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klk5  (R&D Systems)


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    Structured Review

    R&D Systems klk5
    Klk5, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/klk5/product/R&D Systems
    Average 94 stars, based on 13 article reviews
    klk5 - by Bioz Stars, 2026-06
    94/100 stars

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    MedChemExpress klk5
    Elevated <t>KLK5</t> expression correlates with poor survival in ovarian cancer. A . Among the up-regulated genes identified across 29 cancer types, 70 genes were specifically overexpressed in ovarian cancer, as determined from the TCGA datasets analyzed using GEPIA2 ( http://gepia2.cancer-pku.cn/#index ). B . KLK5 emerged as the most significantly up-regulated gene (Log 2 FC = 5.759; P-value < 0.001) among the 70 ovarian cancer-specific genes. C . High levels of KLK5 in tumor tissues were significantly associated with reduced disease-free survival. D . KLK5 expression in tumor tissues was notably increased in advanced stages of ovarian cancer (P-value = 0.0455)
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    R&D Systems klk5
    Elevated <t>KLK5</t> expression correlates with poor survival in ovarian cancer. A . Among the up-regulated genes identified across 29 cancer types, 70 genes were specifically overexpressed in ovarian cancer, as determined from the TCGA datasets analyzed using GEPIA2 ( http://gepia2.cancer-pku.cn/#index ). B . KLK5 emerged as the most significantly up-regulated gene (Log 2 FC = 5.759; P-value < 0.001) among the 70 ovarian cancer-specific genes. C . High levels of KLK5 in tumor tissues were significantly associated with reduced disease-free survival. D . KLK5 expression in tumor tissues was notably increased in advanced stages of ovarian cancer (P-value = 0.0455)
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    Proteintech antibodies against klk5
    Genetic and protein expression analysis. (A) Whole-exome sequencing identified a heterozygous deletion spanning the SPINK gene cluster, including SPINK5 . (B) Sanger sequencing of the patient and his mother revealed a polymorphism in SPINK5 ( NM_006846 ; exon 14, c.1258A>G, p.K420E). (C) LEKTI and <t>KLK5</t> expression in peripheral blood mononuclear cells (PBMCs) from the patient compared to healthy controls (HC, n=3). (D) KLK5 level in the patient’s plasma (seven time points from initial hospitalization) compared with that in healthy controls (HC, n = 8).
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    Jingmei Biotech Co Ltd human klk5 elisa kit
    Genetic and protein expression analysis. (A) Whole-exome sequencing identified a heterozygous deletion spanning the SPINK gene cluster, including SPINK5 . (B) Sanger sequencing of the patient and his mother revealed a polymorphism in SPINK5 ( NM_006846 ; exon 14, c.1258A>G, p.K420E). (C) LEKTI and <t>KLK5</t> expression in peripheral blood mononuclear cells (PBMCs) from the patient compared to healthy controls (HC, n=3). (D) KLK5 level in the patient’s plasma (seven time points from initial hospitalization) compared with that in healthy controls (HC, n = 8).
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    R&D Systems recombinant humane klk5 enzyme
    Fig. 3. Effects of doxycycline on <t>KLK5,</t> LL37, iNOS, iNO and VEGF. (a) Human <t>recombinant</t> KLK5 was preincubated with doxycycline for 5 min and incubated with its fluorogenic substrates for 5 min and the product was detected spectrophotometrically. The IC50 values was calculated using a non-linear fitting model (GraphPad Prism Software 9.2.0). (b/c) NHEKs were preincubated for 3 h with doxycycline at the indicated concentrations and stimulated with 2.5 µg/ml LPS (c; striped bars) or left untreated (b; blank bars) for 6 h. The release of LL-37 was determined by ELISA. (d-j) The iNOS mRNA (d/e), protein (f-h) expression and iNO levels (i/j) were determined in A549 cells stimulated (striped bars) with 5 ng/ml IL1β, 5 ng/ml IFNγ and 5 ng/ml TNFα or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (d/e) iNOS and GADPH mRNA expression was determined by qPCR. iNOS levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (e-h) iNOS and actin levels were determined by western blot technique. (g/h) The optical