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adamts13  (Novus Biologicals)


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    Structured Review

    Novus Biologicals adamts13
    Adamts13, supplied by Novus Biologicals, 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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    Average 94 stars, based on 1 article reviews
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    Chromatin interactions and regulatory landscape at the ABO and <t>ADAMTS13</t> loci in endothelial cells (A) Hi-C data from HUVECs showing chromatin interactions within a segment of chromosome 9, encompassing the ABO and ADAMTS13 loci. Three loop boundaries (L1, L2, L3) are identified, indicating regions anchoring chromatin loops. (B) Detailed epigenomic landscape of the ABO and ADAMTS13 loci, corresponding to the region amplified in (C). Data from multiple assays are shown. RNA-seq data from HUVEC showing gene expression levels at the ABO and ADAMTS13 loci. ADAMTS13 is expressed in HUVECs, whereas ABO shows no detectable expression in this cell type. ChIA-PET (CTCF): identifies CTCF-binding at L1, L2, and L3, suggesting these sites demarcate loop boundaries. DNase-seq: reveals accessible chromatin regions aligning with the loop anchors. ChIP-seq for RAD21 (cohesin): confirms cohesin enrichment at L1, L2, and L3. ChIP-seq data for HBMECs identify CTCF binding sites, while DNase-seq reveals accessible chromatin regions at L1, L2, and L3. (C) Drawn chromatin interaction model of the ABO and ADAMTS13 loci based on epigenomic and chromatin conformation data integrating Hi-C, ChIA-PET, DNase-seq, and ChIP-seq data from HUVEC, created with BioRender.com .
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    ADAMTS13 maintained renal function and attenuated renal fibrosis in vivo . Control mice were treated with vehicle (Control). The STZ-treated mice were infused with vehicle (DN) or <t>rhADAMTS13</t> (DN + rhADAMTS13). rhADAMTS13 (2.6 ug/kg body weight) was injected into the tail vein daily for the subsequent 7 d. (A) The workflow of animal experiments. (B) Representative renal immunohistochemical staining of ADAMTS13 in the kidney. Scale Bar: 30 μm. (C) Representative renal morphological images of mice were shown. Hematoxylin-Eosin (HE), Masson’s trichrome and Periodic Acid-Schiff (PAS) staining of kidney slices. Scale Bar: 30 μm. (D) Body weight. (E) Serum glucose. (F) BUN. (G) Scr. (H) Urinary volume. (I) Proteinuria. (J) Urinary KIM-1. (K) Renal KIM-1 mRNA expression. ADAMTS13: a disintegrin and metalloprotease with a thrombospondin type 1 motif member 13; DN: diabetic nephropathy; BUN: blood urea nitrogen; Scr: serum creatinine; KIM-1: kidney injury molecule-1. Results were presented as mean ± SEM. N = 5, ** P < 0.01, *** P < 0.001, one-way ANOVA followed by Tukey’s post hoc test.
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    ADAMTS13 maintained renal function and attenuated renal fibrosis in vivo . Control mice were treated with vehicle (Control). The STZ-treated mice were infused with vehicle (DN) or <t>rhADAMTS13</t> (DN + rhADAMTS13). rhADAMTS13 (2.6 ug/kg body weight) was injected into the tail vein daily for the subsequent 7 d. (A) The workflow of animal experiments. (B) Representative renal immunohistochemical staining of ADAMTS13 in the kidney. Scale Bar: 30 μm. (C) Representative renal morphological images of mice were shown. Hematoxylin-Eosin (HE), Masson’s trichrome and Periodic Acid-Schiff (PAS) staining of kidney slices. Scale Bar: 30 μm. (D) Body weight. (E) Serum glucose. (F) BUN. (G) Scr. (H) Urinary volume. (I) Proteinuria. (J) Urinary KIM-1. (K) Renal KIM-1 mRNA expression. ADAMTS13: a disintegrin and metalloprotease with a thrombospondin type 1 motif member 13; DN: diabetic nephropathy; BUN: blood urea nitrogen; Scr: serum creatinine; KIM-1: kidney injury molecule-1. Results were presented as mean ± SEM. N = 5, ** P < 0.01, *** P < 0.001, one-way ANOVA followed by Tukey’s post hoc test.
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    ADAMTS13 maintained renal function and attenuated renal fibrosis in vivo . Control mice were treated with vehicle (Control). The STZ-treated mice were infused with vehicle (DN) or <t>rhADAMTS13</t> (DN + rhADAMTS13). rhADAMTS13 (2.6 ug/kg body weight) was injected into the tail vein daily for the subsequent 7 d. (A) The workflow of animal experiments. (B) Representative renal immunohistochemical staining of ADAMTS13 in the kidney. Scale Bar: 30 μm. (C) Representative renal morphological images of mice were shown. Hematoxylin-Eosin (HE), Masson’s trichrome and Periodic Acid-Schiff (PAS) staining of kidney slices. Scale Bar: 30 μm. (D) Body weight. (E) Serum glucose. (F) BUN. (G) Scr. (H) Urinary volume. (I) Proteinuria. (J) Urinary KIM-1. (K) Renal KIM-1 mRNA expression. ADAMTS13: a disintegrin and metalloprotease with a thrombospondin type 1 motif member 13; DN: diabetic nephropathy; BUN: blood urea nitrogen; Scr: serum creatinine; KIM-1: kidney injury molecule-1. Results were presented as mean ± SEM. N = 5, ** P < 0.01, *** P < 0.001, one-way ANOVA followed by Tukey’s post hoc test.
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    ADAMTS13 maintained renal function and attenuated renal fibrosis in vivo . Control mice were treated with vehicle (Control). The STZ-treated mice were infused with vehicle (DN) or <t>rhADAMTS13</t> (DN + rhADAMTS13). rhADAMTS13 (2.6 ug/kg body weight) was injected into the tail vein daily for the subsequent 7 d. (A) The workflow of animal experiments. (B) Representative renal immunohistochemical staining of ADAMTS13 in the kidney. Scale Bar: 30 μm. (C) Representative renal morphological images of mice were shown. Hematoxylin-Eosin (HE), Masson’s trichrome and Periodic Acid-Schiff (PAS) staining of kidney slices. Scale Bar: 30 μm. (D) Body weight. (E) Serum glucose. (F) BUN. (G) Scr. (H) Urinary volume. (I) Proteinuria. (J) Urinary KIM-1. (K) Renal KIM-1 mRNA expression. ADAMTS13: a disintegrin and metalloprotease with a thrombospondin type 1 motif member 13; DN: diabetic nephropathy; BUN: blood urea nitrogen; Scr: serum creatinine; KIM-1: kidney injury molecule-1. Results were presented as mean ± SEM. N = 5, ** P < 0.01, *** P < 0.001, one-way ANOVA followed by Tukey’s post hoc test.
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    Image Search Results


