performed in triplicates. IC 50 values were also indicated in A and D.
    Figure Legend Snippet: Protection against UV-induced cytotoxicity by forced expression of DDB2 . (A, B, C) Sensitivity to UV is presented for stable cell lines indicated or for (D, E, F) HR18 cells which express DDB2. The protein levels of DDB2, DDB1, and β-actin are shown in the insets. The plotted values represent means ± S.D. of experiments performed in triplicates. IC 50 values were also indicated in A and D.

    Techniques Used: Expressing, Stable Transfection

    Overexpression of DDB2 is associated with reduced caspase activation following UV treatment . (A) Reduced caspase activation in cisplatin-resistant cells following UV irradiation. Cell extracts were immunoblotted with the antibodies indicated. (B) Reduced caspase activation in DDB2-expressing cells following UV irradiation.
    Figure Legend Snippet: Overexpression of DDB2 is associated with reduced caspase activation following UV treatment . (A) Reduced caspase activation in cisplatin-resistant cells following UV irradiation. Cell extracts were immunoblotted with the antibodies indicated. (B) Reduced caspase activation in DDB2-expressing cells following UV irradiation.

    Techniques Used: Over Expression, Activation Assay, Irradiation, Expressing

    Stimulation of cFLIP expression and attenuation of UV sensitivity by forced expression of DDB2 . (A) Overexpression of cFLIP in HR3 cells. The plotted values represent means ± S.D. of three experiments (right panel). (B) Stimulation of cFLIP expression by forced expression of DDB2. Whole cell extracts of HR18 cells, treated as indicated, were subjected to immunoblot analysis with specific antibodies. (C) Cell sensitivity to UV after Ad-DDB2 virus infection. The plotted values represent means ± S.D. of three experiments. ** Significant difference against control ( p < 0.05).
    Figure Legend Snippet: Stimulation of cFLIP expression and attenuation of UV sensitivity by forced expression of DDB2 . (A) Overexpression of cFLIP in HR3 cells. The plotted values represent means ± S.D. of three experiments (right panel). (B) Stimulation of cFLIP expression by forced expression of DDB2. Whole cell extracts of HR18 cells, treated as indicated, were subjected to immunoblot analysis with specific antibodies. (C) Cell sensitivity to UV after Ad-DDB2 virus infection. The plotted values represent means ± S.D. of three experiments. ** Significant difference against control ( p < 0.05).

    Techniques Used: Expressing, Over Expression, Western Blot, Infection

    Induction of endogenous cFLIP mRNA levels in cells following Ad-DDB2 infection.
    Figure Legend Snippet: Induction of endogenous cFLIP mRNA levels in cells following Ad-DDB2 infection.

    Techniques Used: Infection

    Upregulation of cFLIP promoter activity by forced expression of DDB2 . HEK293 cells were co-transfected with cFLIP reporter together with either control vector (pcDNA3) or DDB2-expressing vector (pcDNA3-DDB2). After 24 hrs, the luciferase activity was measured. The plotted values represent means ± S.D. from three independent transfections. The schematic presentation of full-length cFLIP promoter (-920/+43) and its deletion mutants are indicated below. Putative cis-elements are also indicated at positions relative to the transcription initiation site (+1). The construct number at the top indicates the length of the tested promoter region upstream of the putative transcription initiation site (designated by the bent arrow at +1). Luciferase activity is shown relative to the full-length cFLIP promoter (-920/+43). Significant difference to the control for each promoter is indicated.
    Figure Legend Snippet: Upregulation of cFLIP promoter activity by forced expression of DDB2 . HEK293 cells were co-transfected with cFLIP reporter together with either control vector (pcDNA3) or DDB2-expressing vector (pcDNA3-DDB2). After 24 hrs, the luciferase activity was measured. The plotted values represent means ± S.D. from three independent transfections. The schematic presentation of full-length cFLIP promoter (-920/+43) and its deletion mutants are indicated below. Putative cis-elements are also indicated at positions relative to the transcription initiation site (+1). The construct number at the top indicates the length of the tested promoter region upstream of the putative transcription initiation site (designated by the bent arrow at +1). Luciferase activity is shown relative to the full-length cFLIP promoter (-920/+43). Significant difference to the control for each promoter is indicated.