densitometry analysis was achieved with Image Lab 6.0 software. The iNOS levels were normalized to actin. Doxycycline treated samples were related to control samples. (i/j) iNO levels were determined by staining of NO with 5 µM DAF-FM-DA and analysing by flow cytometry. The MFI of doxycycline treated samples were related to control samples. (k-n) The VEGF mRNA (k/l) and protein (m/n) expression was determined in HMC 1.2 cells stimulated (striped bars) with 25 ng/ml PMA and 200 nM calcium ionophore A23187 or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (k/l) VEGF and GADPH mRNA expression were determined by qPCR. VEGF levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (m/n) VEGF levels collected from the supernatant were determined by ELISA. The VEGF level of doxycycline treated samples were related to control samples. The experiments were repeated three – five times. To calculate statistical significance two-way ANOVA with Dunnett`s multiple comparisons test was used. *p < 0.05 indicate statistical significance between treated samples and vehicle samples. Abb. CM, cytokine mixture; DOX, doxycycline; iNOS, inducible nitric oxide synthase; iNO, intracellular nitric oxide; VEGF, vascular endothelial growth factor.
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    Bachem boc-vpr-amc (klk5, klk8, klk13)
    Fig. 3. Effects of doxycycline on <t>KLK5,</t> LL37, iNOS, iNO and VEGF. (a) Human <t>recombinant</t> KLK5 was preincubated with doxycycline for 5 min and incubated with its fluorogenic substrates for 5 min and the product was detected spectrophotometrically. The IC50 values was calculated using a non-linear fitting model (GraphPad Prism Software 9.2.0). (b/c) NHEKs were preincubated for 3 h with doxycycline at the indicated concentrations and stimulated with 2.5 µg/ml LPS (c; striped bars) or left untreated (b; blank bars) for 6 h. The release of LL-37 was determined by ELISA. (d-j) The iNOS mRNA (d/e), protein (f-h) expression and iNO levels (i/j) were determined in A549 cells stimulated (striped bars) with 5 ng/ml IL1β, 5 ng/ml IFNγ and 5 ng/ml TNFα or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (d/e) iNOS and GADPH mRNA expression was determined by qPCR. iNOS levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (e-h) iNOS and actin levels were determined by western blot technique. (g/h) The optical densitometry analysis was achieved with Image Lab 6.0 software. The iNOS levels were normalized to actin. Doxycycline treated samples were related to control samples. (i/j) iNO levels were determined by staining of NO with 5 µM DAF-FM-DA and analysing by flow cytometry. The MFI of doxycycline treated samples were related to control samples. (k-n) The VEGF mRNA (k/l) and protein (m/n) expression was determined in HMC 1.2 cells stimulated (striped bars) with 25 ng/ml PMA and 200 nM calcium ionophore A23187 or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (k/l) VEGF and GADPH mRNA expression were determined by qPCR. VEGF levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (m/n) VEGF levels collected from the supernatant were determined by ELISA. The VEGF level of doxycycline treated samples were related to control samples. The experiments were repeated three – five times. To calculate statistical significance two-way ANOVA with Dunnett`s multiple comparisons test was used. *p < 0.05 indicate statistical significance between treated samples and vehicle samples. Abb. CM, cytokine mixture; DOX, doxycycline; iNOS, inducible nitric oxide synthase; iNO, intracellular nitric oxide; VEGF, vascular endothelial growth factor.
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    Elevated KLK5 expression correlates with poor survival in ovarian cancer. A . Among the up-regulated genes identified across 29 cancer types, 70 genes were specifically overexpressed in ovarian cancer, as determined from the TCGA datasets analyzed using GEPIA2 ( http://gepia2.cancer-pku.cn/#index ). B . KLK5 emerged as the most significantly up-regulated gene (Log 2 FC = 5.759; P-value < 0.001) among the 70 ovarian cancer-specific genes. C . High levels of KLK5 in tumor tissues were significantly associated with reduced disease-free survival. D . KLK5 expression in tumor tissues was notably increased in advanced stages of ovarian cancer (P-value = 0.0455)

