annexin v fitc apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc apoptosis detection kit
    Annexin V Fitc Apoptosis Detection Kit, supplied by Vazyme Biotech Co, 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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    annexin v fitc propidium iodide pi apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc propidium iodide pi apoptosis detection kit
    Annexin V Fitc Propidium Iodide Pi Apoptosis Detection Kit, supplied by Vazyme Biotech Co, 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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    annexin v fitc pi apoptosis assay kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc pi apoptosis assay kit
    Annexin V Fitc Pi Apoptosis Assay Kit, supplied by Vazyme Biotech Co, 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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    annexin v fitc pi apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc pi apoptosis detection kit
    Annexin V Fitc Pi Apoptosis Detection Kit, supplied by Vazyme Biotech Co, 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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    annexin v fluorescein isothiocyanate fitc apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fluorescein isothiocyanate fitc apoptosis detection kit
    Annexin V Fluorescein Isothiocyanate Fitc Apoptosis Detection Kit, supplied by Vazyme Biotech Co, 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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    annexin v fitc pi apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc pi apoptosis detection kit
    Silencing circZBTB46 inhibits cell proliferation and migration and induces <t>apoptosis.</t> (A-B) The relative expression of circZBTB46 in HCAECs and HCASMCs transfected with si-NC, si-circZBTB46-1, and si-circZBTB46-2. (C-D) The CCK-8 assay revealed that circZBTB46 knockdown inhibited cell proliferation. (E) Western blot analysis showed that the protein levels of cleaved PARP and cleaved caspase 3 were significantly increased whereas, Cyclin D1 and Cyclin A were significantly decreased upon silencing of circZBTB46. (F-G) The migration of HCAECs and HCASMCs was inhibited by knockdown of circZBTB46. (H-I) Flow cytometric analysis was performed to determine showed the percentages of apoptotic cells after transfection with si-NC, si-circZBTB46-1, and si-circZBTB46-2. * p < 0.05, ** p < 0.01, *** p < 0.001
    Annexin V Fitc Pi Apoptosis Detection Kit, supplied by Vazyme Biotech Co, 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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    annexin v fitc pi apoptosis detection kit - by Bioz Stars, 2023-11
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    1) Product Images from "Circular RNA ZBTB46 depletion alleviates the progression of Atherosclerosis by regulating the ubiquitination and degradation of hnRNPA2B1 via the AKT/mTOR pathway"

    Article Title: Circular RNA ZBTB46 depletion alleviates the progression of Atherosclerosis by regulating the ubiquitination and degradation of hnRNPA2B1 via the AKT/mTOR pathway

    Journal: Immunity & Ageing : I & A

    doi: 10.1186/s12979-023-00386-0

    Silencing circZBTB46 inhibits cell proliferation and migration and induces apoptosis. (A-B) The relative expression of circZBTB46 in HCAECs and HCASMCs transfected with si-NC, si-circZBTB46-1, and si-circZBTB46-2. (C-D) The CCK-8 assay revealed that circZBTB46 knockdown inhibited cell proliferation. (E) Western blot analysis showed that the protein levels of cleaved PARP and cleaved caspase 3 were significantly increased whereas, Cyclin D1 and Cyclin A were significantly decreased upon silencing of circZBTB46. (F-G) The migration of HCAECs and HCASMCs was inhibited by knockdown of circZBTB46. (H-I) Flow cytometric analysis was performed to determine showed the percentages of apoptotic cells after transfection with si-NC, si-circZBTB46-1, and si-circZBTB46-2. * p < 0.05, ** p < 0.01, *** p < 0.001
    Figure Legend Snippet: Silencing circZBTB46 inhibits cell proliferation and migration and induces apoptosis. (A-B) The relative expression of circZBTB46 in HCAECs and HCASMCs transfected with si-NC, si-circZBTB46-1, and si-circZBTB46-2. (C-D) The CCK-8 assay revealed that circZBTB46 knockdown inhibited cell proliferation. (E) Western blot analysis showed that the protein levels of cleaved PARP and cleaved caspase 3 were significantly increased whereas, Cyclin D1 and Cyclin A were significantly decreased upon silencing of circZBTB46. (F-G) The migration of HCAECs and HCASMCs was inhibited by knockdown of circZBTB46. (H-I) Flow cytometric analysis was performed to determine showed the percentages of apoptotic cells after transfection with si-NC, si-circZBTB46-1, and si-circZBTB46-2. * p < 0.05, ** p < 0.01, *** p < 0.001