    Techniques Used: Activity Assay, Expressing, Transfection, Plasmid Preparation, Luciferase, Construct

    Resistance to UV in HR18 cells depends on DDB2 and cFLIP . (A) Attenuation of DDB2 protection against UV-induced apoptosis by knockdown of cFLIP using antisense oligonucleotides. HR18 cells were treated as described in the Materials and methods . The plotted values represent means ± S.D. of experiments performed in triplicates. Inset: immunoblot with specific antibodies. (B) Attenuation of UV-induced caspase activity by forced expression of DDB2, and resensitization by cFLIP antisense oligonucleotides.
    Figure Legend Snippet: Resistance to UV in HR18 cells depends on DDB2 and cFLIP . (A) Attenuation of DDB2 protection against UV-induced apoptosis by knockdown of cFLIP using antisense oligonucleotides. HR18 cells were treated as described in the Materials and methods . The plotted values represent means ± S.D. of experiments performed in triplicates. Inset: immunoblot with specific antibodies. (B) Attenuation of UV-induced caspase activity by forced expression of DDB2, and resensitization by cFLIP antisense oligonucleotides.

    Techniques Used: Western Blot, Activity Assay, Expressing

    Lack of attenuation of UV sensitivity by forced expression of DDB2 in cFLIP-lacking cells . (A) Lack of stimulation of cFLIP expression by forced expression of DDB2 in human VA13 and XP-A cells. Whole cell extracts of infected cells were compared. Cell extracts of cFLIP-transfected cells are also shown as cFLIP protein indicator. (B): Cell sensitivity to UV treatment after Ad-DDB2 virus infection in human VA13 and XP-A cells. The plotted values represent means ± S.D. of three experiments.
    Figure Legend Snippet: Lack of attenuation of UV sensitivity by forced expression of DDB2 in cFLIP-lacking cells . (A) Lack of stimulation of cFLIP expression by forced expression of DDB2 in human VA13 and XP-A cells. Whole cell extracts of infected cells were compared. Cell extracts of cFLIP-transfected cells are also shown as cFLIP protein indicator. (B): Cell sensitivity to UV treatment after Ad-DDB2 virus infection in human VA13 and XP-A cells. The plotted values represent means ± S.D. of three experiments.

    Techniques Used: Expressing, Infection, Transfection

    Protection against UV toxicity by DDB2 in Drosophila . (A) Expression of hDDB2-GFP in Drosophila . Protein extracts from GFP and GFP-hDDB2 expressing embryos were immunoblotted with anti-GFP antibodies. (B) Protection effect of hDDB2 against UV irradiation in fly larvae. GFP or hDDB2 overexpressing larvae were collected and then irradiated with UV (0-100 J/m 2 ). Four days later, surviving adults were counted and the survival rate was calculated. (n>4000). (C) Lack of inhibition of Reaper- or Eiger-induced apoptosis by hDDB2 over-expression. Eye morphology of wild-type and Reaper/eiger-overexpressing flies were examined. To analyze the effect of hDDB2, GMRGal4 was used to drive the expression of Reaper ( GMR>Rpr ) or Eiger ( GMR>eiger ) simultaneously with hDDB2 ( GMR>Rpr, UAS-hDDB2 and GMR>eiger, UAS-hDDB2 , respectively). Panel a-d: Reaper-induced apoptosis, resulting in small eyes, was not rescued by DDB2 overexpression. Panel a, Eye morphology of wild-type OreR fly; Panel b, Eye morphology of Rpr overexpressing fly; Panel c, Eye morphology of Rpr and DDB2 overexpressing fly; Panel d, Eye morphology of Rpr and P35 overexpressing fly. Panel e~g: Eiger-induced apoptosis not rescued by DDB2 overexpression. Panel e, Eye morphology of wild-type OreR fly; Panel f, Eye morphology of eiger overexpressing fly; Panel g, Eye morphology of eiger and DDB2 overexpressing fly.
    Figure Legend Snippet: Protection against UV toxicity by DDB2 in Drosophila . (A) Expression of hDDB2-GFP in Drosophila . Protein extracts from GFP and GFP-hDDB2 expressing embryos were immunoblotted with anti-GFP antibodies. (B) Protection effect of hDDB2 against UV irradiation in fly larvae. GFP or hDDB2 overexpressing larvae were collected and then irradiated with UV (0-100 J/m 2 ). Four days later, surviving adults were counted and the survival rate was calculated. (n>4000). (C) Lack of inhibition of Reaper- or Eiger-induced apoptosis by hDDB2 over-expression. Eye morphology of wild-type and Reaper/eiger-overexpressing flies were examined. To analyze the effect of hDDB2, GMRGal4 was used to drive the expression of Reaper ( GMR>Rpr ) or Eiger ( GMR>eiger ) simultaneously with hDDB2 ( GMR>Rpr, UAS-hDDB2 and GMR>eiger, UAS-hDDB2 , respectively). Panel a-d: Reaper-induced apoptosis, resulting in small eyes, was not rescued by DDB2 overexpression. Panel a, Eye morphology of wild-type OreR fly; Panel b, Eye morphology of Rpr overexpressing fly; Panel c, Eye morphology of Rpr and DDB2 overexpressing fly; Panel d, Eye morphology of Rpr and P35 overexpressing fly. Panel e~g: Eiger-induced apoptosis not rescued by DDB2 overexpression. Panel e, Eye morphology of wild-type OreR fly; Panel f, Eye morphology of eiger overexpressing fly; Panel g, Eye morphology of eiger and DDB2 overexpressing fly.