    Journal: Cancer Cell International

    Article Title: Characterization of KLK5 -high epithelial cells and their interactions with the tumor microenvironment in high-grade serous ovarian cancer

    doi: 10.1186/s12935-026-04273-8

    Figure Lengend Snippet: Elevated KLK5 expression correlates with poor survival in ovarian cancer. A . Among the up-regulated genes identified across 29 cancer types, 70 genes were specifically overexpressed in ovarian cancer, as determined from the TCGA datasets analyzed using GEPIA2 ( http://gepia2.cancer-pku.cn/#index ). B . KLK5 emerged as the most significantly up-regulated gene (Log 2 FC = 5.759; P-value < 0.001) among the 70 ovarian cancer-specific genes. C . High levels of KLK5 in tumor tissues were significantly associated with reduced disease-free survival. D . KLK5 expression in tumor tissues was notably increased in advanced stages of ovarian cancer (P-value = 0.0455)

    Article Snippet: Following wound induction, cells were immediately treated with KLK5 (0, 200, or 400 ng/mL; HY-P70939A, MedChemExpress, USA) and the initial (0 h) images were acquired.

    Techniques: Expressing

    The effect of KLK5 on migration, invasion, apoptosis, and proliferation of HO8910 cells. A . The significantly enhanced of migration in the HO8910 cell line with the addition of KLK5 (400ng/mL; P < 0.05). B .The significantly enhanced of invasion in the HO8910 cells with the addition of KLK5 (400 ng/mL in upper chamber; P < 0.05). C . No significantly differences of invasion in the HO8910 cell line with the addition of KLK5 in lower chamber. D . The apoptosis of HO8910 cells treated with or without KLK5 (200 and 400 ng/mL). E , F . The proliferation of HO8910 cells treated with or without KLK5. The line plot in Fig. 2E and F show the mean ± SEM

    Journal: Cancer Cell International

    Article Title: Characterization of KLK5 -high epithelial cells and their interactions with the tumor microenvironment in high-grade serous ovarian cancer

    doi: 10.1186/s12935-026-04273-8

    Figure Lengend Snippet: The effect of KLK5 on migration, invasion, apoptosis, and proliferation of HO8910 cells. A . The significantly enhanced of migration in the HO8910 cell line with the addition of KLK5 (400ng/mL; P < 0.05). B .The significantly enhanced of invasion in the HO8910 cells with the addition of KLK5 (400 ng/mL in upper chamber; P < 0.05). C . No significantly differences of invasion in the HO8910 cell line with the addition of KLK5 in lower chamber. D . The apoptosis of HO8910 cells treated with or without KLK5 (200 and 400 ng/mL). E , F . The proliferation of HO8910 cells treated with or without KLK5. The line plot in Fig. 2E and F show the mean ± SEM

    Article Snippet: Following wound induction, cells were immediately treated with KLK5 (0, 200, or 400 ng/mL; HY-P70939A, MedChemExpress, USA) and the initial (0 h) images were acquired.

    Techniques: Migration

    KLK5 is significantly elevated in epithelial cells of high-grade serous ovarian cancer based on single-cell RNA sequencing. A . Uniform Manifold Approximation and Projection (UMAP) visualization of 151,729 cells from 60 samples in publicly available single-cell RNA sequencing datasets from GEO ( https://www.ncbi.nlm.nih.gov/geo/ ). Cells were clustered into seven major cell types, including B cells (B), endothelial cells (Endo), epithelial cells (Epi), fibroblasts (Fib), myeloid cells (Mye), plasma cells (Plasma), and T cells/NK cells (T_NK), based on cell type-specific markers. B . Dot plot illustrating the expression of known marker genes for each cell type. C . UMAP plot displaying the expression levels of KLK5 across the cell clusters. D . KLK5 expression was significantly elevated in epithelial cells of high-grade serous ovarian cancer (HGSOC) compared to normal controls (Log2FC = 0.502, adjusted P < 0.001). E . Spatial transcriptomics shows the expression of KLK5 in HGSOC. OCS, ovarian carcinosarcoma; OCCC, ovarian clear-cell carcinoma; OEC, ovarian endometrioid carcinoma; HGSOC, high-grade serous ovarian cancer; LGSOC, low-grade serous ovarian cancer

    Journal: Cancer Cell International

    Article Title: Characterization of KLK5 -high epithelial cells and their interactions with the tumor microenvironment in high-grade serous ovarian cancer

    doi: 10.1186/s12935-026-04273-8

    Figure Lengend Snippet: KLK5 is significantly elevated in epithelial cells of high-grade serous ovarian cancer based on single-cell RNA sequencing. A . Uniform Manifold Approximation and Projection (UMAP) visualization of 151,729 cells from 60 samples in publicly available single-cell RNA sequencing datasets from GEO ( https://www.ncbi.nlm.nih.gov/geo/ ). Cells were clustered into seven major cell types, including B cells (B), endothelial cells (Endo), epithelial cells (Epi), fibroblasts (Fib), myeloid cells (Mye), plasma cells (Plasma), and T cells/NK cells (T_NK), based on cell type-specific markers. B . Dot plot illustrating the expression of known marker genes for each cell type. C . UMAP plot displaying the expression levels of KLK5 across the cell clusters. D . KLK5 expression was significantly elevated in epithelial cells of high-grade serous ovarian cancer (HGSOC) compared to normal controls (Log2FC = 0.502, adjusted P < 0.001). E . Spatial transcriptomics shows the expression of KLK5 in HGSOC. OCS, ovarian carcinosarcoma; OCCC, ovarian clear-cell carcinoma; OEC, ovarian endometrioid carcinoma; HGSOC, high-grade serous ovarian cancer; LGSOC, low-grade serous ovarian cancer

    Article Snippet: Following wound induction, cells were immediately treated with KLK5 (0, 200, or 400 ng/mL; HY-P70939A, MedChemExpress, USA) and the initial (0 h) images were acquired.