    Chromatin interactions and regulatory landscape at the ABO and ADAMTS13 loci in endothelial cells (A) Hi-C data from HUVECs showing chromatin interactions within a segment of chromosome 9, encompassing the ABO and ADAMTS13 loci. Three loop boundaries (L1, L2, L3) are identified, indicating regions anchoring chromatin loops. (B) Detailed epigenomic landscape of the ABO and ADAMTS13 loci, corresponding to the region amplified in (C). Data from multiple assays are shown. RNA-seq data from HUVEC showing gene expression levels at the ABO and ADAMTS13 loci. ADAMTS13 is expressed in HUVECs, whereas ABO shows no detectable expression in this cell type. ChIA-PET (CTCF): identifies CTCF-binding at L1, L2, and L3, suggesting these sites demarcate loop boundaries. DNase-seq: reveals accessible chromatin regions aligning with the loop anchors. ChIP-seq for RAD21 (cohesin): confirms cohesin enrichment at L1, L2, and L3. ChIP-seq data for HBMECs identify CTCF binding sites, while DNase-seq reveals accessible chromatin regions at L1, L2, and L3. (C) Drawn chromatin interaction model of the ABO and ADAMTS13 loci based on epigenomic and chromatin conformation data integrating Hi-C, ChIA-PET, DNase-seq, and ChIP-seq data from HUVEC, created with BioRender.com .