    Techniques Used: Expressing, Irradiation, Inhibition, Over Expression

    ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ddb2
    Primer pairs of real-time RT-PCR analysis.
    Ddb2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Investigation of Radiation-induced Transcriptome Profile of Radioresistant Non-small Cell Lung Cancer A549 Cells Using RNA-seq"

    Article Title: Investigation of Radiation-induced Transcriptome Profile of Radioresistant Non-small Cell Lung Cancer A549 Cells Using RNA-seq

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0059319

    Primer pairs of real-time RT-PCR analysis.
    Figure Legend Snippet: Primer pairs of real-time RT-PCR analysis.

    Techniques Used: Quantitative RT-PCR, Binding Assay

    IPA network analysis of radioresponsive genes in radioresistant A549 cells.
    Figure Legend Snippet: IPA network analysis of radioresponsive genes in radioresistant A549 cells.

    Techniques Used: Modification

    ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ddb2
    Antitumor mechanism of <t>DDB2</t> in different cancers
    Ddb2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "A protein with broad functions: damage-specific DNA-binding protein 2"

    Article Title: A protein with broad functions: damage-specific DNA-binding protein 2

    Journal: Molecular Biology Reports

    doi: 10.1007/s11033-022-07963-4

    Antitumor mechanism of DDB2 in different cancers
    Figure Legend Snippet: Antitumor mechanism of DDB2 in different cancers

    Techniques Used:

    Cancer promoting mechanism of DDB2
    Figure Legend Snippet: Cancer promoting mechanism of DDB2

    Techniques Used:

    Summary of DDB2 mutations in XPE patients
    Figure Legend Snippet: Summary of DDB2 mutations in XPE patients

    Techniques Used:

    ddb2 proteo probe  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ddb2 proteo probe
    Ddb2 Proteo Probe, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ddb2
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    sc ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc sc ddb2
    Sc Ddb2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    sc ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc sc ddb2
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    ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc ddb2
    ERα mediates chemotherapy-induced <t>DDB2</t> gene transcription (A and B) Basal mRNA (A) and protein (B) levels of DDB2 were higher in ER-positive than ER-negative breast cancer cell lines, regardless of their TP53 genetic status. (C) Silencing of ERα by two independent shRNAs suppressed DDB2 protein and mRNA expression. Reduction of both S118-phosphorylated and total ERα revealed the inhibition of ERα activity. (D) ER response elements (EREs) and p53 RE (p53RE) motifs on the DDB2 promoter and the luciferase reporter constructs driven by different lengths of the DDB2 promoter were illustrated (vermilion, red, and pink: EREs; orange: p53RE). (E) Treatment with carboplatin (50 μM) increased the luciferase activity driven by the DDB2 promoter containing both p53RE and EREs in mutp53-expressing T-47D cancer cells. Firefly luciferase activity was normalized with β-gal activity. (F) Silencing of ERα decreased the carboplatin (50 μM)-induced DDB2 promoter activity in T-47D cancer cells, and firefly luciferase activity was normalized with β-gal activity. Data in (A), (C), (E), and (F) were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test.
    Ddb2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "ERα determines the chemo-resistant function of mutant p53 involving the switch between lincRNA-p21 and DDB2 expressions"

    Article Title: ERα determines the chemo-resistant function of mutant p53 involving the switch between lincRNA-p21 and DDB2 expressions