    Techniques: Single Cell, RNA Sequencing, Clinical Proteomics, Expressing, Marker, Spatial Transcriptomics

    Cell-cell interaction network between epithelial cells and the other cells. A . Venn diagram illustrating the cell-cell interaction network among different cell types in each subtype of ovarian cancer. B . Specific cell-cell interactions in HGSOC that correspond to up-regulated genes in epithelial cells from HGSOC. C . Corresponding pathway of the specific cell-cell interactions shown in Fig. 4B. D . Expression levels of KLK5 (Log 2 FC = 1.720; adjusted P < 0.001) in KLK5 -high HGSOC, KLK5 -low HGSOC, and normal controls. E. Expression levels of COL1A1 (Log 2 FC = 1.153; adjusted P = 0.0085), COL1A2 (Log 2 FC = 0.728; adjusted P < 0.001), and COL6A2 (Log 2 FC = 0.546; P < 0.001) were significantly elevated in fibroblast cells from the KLK5 -high HGSOC compared to those in KLK5 -low HGSOC or normal controls. *** indicates the P value < 0.001

    Journal: Cancer Cell International

    Article Title: Characterization of KLK5 -high epithelial cells and their interactions with the tumor microenvironment in high-grade serous ovarian cancer

    doi: 10.1186/s12935-026-04273-8

    Figure Lengend Snippet: Cell-cell interaction network between epithelial cells and the other cells. A . Venn diagram illustrating the cell-cell interaction network among different cell types in each subtype of ovarian cancer. B . Specific cell-cell interactions in HGSOC that correspond to up-regulated genes in epithelial cells from HGSOC. C . Corresponding pathway of the specific cell-cell interactions shown in Fig. 4B. D . Expression levels of KLK5 (Log 2 FC = 1.720; adjusted P < 0.001) in KLK5 -high HGSOC, KLK5 -low HGSOC, and normal controls. E. Expression levels of COL1A1 (Log 2 FC = 1.153; adjusted P = 0.0085), COL1A2 (Log 2 FC = 0.728; adjusted P < 0.001), and COL6A2 (Log 2 FC = 0.546; P < 0.001) were significantly elevated in fibroblast cells from the KLK5 -high HGSOC compared to those in KLK5 -low HGSOC or normal controls. *** indicates the P value < 0.001

    Article Snippet: Following wound induction, cells were immediately treated with KLK5 (0, 200, or 400 ng/mL; HY-P70939A, MedChemExpress, USA) and the initial (0 h) images were acquired.

    Techniques: Expressing

    Transcriptomic changes induced by KLK5 overexpression in ovarian cancer cell lines and the positive relationship between AGRN and KLK5 in single cell RNA datasets of HGSOC. A . Quantitative PCR analysis revealed a significant difference in KLK5 gene expression between the KLK5 -overexpressing SKOV3 cell line (KLK5_OE) and the empty vector control group (Control) ( P < 0.05). B . Transcriptome sequencing analysis identified genes with significant differential expression between KLK5 -overexpressing SKOV3 cells and the empty vector control, where differences with |logFC| > 0.585 and P < 0.05 were considered statistically significant. C . Genes significantly upregulated in KLK5 -overexpressing SKOV3 cells were enriched in the type I interferon synthesis and activation pathways, as indicated by GO enrichment analysis. D . Quantitative PCR analysis revealed a significant difference in KLK5 gene expression between the KLK5 -overexpressing HO-8910 cell line (KLK5_OE) and the empty vector control group (Control) ( P < 0.05). E . Transcriptome sequencing analysis identified genes with significant differential expression between KLK5 -overexpressing HO-8910 cells and the empty vector control, where differences with |logFC| > 0.585 and P < 0.05 were considered statistically significant. F . Venn diagram showing differentially expressed genes (DEGs) between KLK5 -high HGSOC and KLK5 -low HGSOC/normal controls in single cell RNA datasets. G . GO pathway enrichment analysis of common DEGs in epithelial cells from KLK5 -high HGSOC compared to KLK5 -low HGSOC and normal controls, respectively. H . DEGs of epithelial cells between the KLK5 -expression group (Counts ≥ 2) and the null KLK5 -expression group (Counts = 0 in HGSOC. I . KEGG (left) and GO (right) pathway enrichment analyses of DEGs of epithelial cells between the KLK5 -expression group (Counts ≥ 2) and the null KLK5 -expression group (Counts = 0 in HGSOC. J . Positive correlation between KLK5 and AGRN , as demonstrated using the GEPIA2 database ( http://gepia2.cancer-pku.cn/ )