    Techniques Used: Migration, Expressing, Transfection, CCK-8 Assay, Western Blot

    hnRNPA2B1 is upregulated in atherosclerotic plaques, and silencing hnRNPA2B1 inhibits cell proliferation and induces apoptosis. (A-B) The expression of hnRNPA2B1 in different stages of atherosclerosis was analyzed by immunohistochemical staining. (C) The relative expression levels of hnRNPA2B1 in PBMC samples from CAD patients and controls were determined by RT‒PCR. (D-E) The CCK-8 assay revealed that silencing hnRNPA2B1 inhibited cell proliferation. (F-G) Transwell and wound healing assays suggested that cell migration was dramatically suppressed by silencing hnRNPA2B1 expression. (H) Flow cytometric analysis indicated that the proportion of apoptotic cells was notably elevated in the si-hnRNPA2B1 groups. * p < 0.05, ** p < 0.01, *** p < 0.001
    Figure Legend Snippet: hnRNPA2B1 is upregulated in atherosclerotic plaques, and silencing hnRNPA2B1 inhibits cell proliferation and induces apoptosis. (A-B) The expression of hnRNPA2B1 in different stages of atherosclerosis was analyzed by immunohistochemical staining. (C) The relative expression levels of hnRNPA2B1 in PBMC samples from CAD patients and controls were determined by RT‒PCR. (D-E) The CCK-8 assay revealed that silencing hnRNPA2B1 inhibited cell proliferation. (F-G) Transwell and wound healing assays suggested that cell migration was dramatically suppressed by silencing hnRNPA2B1 expression. (H) Flow cytometric analysis indicated that the proportion of apoptotic cells was notably elevated in the si-hnRNPA2B1 groups. * p < 0.05, ** p < 0.01, *** p < 0.001

    Techniques Used: Expressing, Immunohistochemistry, Staining, CCK-8 Assay, Migration

    CircZBTB46 inhibits cell proliferation and migration through hnRNPA2B1 and the PTEN/AKT/mTOR pathway. (A-D) Overexpression of hnRNPA2B1 attenuated the inhibitory effects of circZBTB46 knockdown on the proliferation and migration of HCAECs and HCASMCs. (E) Overexpression of hnRNPA2B1 partially blocked circZBTB46-silencing induced cell apoptosis. (F-G) Silencing circZBTB46 or hnRNPA2B1 increased the expression of PTEN and inhibited AKT and mTOR phosphorylation. * p < 0.05, ** p < 0.01, *** p < 0.001
    Figure Legend Snippet: CircZBTB46 inhibits cell proliferation and migration through hnRNPA2B1 and the PTEN/AKT/mTOR pathway. (A-D) Overexpression of hnRNPA2B1 attenuated the inhibitory effects of circZBTB46 knockdown on the proliferation and migration of HCAECs and HCASMCs. (E) Overexpression of hnRNPA2B1 partially blocked circZBTB46-silencing induced cell apoptosis. (F-G) Silencing circZBTB46 or hnRNPA2B1 increased the expression of PTEN and inhibited AKT and mTOR phosphorylation. * p < 0.05, ** p < 0.01, *** p < 0.001

    Techniques Used: Migration, Over Expression, Expressing

    annexin v fitc apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc apoptosis detection kit
    SiRNA-mediated knockdown of SDC1 and ITGA2 regulates PDAC cell proliferation, <t>apoptosis,</t> and invasion in vitro. ( A ) BxPC-3 and MIA-PaCa2 were transfected with siRNAs. qRT-PCR was used to detect the transfection efficiency. ( B ) Si-SDC1 #1, si-SDC1 #2, si-ITGA2 #1, and si-ITGA2 #3 had better knockdown effects and were selected for further studies, which were detected by western blot. ( C , D ) CCK-8 assay and EdU assay were conducted to examine the BxPC-3 and MIA-PaCa2 cell proliferation viability after the knockdown of SDC1 and ITGA2 . ( E ) Knocking down SDC1 and ITGA2 expression promoted apoptosis in PDAC cells. ( F ) Migration of BxPC-3 and MIA-PaCa2 was detected after transfection with si-SDC1 and si-ITGA2, respectively, for 0 h and 24 h. These data are representative of three independent experiments with similar results. PDAC Pancreatic ductal adenocarcinoma; qRT-PCR Quantitative real-time polymerase chain reaction; CCK-8 Cell Counting Kit-8. (ns P ≥ 0.05; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001).
    Annexin V Fitc Apoptosis Detection Kit, supplied by Vazyme Biotech Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/annexin v fitc apoptosis detection kit/product/Vazyme Biotech Co
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    annexin v fitc apoptosis detection kit - by Bioz Stars, 2023-11
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    1) Product Images from "SDC1 and ITGA2 as novel prognostic biomarkers for PDAC related to IPMN"

    Article Title: SDC1 and ITGA2 as novel prognostic biomarkers for PDAC related to IPMN

    Journal: Scientific Reports

    doi: 10.1038/s41598-023-44646-x

    SiRNA-mediated knockdown of SDC1 and ITGA2 regulates PDAC cell proliferation, apoptosis, and invasion in vitro. ( A ) BxPC-3 and MIA-PaCa2 were transfected with siRNAs. qRT-PCR was used to detect the transfection efficiency. ( B ) Si-SDC1 #1, si-SDC1 #2, si-ITGA2 #1, and si-ITGA2 #3 had better knockdown effects and were selected for further studies, which were detected by western blot. ( C , D ) CCK-8 assay and EdU assay were conducted to examine the BxPC-3 and MIA-PaCa2 cell proliferation viability after the knockdown of SDC1 and ITGA2 . ( E ) Knocking down SDC1 and ITGA2 expression promoted apoptosis in PDAC cells. ( F ) Migration of BxPC-3 and MIA-PaCa2 was detected after transfection with si-SDC1 and si-ITGA2, respectively, for 0 h and 24 h. These data are representative of three independent experiments with similar results. PDAC Pancreatic ductal adenocarcinoma; qRT-PCR Quantitative real-time polymerase chain reaction; CCK-8 Cell Counting Kit-8. (ns P ≥ 0.05; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001).
    Figure Legend Snippet: SiRNA-mediated knockdown of SDC1 and ITGA2 regulates PDAC cell proliferation, apoptosis, and invasion in vitro. ( A ) BxPC-3 and MIA-PaCa2 were transfected with siRNAs. qRT-PCR was used to detect the transfection efficiency. ( B ) Si-SDC1 #1, si-SDC1 #2, si-ITGA2 #1, and si-ITGA2 #3 had better knockdown effects and were selected for further studies, which were detected by western blot. ( C , D ) CCK-8 assay and EdU assay were conducted to examine the BxPC-3 and MIA-PaCa2 cell proliferation viability after the knockdown of SDC1 and ITGA2 . ( E ) Knocking down SDC1 and ITGA2 expression promoted apoptosis in PDAC cells. ( F ) Migration of BxPC-3 and MIA-PaCa2 was detected after transfection with si-SDC1 and si-ITGA2, respectively, for 0 h and 24 h. These data are representative of three independent experiments with similar results. PDAC Pancreatic ductal adenocarcinoma; qRT-PCR Quantitative real-time polymerase chain reaction; CCK-8 Cell Counting Kit-8. (ns P ≥ 0.05; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001).

    Techniques Used: In Vitro, Transfection, Quantitative RT-PCR, Western Blot, CCK-8 Assay, EdU Assay, Expressing, Migration, Real-time Polymerase Chain Reaction, Cell Counting

    annexin v fitc propidium iodide pi apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc propidium iodide pi apoptosis detection kit
    Loss of super enhancer element E_349 in melanoma unlocks tumor growth potential by modulating MEF2A expression. a Epigenetic and 3D genome profiles at the E_349-contained super enhancer and MEF2A locus (GRCh37/hg19 chr15: 99,800,000–100,400,000), including signals of A375 combined Hi-C, H3K27ac, H3K4me1, H3K4me3, ATAC-seq, and HiChIP loops. b Genomic profiles of recurrent DELs and CRISPRi enhancer screen results at the E_349 and MEF2A locus on 297 melanoma samples. c 4C assay result of interaction between the MEF2A promoter and E_349, light blue arrow refers to the 4C viewpoint (VP), and peak region highlighted by yellow arrow represents the chromosome region interacting with the VP. d Expression levels of MEF2A in tumor (T, n = 461 samples) and normal tissues (N, n = 558 samples) were analyzed using the TCGA-SKCM data. e Overall survival analysis of MEF2A in the low MEF2A expressed group and high MEF2A expressed group were compared using the TCGA-SKCM data. f , g The E_349 core sequence (GRCh37/hg19 chr15: 99,982,353–99,983,277) was cloned into pGL3-Promoter vector, and Luciferase assays were performed in 293T cells ( f ), and A375 cells ( g ). h , i Western blotting results of MEF2A protein expression in the E_349-inhibited A375-KRAB ( h ) and E_349-activated A375-VP64 ( i ) cells. j , k Cell <t>apoptosis</t> ( j ) and Plate clone formation ( k ) assay results of the E_349-inhibited A375-KRAB cells with 1 µM vemurafenib or without treatment ( n = 3 samples). l , m The representative three-dimension (3D) modeling graphs and statistical results in calculating tumor volumes for E_349-inhibited A375-KRAB and control cells ( l ) at 2 or 3 weeks after subcutaneous injection in 5-week-old female nude mice, and then the tumors were weighed ( m ) after euthanasia of the mice ( n = 7 mice). CI denotes CRISPR interference, and CA denotes CRISPR activation. Left graph is the representative result, and right graph is the statistical result. All the data are expressed as the means ± SD and analyzed by an unpaired two-tailed Student’s t test. Asterisks indicate significant differences between the indicated experimental groups: *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001
    Annexin V Fitc Propidium Iodide Pi Apoptosis Detection Kit, supplied by Vazyme Biotech Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/annexin v fitc propidium iodide pi apoptosis detection kit/product/Vazyme Biotech Co
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    annexin v fitc propidium iodide pi apoptosis detection kit - by Bioz Stars, 2023-11
    86/100 stars

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    1) Product Images from "Landscape of enhancer disruption and functional screen in melanoma cells"

    Article Title: Landscape of enhancer disruption and functional screen in melanoma cells

    Journal: Genome Biology

    doi: 10.1186/s13059-023-03087-5

    Loss of super enhancer element E_349 in melanoma unlocks tumor growth potential by modulating MEF2A expression. a Epigenetic and 3D genome profiles at the E_349-contained super enhancer and MEF2A locus (GRCh37/hg19 chr15: 99,800,000–100,400,000), including signals of A375 combined Hi-C, H3K27ac, H3K4me1, H3K4me3, ATAC-seq, and HiChIP loops. b Genomic profiles of recurrent DELs and CRISPRi enhancer screen results at the E_349 and MEF2A locus on 297 melanoma samples. c 4C assay result of interaction between the MEF2A promoter and E_349, light blue arrow refers to the 4C viewpoint (VP), and peak region highlighted by yellow arrow represents the chromosome region interacting with the VP. d Expression levels of MEF2A in tumor (T, n = 461 samples) and normal tissues (N, n = 558 samples) were analyzed using the TCGA-SKCM data. e Overall survival analysis of MEF2A in the low MEF2A expressed group and high MEF2A expressed group were compared using the TCGA-SKCM data. f , g The E_349 core sequence (GRCh37/hg19 chr15: 99,982,353–99,983,277) was cloned into pGL3-Promoter vector, and Luciferase assays were performed in 293T cells ( f ), and A375 cells ( g ). h , i Western blotting results of MEF2A protein expression in the E_349-inhibited A375-KRAB ( h ) and E_349-activated A375-VP64 ( i ) cells. j , k Cell apoptosis ( j ) and Plate clone formation ( k ) assay results of the E_349-inhibited A375-KRAB cells with 1 µM vemurafenib or without treatment ( n = 3 samples). l , m The representative three-dimension (3D) modeling graphs and statistical results in calculating tumor volumes for E_349-inhibited A375-KRAB and control cells ( l ) at 2 or 3 weeks after subcutaneous injection in 5-week-old female nude mice, and then the tumors were weighed ( m ) after euthanasia of the mice ( n = 7 mice). CI denotes CRISPR interference, and CA denotes CRISPR activation. Left graph is the representative result, and right graph is the statistical result. All the data are expressed as the means ± SD and analyzed by an unpaired two-tailed Student’s t test. Asterisks indicate significant differences between the indicated experimental groups: *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001
    Figure Legend Snippet: Loss of super enhancer element E_349 in melanoma unlocks tumor growth potential by modulating MEF2A expression. a Epigenetic and 3D genome profiles at the E_349-contained super enhancer and MEF2A locus (GRCh37/hg19 chr15: 99,800,000–100,400,000), including signals of A375 combined Hi-C, H3K27ac, H3K4me1, H3K4me3, ATAC-seq, and HiChIP loops. b Genomic profiles of recurrent DELs and CRISPRi enhancer screen results at the E_349 and MEF2A locus on 297 melanoma samples. c 4C assay result of interaction between the MEF2A promoter and E_349, light blue arrow refers to the 4C viewpoint (VP), and peak region highlighted by yellow arrow represents the chromosome region interacting with the VP. d Expression levels of MEF2A in tumor (T, n = 461 samples) and normal tissues (N, n = 558 samples) were analyzed using the TCGA-SKCM data. e Overall survival analysis of MEF2A in the low MEF2A expressed group and high MEF2A expressed group were compared using the TCGA-SKCM data. f , g The E_349 core sequence (GRCh37/hg19 chr15: 99,982,353–99,983,277) was cloned into pGL3-Promoter vector, and Luciferase assays were performed in 293T cells ( f ), and A375 cells ( g ). h , i Western blotting results of MEF2A protein expression in the E_349-inhibited A375-KRAB ( h ) and E_349-activated A375-VP64 ( i ) cells. j , k Cell apoptosis ( j ) and Plate clone formation ( k ) assay results of the E_349-inhibited A375-KRAB cells with 1 µM vemurafenib or without treatment ( n = 3 samples). l , m The representative three-dimension (3D) modeling graphs and statistical results in calculating tumor volumes for E_349-inhibited A375-KRAB and control cells ( l ) at 2 or 3 weeks after subcutaneous injection in 5-week-old female nude mice, and then the tumors were weighed ( m ) after euthanasia of the mice ( n = 7 mice). CI denotes CRISPR interference, and CA denotes CRISPR activation. Left graph is the representative result, and right graph is the statistical result. All the data are expressed as the means ± SD and analyzed by an unpaired two-tailed Student’s t test. Asterisks indicate significant differences between the indicated experimental groups: *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001

    Techniques Used: Expressing, Hi-C, HiChIP, Sequencing, Clone Assay, Plasmid Preparation, Luciferase, Western Blot, Injection, CRISPR, Activation Assay, Two Tailed Test

    Long-range interaction between E_156 and PTEN maintains melanoma-suppressive function. a Epigenetic and 3D genome profiles at the PTEN and its downstream enhancer locus (GRCh37/hg19 chr10: 89,400,000–90,140,000), including signals of A375 combined Hi-C, H3K27ac, H3K4me1, H3K4me3, ATAC-seq, and HiChIP loops. b Genomic profiles of recurrent DELs and CRISPRi enhancer screen results at the E_156 and PTEN locus on 297 melanoma samples. c 4C assay result of interaction between the PTEN promoter and E_156, light blue arrow refers to the 4C viewpoint (VP), and peak region highlighted by yellow arrow represents the chromosome region interacting with the VP. d Expression levels of PTEN in tumor (T, n = 461 samples) and normal tissues (N, n = 558 samples) were analyzed using the TCGA-SKCM data. e Disease-free survival analysis of PTEN expression were analyzed using the TCGA-SKCM data. Low expression of PTEN predicts shorter disease-free survival. f Western blotting results of MEF2A protein expression in the E_156 (E_155 or E_154 adjacent to E_156)-inhibited A375-KRAB cells. g Western blotting results of PI3K/AKT signaling pathway activation in the E_156 (E_155 or E_154 adjacent to E_156)-inhibited A375-KRAB cells with 1 µM vemurafenib or without treatment. P-AKT denotes Phosphorylated AKT, and T-AKT denotes total AKT. h , i Cell apoptosis ( h ) and Plate clone formation ( i ) assay results of the E_156 (E_155 or E_154 adjacent to E_156)-inhibited A375-KRAB cells with 1 µM vemurafenib or without treatment ( n = 3 samples). j , k The representative three-dimension (3D) modeling graphs and statistical results in calculating tumor volumes for E_156-inhibited A375-KRAB and control cells at 2 or 3 weeks after subcutaneous injection in 5-week-old female nude mice ( j ), and then the tumors were weighed ( k ) after euthanasia of the mice ( n = 7 mice). CI denotes CRISPR interference, and CA denotes CRISPR activation. Left graph is the representative result, and right graph is the statistical result. All the data are expressed as the means ± SD and analyzed by an unpaired two-tailed Student’s t test. Asterisks indicate significant differences between the indicated experimental groups: *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001
    Figure Legend Snippet: Long-range interaction between E_156 and PTEN maintains melanoma-suppressive function. a Epigenetic and 3D genome profiles at the PTEN and its downstream enhancer locus (GRCh37/hg19 chr10: 89,400,000–90,140,000), including signals of A375 combined Hi-C, H3K27ac, H3K4me1, H3K4me3, ATAC-seq, and HiChIP loops. b Genomic profiles of recurrent DELs and CRISPRi enhancer screen results at the E_156 and PTEN locus on 297 melanoma samples. c 4C assay result of interaction between the PTEN promoter and E_156, light blue arrow refers to the 4C viewpoint (VP), and peak region highlighted by yellow arrow represents the chromosome region interacting with the VP. d Expression levels of PTEN in tumor (T, n = 461 samples) and normal tissues (N, n = 558 samples) were analyzed using the TCGA-SKCM data. e Disease-free survival analysis of PTEN expression were analyzed using the TCGA-SKCM data. Low expression of PTEN predicts shorter disease-free survival. f Western blotting results of MEF2A protein expression in the E_156 (E_155 or E_154 adjacent to E_156)-inhibited A375-KRAB cells. g Western blotting results of PI3K/AKT signaling pathway activation in the E_156 (E_155 or E_154 adjacent to E_156)-inhibited A375-KRAB cells with 1 µM vemurafenib or without treatment. P-AKT denotes Phosphorylated AKT, and T-AKT denotes total AKT. h , i Cell apoptosis ( h ) and Plate clone formation ( i ) assay results of the E_156 (E_155 or E_154 adjacent to E_156)-inhibited A375-KRAB cells with 1 µM vemurafenib or without treatment ( n = 3 samples). j , k The representative three-dimension (3D) modeling graphs and statistical results in calculating tumor volumes for E_156-inhibited A375-KRAB and control cells at 2 or 3 weeks after subcutaneous injection in 5-week-old female nude mice ( j ), and then the tumors were weighed ( k ) after euthanasia of the mice ( n = 7 mice). CI denotes CRISPR interference, and CA denotes CRISPR activation. Left graph is the representative result, and right graph is the statistical result. All the data are expressed as the means ± SD and analyzed by an unpaired two-tailed Student’s t test. Asterisks indicate significant differences between the indicated experimental groups: *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001