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2021.07.022

    ERα mediates chemotherapy-induced DDB2 gene transcription (A and B) Basal mRNA (A) and protein (B) levels of DDB2 were higher in ER-positive than ER-negative breast cancer cell lines, regardless of their TP53 genetic status. (C) Silencing of ERα by two independent shRNAs suppressed DDB2 protein and mRNA expression. Reduction of both S118-phosphorylated and total ERα revealed the inhibition of ERα activity. (D) ER response elements (EREs) and p53 RE (p53RE) motifs on the DDB2 promoter and the luciferase reporter constructs driven by different lengths of the DDB2 promoter were illustrated (vermilion, red, and pink: EREs; orange: p53RE). (E) Treatment with carboplatin (50 μM) increased the luciferase activity driven by the DDB2 promoter containing both p53RE and EREs in mutp53-expressing T-47D cancer cells. Firefly luciferase activity was normalized with β-gal activity. (F) Silencing of ERα decreased the carboplatin (50 μM)-induced DDB2 promoter activity in T-47D cancer cells, and firefly luciferase activity was normalized with β-gal activity. Data in (A), (C), (E), and (F) were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test.
    Figure Legend Snippet: ERα mediates chemotherapy-induced DDB2 gene transcription (A and B) Basal mRNA (A) and protein (B) levels of DDB2 were higher in ER-positive than ER-negative breast cancer cell lines, regardless of their TP53 genetic status. (C) Silencing of ERα by two independent shRNAs suppressed DDB2 protein and mRNA expression. Reduction of both S118-phosphorylated and total ERα revealed the inhibition of ERα activity. (D) ER response elements (EREs) and p53 RE (p53RE) motifs on the DDB2 promoter and the luciferase reporter constructs driven by different lengths of the DDB2 promoter were illustrated (vermilion, red, and pink: EREs; orange: p53RE). (E) Treatment with carboplatin (50 μM) increased the luciferase activity driven by the DDB2 promoter containing both p53RE and EREs in mutp53-expressing T-47D cancer cells. Firefly luciferase activity was normalized with β-gal activity. (F) Silencing of ERα decreased the carboplatin (50 μM)-induced DDB2 promoter activity in T-47D cancer cells, and firefly luciferase activity was normalized with β-gal activity. Data in (A), (C), (E), and (F) were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test.

    Techniques Used: Expressing, Inhibition, Activity Assay, Luciferase, Construct

    ERα cooperates with mutp53 to upregulate DDB2 gene transcription and mediates chemoresistance in ER-positive breast cancer cells (A) Silencing of p53 decreased the carboplatin (50 μM)-induced DDB2 promoter activity in T-47D cancer cells. (B) Deletions of EREs, but not p53RE, reduced carboplatin (50 μM)-induced DDB2 promoter activity in T-47D cancer cells. Firefly luciferase activity was normalized with β-gal activity in (A) and (B). (C) Carboplatin (50 μM) induced chromatin-binding affinity of both ERα and mutp53 preferentially on ERE#1 of the DDB2 promoter in T-47D cancer cells in the ChIP assay. (D) Silencing of ERα reduced p53 activity, as evidenced by the acetylation at K382 in T-47D and BT-474 cancer cells. (E) Chemotherapy (50 μM carboplatin or 0.5 μM doxorubicin) induced the protein interaction between p53 and ERα in the coimmunoprecipitation (coIP) assay. (F) Ectopic co-expression of ERα and p53 mutants (R280K and R273H) synergistically enhanced DDB2 expression in HEK293T cells. (G) Silencing of DDB2 by two independent shRNAs enhanced carboplatin (50 μM)-induced DNA damage in the comet assay. The tail moment and tail-length index were calculated from images by Comet Assay III analysis. Data in (A−C) and (G) were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test.
    Figure Legend Snippet: ERα cooperates with mutp53 to upregulate DDB2 gene transcription and mediates chemoresistance in ER-positive breast cancer cells (A) Silencing of p53 decreased the carboplatin (50 μM)-induced DDB2 promoter activity in T-47D cancer cells. (B) Deletions of EREs, but not p53RE, reduced carboplatin (50 μM)-induced DDB2 promoter activity in T-47D cancer cells. Firefly luciferase activity was normalized with β-gal activity in (A) and (B). (C) Carboplatin (50 μM) induced chromatin-binding affinity of both ERα and mutp53 preferentially on ERE#1 of the DDB2 promoter in T-47D cancer cells in the ChIP assay. (D) Silencing of ERα reduced p53 activity, as evidenced by the acetylation at K382 in T-47D and BT-474 cancer cells. (E) Chemotherapy (50 μM carboplatin or 0.5 μM doxorubicin) induced the protein interaction between p53 and ERα in the coimmunoprecipitation (coIP) assay. (F) Ectopic co-expression of ERα and p53 mutants (R280K and R273H) synergistically enhanced DDB2 expression in HEK293T cells. (G) Silencing of DDB2 by two independent shRNAs enhanced carboplatin (50 μM)-induced DNA damage in the comet assay. The tail moment and tail-length index were calculated from images by Comet Assay III analysis. Data in (A−C) and (G) were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test.