    Journal: Cancer Cell International

    Article Title: Characterization of KLK5 -high epithelial cells and their interactions with the tumor microenvironment in high-grade serous ovarian cancer

    doi: 10.1186/s12935-026-04273-8

    Figure Lengend Snippet: Transcriptomic changes induced by KLK5 overexpression in ovarian cancer cell lines and the positive relationship between AGRN and KLK5 in single cell RNA datasets of HGSOC. A . Quantitative PCR analysis revealed a significant difference in KLK5 gene expression between the KLK5 -overexpressing SKOV3 cell line (KLK5_OE) and the empty vector control group (Control) ( P < 0.05). B . Transcriptome sequencing analysis identified genes with significant differential expression between KLK5 -overexpressing SKOV3 cells and the empty vector control, where differences with |logFC| > 0.585 and P < 0.05 were considered statistically significant. C . Genes significantly upregulated in KLK5 -overexpressing SKOV3 cells were enriched in the type I interferon synthesis and activation pathways, as indicated by GO enrichment analysis. D . Quantitative PCR analysis revealed a significant difference in KLK5 gene expression between the KLK5 -overexpressing HO-8910 cell line (KLK5_OE) and the empty vector control group (Control) ( P < 0.05). E . Transcriptome sequencing analysis identified genes with significant differential expression between KLK5 -overexpressing HO-8910 cells and the empty vector control, where differences with |logFC| > 0.585 and P < 0.05 were considered statistically significant. F . Venn diagram showing differentially expressed genes (DEGs) between KLK5 -high HGSOC and KLK5 -low HGSOC/normal controls in single cell RNA datasets. G . GO pathway enrichment analysis of common DEGs in epithelial cells from KLK5 -high HGSOC compared to KLK5 -low HGSOC and normal controls, respectively. H . DEGs of epithelial cells between the KLK5 -expression group (Counts ≥ 2) and the null KLK5 -expression group (Counts = 0 in HGSOC. I . KEGG (left) and GO (right) pathway enrichment analyses of DEGs of epithelial cells between the KLK5 -expression group (Counts ≥ 2) and the null KLK5 -expression group (Counts = 0 in HGSOC. J . Positive correlation between KLK5 and AGRN , as demonstrated using the GEPIA2 database ( http://gepia2.cancer-pku.cn/ )

    Article Snippet: Following wound induction, cells were immediately treated with KLK5 (0, 200, or 400 ng/mL; HY-P70939A, MedChemExpress, USA) and the initial (0 h) images were acquired.

    Techniques: Over Expression, Single Cell, Real-time Polymerase Chain Reaction, Gene Expression, Plasmid Preparation, Control, Sequencing, Quantitative Proteomics, Activation Assay, Expressing

    Enhanced tumor-associated macrophages in KLK5-high HGSOC. A. Immune cell infiltration profiles of TCGA-KLK5 High , TCGA-KLK5 Low and normal controls, analyzed using the ssGSEA algorithm. B . Subtypes and their proportions of monocytes and macrophages. C . Unsupervised trajectory analysis illustrating state transitions between monocytes and macrophages. The branched trajectory is color-coded by cell states and cell subtypes. D . GO terms enriched from up-regulated genes in macrophage subtypes. E . Differentially expressed genes (DEGs) in THP-1-derived macrophages after co-culture with KLK5-overexpressing (versus empty vector control) HO-8910 cells. (|log₂FC| > 0.585 and P < 0.05). F . Differentially expressed genes (DEGs) in THP-1-derived macrophages after co-culture with KLK5-overexpressing (versus empty vector control) SKOV3 cells. (|log₂FC| > 0.585 and P < 0.05)

    Journal: Cancer Cell International

    Article Title: Characterization of KLK5 -high epithelial cells and their interactions with the tumor microenvironment in high-grade serous ovarian cancer

    doi: 10.1186/s12935-026-04273-8

    Figure Lengend Snippet: Enhanced tumor-associated macrophages in KLK5-high HGSOC. A. Immune cell infiltration profiles of TCGA-KLK5 High , TCGA-KLK5 Low and normal controls, analyzed using the ssGSEA algorithm. B . Subtypes and their proportions of monocytes and macrophages. C . Unsupervised trajectory analysis illustrating state transitions between monocytes and macrophages. The branched trajectory is color-coded by cell states and cell subtypes. D . GO terms enriched from up-regulated genes in macrophage subtypes. E . Differentially expressed genes (DEGs) in THP-1-derived macrophages after co-culture with KLK5-overexpressing (versus empty vector control) HO-8910 cells. (|log₂FC| > 0.585 and P < 0.05). F . Differentially expressed genes (DEGs) in THP-1-derived macrophages after co-culture with KLK5-overexpressing (versus empty vector control) SKOV3 cells. (|log₂FC| > 0.585 and P < 0.05)

    Article Snippet: Following wound induction, cells were immediately treated with KLK5 (0, 200, or 400 ng/mL; HY-P70939A, MedChemExpress, USA) and the initial (0 h) images were acquired.