    Journal: Human Genetics and Genomics Advances

    Article Title: A non-coding ABO regulatory variant associatedwith VWF levels, thrombosis risk, and COVID-19 severity is topologically linked to ADAMTS13 in endothelial cells

    doi: 10.1016/j.xhgg.2025.100550

    Figure Lengend Snippet: Chromatin interactions and regulatory landscape at the ABO and ADAMTS13 loci in endothelial cells (A) Hi-C data from HUVECs showing chromatin interactions within a segment of chromosome 9, encompassing the ABO and ADAMTS13 loci. Three loop boundaries (L1, L2, L3) are identified, indicating regions anchoring chromatin loops. (B) Detailed epigenomic landscape of the ABO and ADAMTS13 loci, corresponding to the region amplified in (C). Data from multiple assays are shown. RNA-seq data from HUVEC showing gene expression levels at the ABO and ADAMTS13 loci. ADAMTS13 is expressed in HUVECs, whereas ABO shows no detectable expression in this cell type. ChIA-PET (CTCF): identifies CTCF-binding at L1, L2, and L3, suggesting these sites demarcate loop boundaries. DNase-seq: reveals accessible chromatin regions aligning with the loop anchors. ChIP-seq for RAD21 (cohesin): confirms cohesin enrichment at L1, L2, and L3. ChIP-seq data for HBMECs identify CTCF binding sites, while DNase-seq reveals accessible chromatin regions at L1, L2, and L3. (C) Drawn chromatin interaction model of the ABO and ADAMTS13 loci based on epigenomic and chromatin conformation data integrating Hi-C, ChIA-PET, DNase-seq, and ChIP-seq data from HUVEC, created with BioRender.com .

    Article Snippet: Quantitative PCR was conducted with TaqMan Fast Advanced Master Mix (Applied Biosystems, catalog no. 4444556) and TaqMan probes for ADAMTS13 (Applied Biosystems, catalog no. Hs00260148_m1) and glyceraldehyde 3-phosphate dehydrogenase (Applied Biosystems, catalog no. Hs02786624_g1).

    Techniques: Hi-C, Amplification, RNA Sequencing, Gene Expression, Expressing, ChIA Pet Assay, Binding Assay, ChIP-sequencing

    Functional testing and motif evaluation of non-coding variants at the ABO locus (A) Tables summarizing phenotypes previously associated with the non-coding variants rs657152 and rs505922 at the ABO locus. (B) Results of CRISPRa activation assays targeting the regions containing rs657152 and rs505922 in HUVECs. Three sgRNAs were used to activate transcription at each locus. The region harboring rs657152 demonstrated a significant increase in ADAMTS13 expression ( p < 0.05), supporting its role as a cis -regulatory element. In contrast, targeting the rs505922 region showed no significant activation. Data are represented as average fold change relative to control, with each point being a technical replicate ( n = 3). (C) Results of luciferase reporter assays for the genomic regions containing rs657152 and rs505922. For each variant, constructs containing either the risk or non-risk allele were tested in HUVECs to evaluate allele-specific transcriptional activity. The assay showed that the risk allele of rs505922 significantly reduced luciferase activity compared to the non-risk allele ( p < 0.05). In contrast, no statistically significant difference was observed between the alleles of rs657152. Data are represented as average luciferase activity relative to control, normalized with Renilla luciferase activity, with each point being a technical replicate ( n = 3) for each variant. (D) Motif analysis for the genomic regions containing rs657152 and rs505922. The in silico analysis demonstrated allele-specific transcription factor binding motifs for both variants. Substitution of the risk and non-risk alleles resulted in distinct motif profiles.

    Journal: Human Genetics and Genomics Advances

    Article Title: A non-coding ABO regulatory variant associatedwith VWF levels, thrombosis risk, and COVID-19 severity is topologically linked to ADAMTS13 in endothelial cells

    doi: 10.1016/j.xhgg.2025.100550

    Figure Lengend Snippet: Functional testing and motif evaluation of non-coding variants at the ABO locus (A) Tables summarizing phenotypes previously associated with the non-coding variants rs657152 and rs505922 at the ABO locus. (B) Results of CRISPRa activation assays targeting the regions containing rs657152 and rs505922 in HUVECs. Three sgRNAs were used to activate transcription at each locus. The region harboring rs657152 demonstrated a significant increase in ADAMTS13 expression ( p < 0.05), supporting its role as a cis -regulatory element. In contrast, targeting the rs505922 region showed no significant activation. Data are represented as average fold change relative to control, with each point being a technical replicate ( n = 3). (C) Results of luciferase reporter assays for the genomic regions containing rs657152 and rs505922. For each variant, constructs containing either the risk or non-risk allele were tested in HUVECs to evaluate allele-specific transcriptional activity. The assay showed that the risk allele of rs505922 significantly reduced luciferase activity compared to the non-risk allele ( p < 0.05). In contrast, no statistically significant difference was observed between the alleles of rs657152. Data are represented as average luciferase activity relative to control, normalized with Renilla luciferase activity, with each point being a technical replicate ( n = 3) for each variant. (D) Motif analysis for the genomic regions containing rs657152 and rs505922. The in silico analysis demonstrated allele-specific transcription factor binding motifs for both variants. Substitution of the risk and non-risk alleles resulted in distinct motif profiles.

    Article Snippet: Quantitative PCR was conducted with TaqMan Fast Advanced Master Mix (Applied Biosystems, catalog no. 4444556) and TaqMan probes for ADAMTS13 (Applied Biosystems, catalog no. Hs00260148_m1) and glyceraldehyde 3-phosphate dehydrogenase (Applied Biosystems, catalog no. Hs02786624_g1).

    Techniques: Functional Assay, Activation Assay, Expressing, Control, Luciferase, Variant Assay, Construct, Activity Assay, In Silico, Binding Assay

    ADAMTS13 maintained renal function and attenuated renal fibrosis in vivo . Control mice were treated with vehicle (Control). The STZ-treated mice were infused with vehicle (DN) or rhADAMTS13 (DN + rhADAMTS13). rhADAMTS13 (2.6 ug/kg body weight) was injected into the tail vein daily for the subsequent 7 d. (A) The workflow of animal experiments. (B) Representative renal immunohistochemical staining of ADAMTS13 in the kidney. Scale Bar: 30 μm. (C) Representative renal morphological images of mice were shown. Hematoxylin-Eosin (HE), Masson’s trichrome and Periodic Acid-Schiff (PAS) staining of kidney slices. Scale Bar: 30 μm. (D) Body weight. (E) Serum glucose. (F) BUN. (G) Scr. (H) Urinary volume. (I) Proteinuria. (J) Urinary KIM-1. (K) Renal KIM-1 mRNA expression. ADAMTS13: a disintegrin and metalloprotease with a thrombospondin type 1 motif member 13; DN: diabetic nephropathy; BUN: blood urea nitrogen; Scr: serum creatinine; KIM-1: kidney injury molecule-1. Results were presented as mean ± SEM. N = 5, ** P < 0.01, *** P < 0.001, one-way ANOVA followed by Tukey’s post hoc test.

    Journal: Renal Failure

    Article Title: ADAMTS13 ameliorates diabetic nephropathy by Nrf2/GPX4/eNOS signaling pathway

    doi: 10.1080/0886022X.2026.2646089

    Figure Lengend Snippet: ADAMTS13 maintained renal function and attenuated renal fibrosis in vivo . Control mice were treated with vehicle (Control). The STZ-treated mice were infused with vehicle (DN) or rhADAMTS13 (DN + rhADAMTS13). rhADAMTS13 (2.6 ug/kg body weight) was injected into the tail vein daily for the subsequent 7 d. (A) The workflow of animal experiments. (B) Representative renal immunohistochemical staining of ADAMTS13 in the kidney. Scale Bar: 30 μm. (C) Representative renal morphological images of mice were shown. Hematoxylin-Eosin (HE), Masson’s trichrome and Periodic Acid-Schiff (PAS) staining of kidney slices. Scale Bar: 30 μm. (D) Body weight. (E) Serum glucose. (F) BUN. (G) Scr. (H) Urinary volume. (I) Proteinuria. (J) Urinary KIM-1. (K) Renal KIM-1 mRNA expression. ADAMTS13: a disintegrin and metalloprotease with a thrombospondin type 1 motif member 13; DN: diabetic nephropathy; BUN: blood urea nitrogen; Scr: serum creatinine; KIM-1: kidney injury molecule-1. Results were presented as mean ± SEM. N = 5, ** P < 0.01, *** P < 0.001, one-way ANOVA followed by Tukey’s post hoc test.

    Article Snippet: Hyperglycemia was defined as a fasting blood glucose ≥11.1 mmol/L or random blood glucose ≥16.7 mmol/L. rhADAMTS13 (4245-AD, R&D Systems, Minneapolis, MN) was dissolved in saline and administered to mice via tail vein injections.

    Techniques: In Vivo, Control, Injection, Immunohistochemical staining, Staining, Expressing