    Techniques Used: Activity Assay, Luciferase, Binding Assay, Co-Immunoprecipitation Assay, Expressing, Single Cell Gel Electrophoresis

    ERα hijacks mutp53 from the G-quadruplex DNA (GQ) structure of the lincRNA-p21 promoter to EREs of the DDB2 promoter (A) Illustration of the predicted non-B structure and p53RE on the lincRNA-p21 promoter and two luciferase-reporter constructs driven by lincRNA-p21 promoters containing different motifs. (B and C) GQ motif is required for mutp53-increased lincRNA-p21 promoter activity, and firefly luciferase activity was normalized with β-gal activity. (D) The binding efficacy of endogenous mutp53 on different motifs of the lincRNA-p21 promoter in response to chemotherapies (50 μM carboplatin and 0.5 μM doxorubicin) in the ChIP assay. (E and F) Carboplatin (50 μM) and two GQ stabilizers (1 μM NMM and 5 μM auramine) increased the binding of mutp53 to the GQ motif of the 5′-biotinylated lincRNA-p21 promoters in the in vitro pull-down assay. (G) GQ stabilizers increased lincRNA-p21 expression in MDA-MB-231 cancer cells. (H) Silencing of ERα switched the chromatin-binding activity of mutp53 from EREs of the DDB2 promoter (left) to the non-B DNA motifs of the lincRNA-p21 promoter (right) in ER-positive/p53 L194F T-47D cancer cells. (I) The inversed correlation between the ex vivo induction of lincRNA-p21 and DDB2 expression by carboplatin (50 μM) treatments in human primary breast cancer tissues in an ER status-dependent manner. Data in (B−D), (G), and (H) were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test.
    Figure Legend Snippet: ERα hijacks mutp53 from the G-quadruplex DNA (GQ) structure of the lincRNA-p21 promoter to EREs of the DDB2 promoter (A) Illustration of the predicted non-B structure and p53RE on the lincRNA-p21 promoter and two luciferase-reporter constructs driven by lincRNA-p21 promoters containing different motifs. (B and C) GQ motif is required for mutp53-increased lincRNA-p21 promoter activity, and firefly luciferase activity was normalized with β-gal activity. (D) The binding efficacy of endogenous mutp53 on different motifs of the lincRNA-p21 promoter in response to chemotherapies (50 μM carboplatin and 0.5 μM doxorubicin) in the ChIP assay. (E and F) Carboplatin (50 μM) and two GQ stabilizers (1 μM NMM and 5 μM auramine) increased the binding of mutp53 to the GQ motif of the 5′-biotinylated lincRNA-p21 promoters in the in vitro pull-down assay. (G) GQ stabilizers increased lincRNA-p21 expression in MDA-MB-231 cancer cells. (H) Silencing of ERα switched the chromatin-binding activity of mutp53 from EREs of the DDB2 promoter (left) to the non-B DNA motifs of the lincRNA-p21 promoter (right) in ER-positive/p53 L194F T-47D cancer cells. (I) The inversed correlation between the ex vivo induction of lincRNA-p21 and DDB2 expression by carboplatin (50 μM) treatments in human primary breast cancer tissues in an ER status-dependent manner. Data in (B−D), (G), and (H) were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test.

    Techniques Used: Luciferase, Construct, Activity Assay, Binding Assay, In Vitro, Pull Down Assay, Expressing, Ex Vivo