    Techniques: Derivative Assay, Co-Culture Assay, Plasmid Preparation, Control

    Immune cell-cell interactions in KLK5 -high HGSOC. A . Uniform Manifold Approximation and Projection (UMAP) plot of T and NK cells, color-coded by cell subtypes. B . Relative proportions of T and NK cell subsets in each group. C . GO terms enriched from up-regulated genes in T_CD8_Cytotoxic cells. D . GO terms enriched from up-regulated genes in NK_XCL1 cells. E . Unique Cell-cell interactions between myeloid cells (Mye) and T-NK cells in KLK5 -high HGSOC

    Journal: Cancer Cell International

    Article Title: Characterization of KLK5 -high epithelial cells and their interactions with the tumor microenvironment in high-grade serous ovarian cancer

    doi: 10.1186/s12935-026-04273-8

    Figure Lengend Snippet: Immune cell-cell interactions in KLK5 -high HGSOC. A . Uniform Manifold Approximation and Projection (UMAP) plot of T and NK cells, color-coded by cell subtypes. B . Relative proportions of T and NK cell subsets in each group. C . GO terms enriched from up-regulated genes in T_CD8_Cytotoxic cells. D . GO terms enriched from up-regulated genes in NK_XCL1 cells. E . Unique Cell-cell interactions between myeloid cells (Mye) and T-NK cells in KLK5 -high HGSOC

    Article Snippet: Following wound induction, cells were immediately treated with KLK5 (0, 200, or 400 ng/mL; HY-P70939A, MedChemExpress, USA) and the initial (0 h) images were acquired.

    Techniques:

    Genetic and protein expression analysis. (A) Whole-exome sequencing identified a heterozygous deletion spanning the SPINK gene cluster, including SPINK5 . (B) Sanger sequencing of the patient and his mother revealed a polymorphism in SPINK5 ( NM_006846 ; exon 14, c.1258A>G, p.K420E). (C) LEKTI and KLK5 expression in peripheral blood mononuclear cells (PBMCs) from the patient compared to healthy controls (HC, n=3). (D) KLK5 level in the patient’s plasma (seven time points from initial hospitalization) compared with that in healthy controls (HC, n = 8).

    Journal: Frontiers in Immunology

    Article Title: Clinical and immunological characterization of a Netherton syndrome infant with a large SPINK gene cluster deletion and a c.1258A>G polymorphism in SPINK5

    doi: 10.3389/fimmu.2025.1658444

    Figure Lengend Snippet: Genetic and protein expression analysis. (A) Whole-exome sequencing identified a heterozygous deletion spanning the SPINK gene cluster, including SPINK5 . (B) Sanger sequencing of the patient and his mother revealed a polymorphism in SPINK5 ( NM_006846 ; exon 14, c.1258A>G, p.K420E). (C) LEKTI and KLK5 expression in peripheral blood mononuclear cells (PBMCs) from the patient compared to healthy controls (HC, n=3). (D) KLK5 level in the patient’s plasma (seven time points from initial hospitalization) compared with that in healthy controls (HC, n = 8).

    Article Snippet: Membranes were blocked in 5% skim milk and incubated overnight at 4°C with primary antibodies against LEKTI (29808-1-AP, Proteintech, USA), antibodies against KLK5 (38528, SAB, USA) and HRP-conjugated β-actin recombinant rabbit monoclonal antibody (ET1702-67, HUABIO, China).

    Techniques: Expressing, Sequencing, Clinical Proteomics

    Genetic and protein expression analysis. (A) Whole-exome sequencing identified a heterozygous deletion spanning the SPINK gene cluster, including SPINK5 . (B) Sanger sequencing of the patient and his mother revealed a polymorphism in SPINK5 ( NM_006846 ; exon 14, c.1258A>G, p.K420E). (C) LEKTI and KLK5 expression in peripheral blood mononuclear cells (PBMCs) from the patient compared to healthy controls (HC, n=3). (D) KLK5 level in the patient’s plasma (seven time points from initial hospitalization) compared with that in healthy controls (HC, n = 8).