    Techniques Used: Hi-C, HiChIP, Expressing, Western Blot, Activation Assay, Injection, CRISPR, Two Tailed Test

    annexin v fitc pi apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc pi apoptosis detection kit
    ACQA enhanced fatty acid β-oxidation and reduced injury caused by steatosis in HepG2 cells. ( A ) The rate of fatty acid β-oxidation in HepG2 cells was detected. The reduction rate of micromole ferricyanide was used to characterize the β-oxidation rate of fatty acids. ( B , C ) After the group was treated with chlorogenic acid, the culture medium was collected, and the ALT and AST levels in the culture medium were detected. ( D ) <t>Apoptosis</t> was assessed with annexin V/PI staining. ( E ) The data for analysis are expressed as the ratio of total apoptotic cells to the number of normal cells. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001, and compared with OA group, n = 3.
    Annexin V Fitc Pi Apoptosis Detection Kit, supplied by Vazyme Biotech Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/annexin v fitc pi apoptosis detection kit/product/Vazyme Biotech Co
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    annexin v fitc pi apoptosis detection kit - by Bioz Stars, 2023-11
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    1) Product Images from "Chlorogenic Acid from Burdock Roots Ameliorates Oleic Acid-Induced Steatosis in HepG2 Cells through AMPK/ACC/CPT-1 Pathway"

    Article Title: Chlorogenic Acid from Burdock Roots Ameliorates Oleic Acid-Induced Steatosis in HepG2 Cells through AMPK/ACC/CPT-1 Pathway

    Journal: Molecules

    doi: 10.3390/molecules28217257

    ACQA enhanced fatty acid β-oxidation and reduced injury caused by steatosis in HepG2 cells. ( A ) The rate of fatty acid β-oxidation in HepG2 cells was detected. The reduction rate of micromole ferricyanide was used to characterize the β-oxidation rate of fatty acids. ( B , C ) After the group was treated with chlorogenic acid, the culture medium was collected, and the ALT and AST levels in the culture medium were detected. ( D ) Apoptosis was assessed with annexin V/PI staining. ( E ) The data for analysis are expressed as the ratio of total apoptotic cells to the number of normal cells. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001, and compared with OA group, n = 3.
    Figure Legend Snippet: ACQA enhanced fatty acid β-oxidation and reduced injury caused by steatosis in HepG2 cells. ( A ) The rate of fatty acid β-oxidation in HepG2 cells was detected. The reduction rate of micromole ferricyanide was used to characterize the β-oxidation rate of fatty acids. ( B , C ) After the group was treated with chlorogenic acid, the culture medium was collected, and the ALT and AST levels in the culture medium were detected. ( D ) Apoptosis was assessed with annexin V/PI staining. ( E ) The data for analysis are expressed as the ratio of total apoptotic cells to the number of normal cells. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001, and compared with OA group, n = 3.

    Techniques Used: Staining

    annexin v fitc pi apoptosis detection kit  (Vazyme Biotech Co)


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    Vazyme Biotech Co annexin v fitc pi apoptosis detection kit
    a Representative photographs of DHE fluorescent imaging of lung tissue sections. Scale bars: 100 μm. b The levels of MDA in the lung tissues of 8 M and HFD mice were detected. c Representative TEM images of AECIIs from the Control and Sohlh2 KI mice after 8-week HFD treatment. Mitochondrial profiles showed enlarged swollen mitochondria in Sohlh2 KI AECIIs. Boxed regions are enlarged at the right. Scale bars: 1 μm. d Under an inverted phase-contrast microscope, the morphology of murine primary AECIIs (left). Scale bars: 50 μm; the expression of cell surfactant protein SP-C was measured by immunofluorescence staining (right). Scale bars: 50 μm. e ROS levels were measured by DHE fluorescent intensity in murine primary AECIIs and A549 cells treated with or without 300 μM PA. Scale bars: 50 μm. f Detection of ROS level and average immunofluorescence intensity of mouse primary AECIIs and human A549 cells treated with or without PA by FACS. g The levels of MDA were shown in Sohlh2 overexpression A549 cells treated by PA. h qPCR analysis of proinflammatory cytokines mRNA levels from mouse primary AECIIs and human A549 cells treated by PA. ( n = 3). i ELISA analysis of IL-6, TNF-α, and TGF-β1 in the culture medium of Sohlh2 overexpression A549 cells treated by PA. j Representative images and quantification analysis of TUNEL staining in mouse primary AECIIs and human A549 cells treated with or without PA. ( n = 3). Scale bars: 20 μm. k Percentages of Annexin V-positive cells upon PA treatment were examined by FACS. Cells treated with PBS served as the control. ( n = 3). Data are presented as the mean ± SD. ns. P > 0.05, * P < 0.05, ** P < 0.01, and *** P < 0.001.
    Annexin V Fitc Pi Apoptosis Detection Kit, supplied by Vazyme Biotech Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/annexin v fitc pi apoptosis detection kit/product/Vazyme Biotech Co
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    annexin v fitc pi apoptosis detection kit - by Bioz Stars, 2023-11
    86/100 stars

    Images

    1) Product Images from "Sohlh2 promotes pulmonary fibrosis via repression of p62/Keap1/Nrf2 mediated anti-oxidative signaling pathway"

    Article Title: Sohlh2 promotes pulmonary fibrosis via repression of p62/Keap1/Nrf2 mediated anti-oxidative signaling pathway

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-023-06179-z

    a Representative photographs of DHE fluorescent imaging of lung tissue sections. Scale bars: 100 μm. b The levels of MDA in the lung tissues of 8 M and HFD mice were detected. c Representative TEM images of AECIIs from the Control and Sohlh2 KI mice after 8-week HFD treatment. Mitochondrial profiles showed enlarged swollen mitochondria in Sohlh2 KI AECIIs. Boxed regions are enlarged at the right. Scale bars: 1 μm. d Under an inverted phase-contrast microscope, the morphology of murine primary AECIIs (left). Scale bars: 50 μm; the expression of cell surfactant protein SP-C was measured by immunofluorescence staining (right). Scale bars: 50 μm. e ROS levels were measured by DHE fluorescent intensity in murine primary AECIIs and A549 cells treated with or without 300 μM PA. Scale bars: 50 μm. f Detection of ROS level and average immunofluorescence intensity of mouse primary AECIIs and human A549 cells treated with or without PA by FACS. g The levels of MDA were shown in Sohlh2 overexpression A549 cells treated by PA. h qPCR analysis of proinflammatory cytokines mRNA levels from mouse primary AECIIs and human A549 cells treated by PA. ( n = 3). i ELISA analysis of IL-6, TNF-α, and TGF-β1 in the culture medium of Sohlh2 overexpression A549 cells treated by PA. j Representative images and quantification analysis of TUNEL staining in mouse primary AECIIs and human A549 cells treated with or without PA. ( n = 3). Scale bars: 20 μm. k Percentages of Annexin V-positive cells upon PA treatment were examined by FACS. Cells treated with PBS served as the control. ( n = 3). Data are presented as the mean ± SD. ns. P > 0.05, * P < 0.05, ** P < 0.01, and *** P < 0.001.
    Figure Legend Snippet: a Representative photographs of DHE fluorescent imaging of lung tissue sections. Scale bars: 100 μm. b The levels of MDA in the lung tissues of 8 M and HFD mice were detected. c Representative TEM images of AECIIs from the Control and Sohlh2 KI mice after 8-week HFD treatment. Mitochondrial profiles showed enlarged swollen mitochondria in Sohlh2 KI AECIIs. Boxed regions are enlarged at the right. Scale bars: 1 μm. d Under an inverted phase-contrast microscope, the morphology of murine primary AECIIs (left). Scale bars: 50 μm; the expression of cell surfactant protein SP-C was measured by immunofluorescence staining (right). Scale bars: 50 μm. e ROS levels were measured by DHE fluorescent intensity in murine primary AECIIs and A549 cells treated with or without 300 μM PA. Scale bars: 50 μm. f Detection of ROS level and average immunofluorescence intensity of mouse primary AECIIs and human A549 cells treated with or without PA by FACS. g The levels of MDA were shown in Sohlh2 overexpression A549 cells treated by PA. h qPCR analysis of proinflammatory cytokines mRNA levels from mouse primary AECIIs and human A549 cells treated by PA. ( n = 3). i ELISA analysis of IL-6, TNF-α, and TGF-β1 in the culture medium of Sohlh2 overexpression A549 cells treated by PA. j Representative images and quantification analysis of TUNEL staining in mouse primary AECIIs and human A549 cells treated with or without PA. ( n = 3). Scale bars: 20 μm. k Percentages of Annexin V-positive cells upon PA treatment were examined by FACS. Cells treated with PBS served as the control. ( n = 3). Data are presented as the mean ± SD. ns. P > 0.05, * P < 0.05, ** P < 0.01, and *** P < 0.001.

    Techniques Used: Imaging, Microscopy, Expressing, Immunofluorescence, Staining, Over Expression, Enzyme-linked Immunosorbent Assay, TUNEL Assay

    p62 overexpression or control plasmid was transfected into the control and Sohlh2 overexpressing A549 cells. a ROS levels were measured by DHE fluorescent intensity in four group A549 cells treated by PA. Scale bars: 50 μm. b Detection of ROS levels in four group A549 cells treated by PA by FACS. c Representative images and quantification analysis of TUNEL staining in four group A549 cells treated by PA. ( n = 3). Scale bars: 20 μm. d Percentages of Annexin V-positive cells upon PA treatment were examined by FACS. e , f qPCR and ELISA analysis of the expression of proinflammatory cytokines from four group A549 cells treated by PA. g Representative Western blot images and quantification analysis showing the expression levels of Sohlh2, total Nrf2, and nuclear Nrf2 in the indicated A549 cells. h Representative Western blot images and quantification analysis showing the expression levels of Sohlh2, p62, Keap1, and total Nrf2 in the indicated A549 cells. i qPCR analysis of the expression of Nrf2 target genes (HO1, NQO1, Gsta1) in the indicated A549 cells. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, and *** P < 0.001.
    Figure Legend Snippet: p62 overexpression or control plasmid was transfected into the control and Sohlh2 overexpressing A549 cells. a ROS levels were measured by DHE fluorescent intensity in four group A549 cells treated by PA. Scale bars: 50 μm. b Detection of ROS levels in four group A549 cells treated by PA by FACS. c Representative images and quantification analysis of TUNEL staining in four group A549 cells treated by PA. ( n = 3). Scale bars: 20 μm. d Percentages of Annexin V-positive cells upon PA treatment were examined by FACS. e , f qPCR and ELISA analysis of the expression of proinflammatory cytokines from four group A549 cells treated by PA. g Representative Western blot images and quantification analysis showing the expression levels of Sohlh2, total Nrf2, and nuclear Nrf2 in the indicated A549 cells. h Representative Western blot images and quantification analysis showing the expression levels of Sohlh2, p62, Keap1, and total Nrf2 in the indicated A549 cells. i qPCR analysis of the expression of Nrf2 target genes (HO1, NQO1, Gsta1) in the indicated A549 cells. Data are presented as the mean ± SD. * P < 0.05, ** P < 0.01, and *** P < 0.001.

    Techniques Used: Over Expression, Plasmid Preparation, Transfection, TUNEL Assay, Staining, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

    In the occurrence and progression of pulmonary fibrosis, Sohlh2 can downregulate the transcriptional activity of p62 by directly binding to the promoter region of p62, activating the Keap1/Nrf2 signaling pathway to result in the production of ROS in AECIIs, leading to inflammation, cells apoptosis, and fibrosis of lung tissues under different conditions. Therefore, targeted Sohlh2 may prevent age-related and stress-induced pulmonary fibrosis and provide a new way for clinical treatment of IPF with anti-oxidation.
    Figure Legend Snippet: In the occurrence and progression of pulmonary fibrosis, Sohlh2 can downregulate the transcriptional activity of p62 by directly binding to the promoter region of p62, activating the Keap1/Nrf2 signaling pathway to result in the production of ROS in AECIIs, leading to inflammation, cells apoptosis, and fibrosis of lung tissues under different conditions. Therefore, targeted Sohlh2 may prevent age-related and stress-induced pulmonary fibrosis and provide a new way for clinical treatment of IPF with anti-oxidation.

    Techniques Used: Activity Assay, Binding Assay

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