    lincRNA-p21 reduces the growth and chemoresistance of the ER-positive tumor in vivo (A) The T-47D#Tet-On-LincRNA-p21 stable clone was treated with or without tetracycline (10 μg/mL), and the expressions of lincRNA-p21 and DDB2 were detected by quantitative real-time PCR analysis and western blot assay, respectively. Data were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test. (B) Illustration of the treatment timeline in the tumor-xenograft mouse model (yellow arrow: the starting point for tetracycline administration [0.2 mg/mL]; red arrow: the points for the intraperitoneal injection with doxorubicin [2.5 mg/kg]). (C and D) The tumor growth rate (C) and size at the end point (D) in four groups of these mice. Data were representative of n = 3 in every group and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test. (E) The expressions of lincRNA-p21, DDB2, Ki67, and cleaved caspase-3 in the tumor tissues were examined in the in situ hybridization and immunohistochemistry assays.
    Figure Legend Snippet: lincRNA-p21 reduces the growth and chemoresistance of the ER-positive tumor in vivo (A) The T-47D#Tet-On-LincRNA-p21 stable clone was treated with or without tetracycline (10 μg/mL), and the expressions of lincRNA-p21 and DDB2 were detected by quantitative real-time PCR analysis and western blot assay, respectively. Data were representative of three experiments and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test. (B) Illustration of the treatment timeline in the tumor-xenograft mouse model (yellow arrow: the starting point for tetracycline administration [0.2 mg/mL]; red arrow: the points for the intraperitoneal injection with doxorubicin [2.5 mg/kg]). (C and D) The tumor growth rate (C) and size at the end point (D) in four groups of these mice. Data were representative of n = 3 in every group and were shown as the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001 versus the control group, Student’s t test. (E) The expressions of lincRNA-p21, DDB2, Ki67, and cleaved caspase-3 in the tumor tissues were examined in the in situ hybridization and immunohistochemistry assays.

    Techniques Used: In Vivo, Stable Transfection, Real-time Polymerase Chain Reaction, Western Blot, Injection, In Situ Hybridization, Immunohistochemistry

    The proposed model of ERα/mutp53 mediated DDB2 and lincRNA-p21 in contributing to chemoresistance The proposed model illustrates how ERα determined chemoresistance of breast cancer by disrupting the balance between mutp53-dependent DDB2 and lincRNA-p21 transcriptions. In the ER-negative cancer cells (left), lincRNA-p21 , transcribed by mutp53 in a G-quadruplex of non-B structure-dependent fashion, mediate apoptosis for chemosensitivity. In the ER-positive cancer cells (right), however, ERα switches mutp53 to preferentially mediate DDB2 transcription via targeting its EREs and thereby reduces lincRNA-p21 expression, conferring chemoresistance (p53∗, mutp53).
    Figure Legend Snippet: The proposed model of ERα/mutp53 mediated DDB2 and lincRNA-p21 in contributing to chemoresistance The proposed model illustrates how ERα determined chemoresistance of breast cancer by disrupting the balance between mutp53-dependent DDB2 and lincRNA-p21 transcriptions. In the ER-negative cancer cells (left), lincRNA-p21 , transcribed by mutp53 in a G-quadruplex of non-B structure-dependent fashion, mediate apoptosis for chemosensitivity. In the ER-positive cancer cells (right), however, ERα switches mutp53 to preferentially mediate DDB2 transcription via targeting its EREs and thereby reduces lincRNA-p21 expression, conferring chemoresistance (p53∗, mutp53).

    Techniques Used: Expressing

    sc ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc sc ddb2
    Sc Ddb2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti ddb2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti ddb2
    USP44 deubiquitinates <t>DDB2</t> following UVC exposure. (A,B) MEFs of the indicated genotype were exposed to 30 J/m 2 UVC and samples were collected for immunoblot at the indicated times. The doublet bands were consistently observed in these mouse cells, and were both quantitated to represent DDB2 using imageJ. The graph represents the mean ± SEM for three independent MEF lines. “*” denotes p < 0.05. (C) MEFs were transduced with the indicated constructs and subjected to immunoprecipitation for the FLAG epitope and probed as indicated. (D) Purified CRL-DDB2 was auto-ubiquitinated by the addition of UbE1, UBCH5a, and ubiquitin, and subsequently incubated with either wild type or catalytic mutant (C281A) immunopurified USP44 as indicated. Rxn = reaction.
    Anti Ddb2, supplied by Cell Signaling Technology Inc, 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/result/anti ddb2/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    1) Product Images from "USP44 Stabilizes DDB2 to Facilitate Nucleotide Excision Repair and Prevent Tumors"

    Article Title: USP44 Stabilizes DDB2 to Facilitate Nucleotide Excision Repair and Prevent Tumors

    Journal: Frontiers in Cell and Developmental Biology

    doi: 10.3389/fcell.2021.663411

    USP44 deubiquitinates DDB2 following UVC exposure. (A,B) MEFs of the indicated genotype were exposed to 30 J/m 2 UVC and samples were collected for immunoblot at the indicated times. The doublet bands were consistently observed in these mouse cells, and were both quantitated to represent DDB2 using imageJ. The graph represents the mean ± SEM for three independent MEF lines. “*” denotes p < 0.05. (C) MEFs were transduced with the indicated constructs and subjected to immunoprecipitation for the FLAG epitope and probed as indicated. (D) Purified CRL-DDB2 was auto-ubiquitinated by the addition of UbE1, UBCH5a, and ubiquitin, and subsequently incubated with either wild type or catalytic mutant (C281A) immunopurified USP44 as indicated. Rxn = reaction.
    Figure Legend Snippet: USP44 deubiquitinates DDB2 following UVC exposure. (A,B) MEFs of the indicated genotype were exposed to 30 J/m 2 UVC and samples were collected for immunoblot at the indicated times. The doublet bands were consistently observed in these mouse cells, and were both quantitated to represent DDB2 using imageJ. The graph represents the mean ± SEM for three independent MEF lines. “*” denotes p < 0.05. (C) MEFs were transduced with the indicated constructs and subjected to immunoprecipitation for the FLAG epitope and probed as indicated. (D) Purified CRL-DDB2 was auto-ubiquitinated by the addition of UbE1, UBCH5a, and ubiquitin, and subsequently incubated with either wild type or catalytic mutant (C281A) immunopurified USP44 as indicated. Rxn = reaction.

    Techniques Used: Western Blot, Transduction, Construct, Immunoprecipitation, FLAG-tag, Purification, Incubation, Mutagenesis

    Incomplete CPD repair in Usp44 null cells associated with inadequate DDB2 recruitment to sites of damage. (A,B) VH10 cells expressing DDB2-GFP were transfected with control or USP44 targeting siRNA and then locally irradiated. The DDB-GFP fluorescence was monitored over time using live-cell confocal imaging and quantified to pre-damage intensity set at 100. The graph represents the mean ± SEM for 31–36 cells per condition. (C) MEFs of the indicated genotypes were transduced with wild-type, catalytic mutant (USP44 C I ; C281A), centrin-binding deficient (USP44 C BM ; W162A) USP44, or DDB2 as indicated. The cells were exposed to UVC (10 J/m 2 ) and CPD levels were monitored at the indicated times. The graph represents the means of three independent experiments for each condition.
    Figure Legend Snippet: Incomplete CPD repair in Usp44 null cells associated with inadequate DDB2 recruitment to sites of damage. (A,B) VH10 cells expressing DDB2-GFP were transfected with control or USP44 targeting siRNA and then locally irradiated. The DDB-GFP fluorescence was monitored over time using live-cell confocal imaging and quantified to pre-damage intensity set at 100. The graph represents the mean ± SEM for 31–36 cells per condition. (C) MEFs of the indicated genotypes were transduced with wild-type, catalytic mutant (USP44 C I ; C281A), centrin-binding deficient (USP44 C BM ; W162A) USP44, or DDB2 as indicated. The cells were exposed to UVC (10 J/m 2 ) and CPD levels were monitored at the indicated times. The graph represents the means of three independent experiments for each condition.

    Techniques Used: Expressing, Transfection, Irradiation, Fluorescence, Imaging, Transduction, Mutagenesis, Binding Assay

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    anti ddb2  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc anti ddb2
    USP44 deubiquitinates <t>DDB2</t> following UVC exposure. (A,B) MEFs of the indicated genotype were exposed to 30 J/m 2 UVC and samples were collected for immunoblot at the indicated times. The doublet bands were consistently observed in these mouse cells, and were both quantitated to represent DDB2 using imageJ. The graph represents the mean ± SEM for three independent MEF lines. “*” denotes p < 0.05. (C) MEFs were transduced with the indicated constructs and subjected to immunoprecipitation for the FLAG epitope and probed as indicated. (D) Purified CRL-DDB2 was auto-ubiquitinated by the addition of UbE1, UBCH5a, and ubiquitin, and subsequently incubated with either wild type or catalytic mutant (C281A) immunopurified USP44 as indicated. Rxn = reaction.
    Anti Ddb2, supplied by Cell Signaling Technology Inc, 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/result/anti ddb2/product/Cell Signaling Technology Inc
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    USP44 deubiquitinates DDB2 following UVC exposure. (A,B) MEFs of the indicated genotype were exposed to 30 J/m 2 UVC and samples were collected for immunoblot at the indicated times. The doublet bands were consistently observed in these mouse cells, and were both quantitated to represent DDB2 using imageJ. The graph represents the mean ± SEM for three independent MEF lines. “*” denotes p < 0.05. (C) MEFs were transduced with the indicated constructs and subjected to immunoprecipitation for the FLAG epitope and probed as indicated. (D) Purified CRL-DDB2 was auto-ubiquitinated by the addition of UbE1, UBCH5a, and ubiquitin, and subsequently incubated with either wild type or catalytic mutant (C281A) immunopurified USP44 as indicated. Rxn = reaction.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: USP44 Stabilizes DDB2 to Facilitate Nucleotide Excision Repair and Prevent Tumors