    Journal: Frontiers in Immunology

    Article Title: Clinical and immunological characterization of a Netherton syndrome infant with a large SPINK gene cluster deletion and a c.1258A>G polymorphism in SPINK5

    doi: 10.3389/fimmu.2025.1658444

    Figure Lengend Snippet: Genetic and protein expression analysis. (A) Whole-exome sequencing identified a heterozygous deletion spanning the SPINK gene cluster, including SPINK5 . (B) Sanger sequencing of the patient and his mother revealed a polymorphism in SPINK5 ( NM_006846 ; exon 14, c.1258A>G, p.K420E). (C) LEKTI and KLK5 expression in peripheral blood mononuclear cells (PBMCs) from the patient compared to healthy controls (HC, n=3). (D) KLK5 level in the patient’s plasma (seven time points from initial hospitalization) compared with that in healthy controls (HC, n = 8).

    Article Snippet: Plasma was collected from peripheral blood samples, and the level of KLK5 was measured using a Human KLK5 ELISA Kit (JM-6832H2, JINGMEI, China).

    Techniques: Expressing, Sequencing, Clinical Proteomics

    Fig. 3. Effects of doxycycline on KLK5, LL37, iNOS, iNO and VEGF. (a) Human recombinant KLK5 was preincubated with doxycycline for 5 min and incubated with its fluorogenic substrates for 5 min and the product was detected spectrophotometrically. The IC50 values was calculated using a non-linear fitting model (GraphPad Prism Software 9.2.0). (b/c) NHEKs were preincubated for 3 h with doxycycline at the indicated concentrations and stimulated with 2.5 µg/ml LPS (c; striped bars) or left untreated (b; blank bars) for 6 h. The release of LL-37 was determined by ELISA. (d-j) The iNOS mRNA (d/e), protein (f-h) expression and iNO levels (i/j) were determined in A549 cells stimulated (striped bars) with 5 ng/ml IL1β, 5 ng/ml IFNγ and 5 ng/ml TNFα or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (d/e) iNOS and GADPH mRNA expression was determined by qPCR. iNOS levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (e-h) iNOS and actin levels were determined by western blot technique. (g/h) The optical densitometry analysis was achieved with Image Lab 6.0 software. The iNOS levels were normalized to actin. Doxycycline treated samples were related to control samples. (i/j) iNO levels were determined by staining of NO with 5 µM DAF-FM-DA and analysing by flow cytometry. The MFI of doxycycline treated samples were related to control samples. (k-n) The VEGF mRNA (k/l) and protein (m/n) expression was determined in HMC 1.2 cells stimulated (striped bars) with 25 ng/ml PMA and 200 nM calcium ionophore A23187 or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (k/l) VEGF and GADPH mRNA expression were determined by qPCR. VEGF levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (m/n) VEGF levels collected from the supernatant were determined by ELISA. The VEGF level of doxycycline treated samples were related to control samples. The experiments were repeated three – five times. To calculate statistical significance two-way ANOVA with Dunnett`s multiple comparisons test was used. *p < 0.05 indicate statistical significance between treated samples and vehicle samples. Abb. CM, cytokine mixture; DOX, doxycycline; iNOS, inducible nitric oxide synthase; iNO, intracellular nitric oxide; VEGF, vascular endothelial growth factor.

    Journal: Scientific reports

    Article Title: Influence of sodium Bituminosulfonate and Doxycycline on signal molecules relevant for rosacea symptoms.

    doi: 10.1038/s41598-025-02796-0

    Figure Lengend Snippet: Fig. 3. Effects of doxycycline on KLK5, LL37, iNOS, iNO and VEGF. (a) Human recombinant KLK5 was preincubated with doxycycline for 5 min and incubated with its fluorogenic substrates for 5 min and the product was detected spectrophotometrically. The IC50 values was calculated using a non-linear fitting model (GraphPad Prism Software 9.2.0). (b/c) NHEKs were preincubated for 3 h with doxycycline at the indicated concentrations and stimulated with 2.5 µg/ml LPS (c; striped bars) or left untreated (b; blank bars) for 6 h. The release of LL-37 was determined by ELISA. (d-j) The iNOS mRNA (d/e), protein (f-h) expression and iNO levels (i/j) were determined in A549 cells stimulated (striped bars) with 5 ng/ml IL1β, 5 ng/ml IFNγ and 5 ng/ml TNFα or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (d/e) iNOS and GADPH mRNA expression was determined by qPCR. iNOS levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (e-h) iNOS and actin levels were determined by western blot technique. (g/h) The optical densitometry analysis was achieved with Image Lab 6.0 software. The iNOS levels were normalized to actin. Doxycycline treated samples were related to control samples. (i/j) iNO levels were determined by staining of NO with 5 µM DAF-FM-DA and analysing by flow cytometry. The MFI of doxycycline treated samples were related to control samples. (k-n) The VEGF mRNA (k/l) and protein (m/n) expression was determined in HMC 1.2 cells stimulated (striped bars) with 25 ng/ml PMA and 200 nM calcium ionophore A23187 or unstimulated (blank bars) in presence or absence of doxycycline in the indicated concentrations. (k/l) VEGF and GADPH mRNA expression were determined by qPCR. VEGF levels were normalized to GAPDH. Doxycycline treated samples were related to control samples. (m/n) VEGF levels collected from the supernatant were determined by ELISA. The VEGF level of doxycycline treated samples were related to control samples. The experiments were repeated three – five times. To calculate statistical significance two-way ANOVA with Dunnett`s multiple comparisons test was used. *p < 0.05 indicate statistical significance between treated samples and vehicle samples. Abb. CM, cytokine mixture; DOX, doxycycline; iNOS, inducible nitric oxide synthase; iNO, intracellular nitric oxide; VEGF, vascular endothelial growth factor.