    doi: 10.3389/fcell.2021.663411

    Figure Lengend Snippet: USP44 deubiquitinates DDB2 following UVC exposure. (A,B) MEFs of the indicated genotype were exposed to 30 J/m 2 UVC and samples were collected for immunoblot at the indicated times. The doublet bands were consistently observed in these mouse cells, and were both quantitated to represent DDB2 using imageJ. The graph represents the mean ± SEM for three independent MEF lines. “*” denotes p < 0.05. (C) MEFs were transduced with the indicated constructs and subjected to immunoprecipitation for the FLAG epitope and probed as indicated. (D) Purified CRL-DDB2 was auto-ubiquitinated by the addition of UbE1, UBCH5a, and ubiquitin, and subsequently incubated with either wild type or catalytic mutant (C281A) immunopurified USP44 as indicated. Rxn = reaction.

    Article Snippet: Antibodies used in this study include anti-DDB2 (#5416), FLAG (DYKDDDDK, #2368), histone H2B (#5546), α-actin (#4970) (Cell Signaling Inc. Danvers, MA, United States), HA (3F10, Millipore-Sigma, St. Louis, MO, United States), V5 (Bethyl Laboratories, Montgomery, TX, United States), CPD (clone TDM-2; CosmoBio) XPC (graciously supplied by Jeff Salisbury) ( ).

    Techniques: Western Blot, Transduction, Construct, Immunoprecipitation, FLAG-tag, Purification, Incubation, Mutagenesis

    Incomplete CPD repair in Usp44 null cells associated with inadequate DDB2 recruitment to sites of damage. (A,B) VH10 cells expressing DDB2-GFP were transfected with control or USP44 targeting siRNA and then locally irradiated. The DDB-GFP fluorescence was monitored over time using live-cell confocal imaging and quantified to pre-damage intensity set at 100. The graph represents the mean ± SEM for 31–36 cells per condition. (C) MEFs of the indicated genotypes were transduced with wild-type, catalytic mutant (USP44 C I ; C281A), centrin-binding deficient (USP44 C BM ; W162A) USP44, or DDB2 as indicated. The cells were exposed to UVC (10 J/m 2 ) and CPD levels were monitored at the indicated times. The graph represents the means of three independent experiments for each condition.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: USP44 Stabilizes DDB2 to Facilitate Nucleotide Excision Repair and Prevent Tumors

    doi: 10.3389/fcell.2021.663411

    Figure Lengend Snippet: Incomplete CPD repair in Usp44 null cells associated with inadequate DDB2 recruitment to sites of damage. (A,B) VH10 cells expressing DDB2-GFP were transfected with control or USP44 targeting siRNA and then locally irradiated. The DDB-GFP fluorescence was monitored over time using live-cell confocal imaging and quantified to pre-damage intensity set at 100. The graph represents the mean ± SEM for 31–36 cells per condition. (C) MEFs of the indicated genotypes were transduced with wild-type, catalytic mutant (USP44 C I ; C281A), centrin-binding deficient (USP44 C BM ; W162A) USP44, or DDB2 as indicated. The cells were exposed to UVC (10 J/m 2 ) and CPD levels were monitored at the indicated times. The graph represents the means of three independent experiments for each condition.

    Article Snippet: Antibodies used in this study include anti-DDB2 (#5416), FLAG (DYKDDDDK, #2368), histone H2B (#5546), α-actin (#4970) (Cell Signaling Inc. Danvers, MA, United States), HA (3F10, Millipore-Sigma, St. Louis, MO, United States), V5 (Bethyl Laboratories, Montgomery, TX, United States), CPD (clone TDM-2; CosmoBio) XPC (graciously supplied by Jeff Salisbury) ( ).

    Techniques: Expressing, Transfection, Irradiation, Fluorescence, Imaging, Transduction, Mutagenesis, Binding Assay