    Article Snippet: Briefly, recombinant humane KLK5 enzyme (R&D Systems, Wiesbaden, Germany) and the fluorogenic substrate Boc-V-P-R-AMC substrate (Boc: t-Butyloxycarbonyl; AMC: 7-Amino-4-methylcoumarin) (R&D Systems, Wiesbaden, Germany) were used. rhKLK5 was diluted in 1 M NaH2PO4 pH 8 and doxycycline (0.48 μg/ml – 480 μg/ml) or water (background control (C) with enzyme without compound) was added and incubated for 5 min at RT.

    Techniques: Recombinant, Incubation, Software, Enzyme-linked Immunosorbent Assay, Expressing, Control, Western Blot, Staining, Flow Cytometry

    Fig. 5. Potential contribution of SBDS and doxycycline in inflammatory and vascular-modifying pathways (created with Biorender). Macrophages release the vasoconstrictive TXB2. the vasodilatory NO and PGE2, which mediates either vasodilatory or vasoconstrictive effects depending on the interacting EP receptor. SBDS impairs the release of NO in murine macrophages and the release of PGE2 and TXB2 in human primary macrophages. Cytokines released by macrophages activate neutrophils and keratinocytes, which among others, release the antimicrobial peptide LL-37. KLK5 is responsible for cleaving the inactive precursor protein hCAP18 to form the active antimicrobial peptide LL-37. Both SBDS and doxycycline inhibit KLK5. SBDS specifically inhibits the release of LL-37 in neutrophils. LL-37 promotes the release of VEGF from neutrophils and mast cells. SBDS reduced the release of VEGF from both neutrophils and mast cells, while doxycycline reduced the release of VEGF from mast cells. Inhibitory arrows for macrophages are depicted in light purple, for neutrophils in blue, for the enzyme KLK5 in red, and for mast cells in yellow.

    Journal: Scientific reports

    Article Title: Influence of sodium Bituminosulfonate and Doxycycline on signal molecules relevant for rosacea symptoms.

    doi: 10.1038/s41598-025-02796-0

    Figure Lengend Snippet: Fig. 5. Potential contribution of SBDS and doxycycline in inflammatory and vascular-modifying pathways (created with Biorender). Macrophages release the vasoconstrictive TXB2. the vasodilatory NO and PGE2, which mediates either vasodilatory or vasoconstrictive effects depending on the interacting EP receptor. SBDS impairs the release of NO in murine macrophages and the release of PGE2 and TXB2 in human primary macrophages. Cytokines released by macrophages activate neutrophils and keratinocytes, which among others, release the antimicrobial peptide LL-37. KLK5 is responsible for cleaving the inactive precursor protein hCAP18 to form the active antimicrobial peptide LL-37. Both SBDS and doxycycline inhibit KLK5. SBDS specifically inhibits the release of LL-37 in neutrophils. LL-37 promotes the release of VEGF from neutrophils and mast cells. SBDS reduced the release of VEGF from both neutrophils and mast cells, while doxycycline reduced the release of VEGF from mast cells. Inhibitory arrows for macrophages are depicted in light purple, for neutrophils in blue, for the enzyme KLK5 in red, and for mast cells in yellow.

    Article Snippet: Briefly, recombinant humane KLK5 enzyme (R&D Systems, Wiesbaden, Germany) and the fluorogenic substrate Boc-V-P-R-AMC substrate (Boc: t-Butyloxycarbonyl; AMC: 7-Amino-4-methylcoumarin) (R&D Systems, Wiesbaden, Germany) were used. rhKLK5 was diluted in 1 M NaH2PO4 pH 8 and doxycycline (0.48 μg/ml – 480 μg/ml) or water (background control (C) with enzyme without compound) was added and incubated for 5 min at RT.

    Techniques: