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recombinant mouse cst6 (R&D Systems)

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R&D Systems recombinant mouse cst6

Regulation of epidermal protease activity by <t>CST6.</t> Model of the regulatory role of CST6 in processes that control epidermal cornification, desquamation and HF maintenance. 1 ) Inhibition of CTSL activity by CST6 is important in the cornification process, as CTSL is the elusive processing and activating enzyme for (TGM)-3. CTSL is also able to process CTSD, which in turn can activate TGM-1. 2 ) Inhibition of CTSV regulates desquamation, as CTSV is able to degrade desmosomal and corneodesmosomal proteins, such as desmoglein-1, desmocollin-1, and corneodesmosin. As CTSV is expressed only in humans, murine CTSL probably controls the specific functional enzymatic activities of both human CTSL and CTSV. 3 ) The findings in the present study suggest that inhibition of CtsB by Cst6 protects HF maintenance in mice. 4 ) Inhibition of human LGMN regulates the processing of (pro)-cathepsins; however mouse LGMN is not inhibited by mouse Cst6.

Recombinant Mouse Cst6, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+mouse+cst6/pmc05602906-61-4-7?v=R%26D+Systems
Average 90 stars, based on 1 article reviews

recombinant mouse cst6 - by Bioz Stars, 2026-06

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1) Product Images from "Cathepsin B as a potential cystatin M/E target in the mouse hair follicle"

Article Title: Cathepsin B as a potential cystatin M/E target in the mouse hair follicle

Journal: The FASEB Journal

doi: 10.1096/fj.201700267R

Regulation of epidermal protease activity by CST6. Model of the regulatory role of CST6 in processes that control epidermal cornification, desquamation and HF maintenance. 1 ) Inhibition of CTSL activity by CST6 is important in the cornification process, as CTSL is the elusive processing and activating enzyme for (TGM)-3. CTSL is also able to process CTSD, which in turn can activate TGM-1. 2 ) Inhibition of CTSV regulates desquamation, as CTSV is able to degrade desmosomal and corneodesmosomal proteins, such as desmoglein-1, desmocollin-1, and corneodesmosin. As CTSV is expressed only in humans, murine CTSL probably controls the specific functional enzymatic activities of both human CTSL and CTSV. 3 ) The findings in the present study suggest that inhibition of CtsB by Cst6 protects HF maintenance in mice. 4 ) Inhibition of human LGMN regulates the processing of (pro)-cathepsins; however mouse LGMN is not inhibited by mouse Cst6.

Figure Legend Snippet: Regulation of epidermal protease activity by CST6. Model of the regulatory role of CST6 in processes that control epidermal cornification, desquamation and HF maintenance. 1 ) Inhibition of CTSL activity by CST6 is important in the cornification process, as CTSL is the elusive processing and activating enzyme for (TGM)-3. CTSL is also able to process CTSD, which in turn can activate TGM-1. 2 ) Inhibition of CTSV regulates desquamation, as CTSV is able to degrade desmosomal and corneodesmosomal proteins, such as desmoglein-1, desmocollin-1, and corneodesmosin. As CTSV is expressed only in humans, murine CTSL probably controls the specific functional enzymatic activities of both human CTSL and CTSV. 3 ) The findings in the present study suggest that inhibition of CtsB by Cst6 protects HF maintenance in mice. 4 ) Inhibition of human LGMN regulates the processing of (pro)-cathepsins; however mouse LGMN is not inhibited by mouse Cst6.

Techniques Used: Activity Assay, Inhibition, Functional Assay

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CST6 suppresses osteoclastogenesis and bone metastasis. ( A ) Osteoclastogenesis of murine primary bone marrow cells with conditioned medium (CM) from CST6 -overexpressing or control SCP2 (n = 3 independent experiments). Ctrl, control. ( B ) Osteoclastogenesis of primary bone marrow culture with CM from CST6 knockdown or control SCP4 cells (n = 3 independent experiments). ( C-F ) Intracardiac injection of SCP2 cells with CST6 overexpression for bone metastasis analysis (n = 10 mice per group). Shown are representative bioluminescence imaging (BLI), micro-CT, H&E and TRAP staining of the hind legs ( C ), ex vivo BLI analysis of hind legs of the mice ( D ), BLI quantitation of limb metastasis ( E ) and quantitation of TRAP + cells along the tumor-bone interface ( F ). White and black arrows ( C ) point to the area of bone damage and osteoclasts, respectively. Scale bar, 200 μm. ( G ) Intracardiac injection of SCP4 cells with CST6 knockdown for bone metastasis analysis. ( H ) Osteoclastogenesis of primary bone marrow cells treated with 32 nM human or mouse (mCST6) recombinant CST6 proteins. ( I ) Osteoclastogenesis of RAW264.7 cells cultured with RANKL and treated with 32 nM human CST6 protein or 32 nM human CST6 and 7 µg/ml CST6 neutralizing antibody. ( J ) Expression of various gene markers of osteoclast differentiation in RAW264.7 cells treated with CST6 recombinant protein or CST6 recombinant protein and CST6 neutralizing antibody (n = 3 biological repeats). Scale bar, 150 μm. * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Journal: Theranostics

Article Title: CST6 protein and peptides inhibit breast cancer bone metastasis by suppressing CTSB activity and osteoclastogenesis

doi: 10.7150/thno.62187

Figure Lengend Snippet: CST6 suppresses osteoclastogenesis and bone metastasis. ( A ) Osteoclastogenesis of murine primary bone marrow cells with conditioned medium (CM) from CST6 -overexpressing or control SCP2 (n = 3 independent experiments). Ctrl, control. ( B ) Osteoclastogenesis of primary bone marrow culture with CM from CST6 knockdown or control SCP4 cells (n = 3 independent experiments). ( C-F ) Intracardiac injection of SCP2 cells with CST6 overexpression for bone metastasis analysis (n = 10 mice per group). Shown are representative bioluminescence imaging (BLI), micro-CT, H&E and TRAP staining of the hind legs ( C ), ex vivo BLI analysis of hind legs of the mice ( D ), BLI quantitation of limb metastasis ( E ) and quantitation of TRAP + cells along the tumor-bone interface ( F ). White and black arrows ( C ) point to the area of bone damage and osteoclasts, respectively. Scale bar, 200 μm. ( G ) Intracardiac injection of SCP4 cells with CST6 knockdown for bone metastasis analysis. ( H ) Osteoclastogenesis of primary bone marrow cells treated with 32 nM human or mouse (mCST6) recombinant CST6 proteins. ( I ) Osteoclastogenesis of RAW264.7 cells cultured with RANKL and treated with 32 nM human CST6 protein or 32 nM human CST6 and 7 µg/ml CST6 neutralizing antibody. ( J ) Expression of various gene markers of osteoclast differentiation in RAW264.7 cells treated with CST6 recombinant protein or CST6 recombinant protein and CST6 neutralizing antibody (n = 3 biological repeats). Scale bar, 150 μm. * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Article Snippet: Other reagents used in this study included CST6 neutralizing antibody (MAB1286, R&D), CA-074Me (HY-100350, Medchem Express), Z-FY(t-Bu)-DMK (219427, Merck), SB203580 (1076, Selleck) and recombinant mouse CST6 protein (1284, R&D).

Techniques: Control, Knockdown, Injection, Over Expression, Imaging, Micro-CT, Staining, Ex Vivo, Quantitation Assay, Recombinant, Cell Culture, Expressing

CST6 regulates osteoclastogenesis by inhibiting CTSB. ( A ) CTSB enzymatic activity in lysates of SCP2 cells expressing wild type or mutant CST6 (n = 3 independent experiments). ∆N, N64A; ∆W, W135A; ∆NW, N64A and W135A double mutant. ( B, C ) Osteoclastogenesis of primary bone marrow treated with CM from SCP2 overexpressing CST6 mutants (n = 3 independent experiments). Representative images of TRAP staining were shown in C . Scale bar, 150 μm. ( D, E ) In vivo bone metastasis analysis of SCP2 cells expressing CST6 mutants (n = 10 mice per group). Shown are representative images of BLI, H&E and TRAP staining of bone metastases in hind legs at week 6 after SCP2 injection ( D ), and quantitation of BLI signal and TRAP + cells ( E ). Scale bar, 200 μm. ( F ) Osteoclastogenesis of primary bone marrow treated with 10 μM Z-FY(t-Bu)-DMK (Z-FY) or CA-074Me (n = 3 independent experiments). ( G ) RAW264.7 osteoclastogenesis after treatment with Z-FY or CA074Me (n = 3 independent experiments). ( H ) Osteoclastogenesis of murine primary bone marrow cells transfected with Ctsb siRNA. ( I ) Intracellular CTSB activity of RAW264.7 after treatment with 32 nM CST6 protein. ( J ) RAW264.7 was cultured with recombinant His-tagged CST6 protein for the indicated time, and intracellular CST6-His level was analyzed by Western blots after PBS washing of the cells. α-Tub, α-Tubulin. ( K ) Western blot analysis of intracellular CST6-His level of RAW264.7 after culturing the cells with CST6-His protein and various concentrations of Dynasore. ( L ) RAW264.7 osteoclastogenesis after CST6 protein and Dynasore treatment. Scale bar, 150 μm. * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Journal: Theranostics

Article Title: CST6 protein and peptides inhibit breast cancer bone metastasis by suppressing CTSB activity and osteoclastogenesis

doi: 10.7150/thno.62187

Figure Lengend Snippet: CST6 regulates osteoclastogenesis by inhibiting CTSB. ( A ) CTSB enzymatic activity in lysates of SCP2 cells expressing wild type or mutant CST6 (n = 3 independent experiments). ∆N, N64A; ∆W, W135A; ∆NW, N64A and W135A double mutant. ( B, C ) Osteoclastogenesis of primary bone marrow treated with CM from SCP2 overexpressing CST6 mutants (n = 3 independent experiments). Representative images of TRAP staining were shown in C . Scale bar, 150 μm. ( D, E ) In vivo bone metastasis analysis of SCP2 cells expressing CST6 mutants (n = 10 mice per group). Shown are representative images of BLI, H&E and TRAP staining of bone metastases in hind legs at week 6 after SCP2 injection ( D ), and quantitation of BLI signal and TRAP + cells ( E ). Scale bar, 200 μm. ( F ) Osteoclastogenesis of primary bone marrow treated with 10 μM Z-FY(t-Bu)-DMK (Z-FY) or CA-074Me (n = 3 independent experiments). ( G ) RAW264.7 osteoclastogenesis after treatment with Z-FY or CA074Me (n = 3 independent experiments). ( H ) Osteoclastogenesis of murine primary bone marrow cells transfected with Ctsb siRNA. ( I ) Intracellular CTSB activity of RAW264.7 after treatment with 32 nM CST6 protein. ( J ) RAW264.7 was cultured with recombinant His-tagged CST6 protein for the indicated time, and intracellular CST6-His level was analyzed by Western blots after PBS washing of the cells. α-Tub, α-Tubulin. ( K ) Western blot analysis of intracellular CST6-His level of RAW264.7 after culturing the cells with CST6-His protein and various concentrations of Dynasore. ( L ) RAW264.7 osteoclastogenesis after CST6 protein and Dynasore treatment. Scale bar, 150 μm. * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Techniques: Activity Assay, Expressing, Mutagenesis, Staining, In Vivo, Injection, Quantitation Assay, Transfection, Cell Culture, Recombinant, Western Blot

CST6 regulates osteoclastogenesis by stabilizing SPHK1 and inhibiting p38. ( A ) SPHK1 and phosphorylation of p38 in murine primary bone marrow cells transfected with Ctsb siRNA. ( B ) SPHK1 and phosphorylation of p38 in RAW264.7 after treatment with CA074Me or CST6 protein. ( C ) RAW264.7 osteoclastogenesis after Sphk1 overexpression and Sphk1 knockdown. ( d-f ) SPHK1 expression ( D ) and osteoclastogenesis ( E, F ) of murine primary bone marrow cells with Ctsb and Sphk1 knockdown. ( G, H ) SPHK1 expression ( G ) and osteoclastogenesis ( H ) of RAW264.7 after Sphk1 knockdown and recombinant CST6 treatment. ( I ) Phosphorylation of p38 in primary bone marrow cells with Ctsb knockdown (left) and in RAW264.7 cells after Sphk1 knockdown (right), together with RANKL treatment of various time. ( J ) Phosphorylation of p38 in RAW264.7 cells treated with CM from CST6 -ovexpressing or control SCP2 cells, together with RANKL treatment of various time. ( K, L ) Phosphorylation of p38 ( K ) and osteoclastogenesis ( L ) of RAW264.7 treated with RANKL, SB203580 and CM from CST6 -knockdown or control SCP4 cells. * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Journal: Theranostics

Article Title: CST6 protein and peptides inhibit breast cancer bone metastasis by suppressing CTSB activity and osteoclastogenesis

doi: 10.7150/thno.62187

Figure Lengend Snippet: CST6 regulates osteoclastogenesis by stabilizing SPHK1 and inhibiting p38. ( A ) SPHK1 and phosphorylation of p38 in murine primary bone marrow cells transfected with Ctsb siRNA. ( B ) SPHK1 and phosphorylation of p38 in RAW264.7 after treatment with CA074Me or CST6 protein. ( C ) RAW264.7 osteoclastogenesis after Sphk1 overexpression and Sphk1 knockdown. ( d-f ) SPHK1 expression ( D ) and osteoclastogenesis ( E, F ) of murine primary bone marrow cells with Ctsb and Sphk1 knockdown. ( G, H ) SPHK1 expression ( G ) and osteoclastogenesis ( H ) of RAW264.7 after Sphk1 knockdown and recombinant CST6 treatment. ( I ) Phosphorylation of p38 in primary bone marrow cells with Ctsb knockdown (left) and in RAW264.7 cells after Sphk1 knockdown (right), together with RANKL treatment of various time. ( J ) Phosphorylation of p38 in RAW264.7 cells treated with CM from CST6 -ovexpressing or control SCP2 cells, together with RANKL treatment of various time. ( K, L ) Phosphorylation of p38 ( K ) and osteoclastogenesis ( L ) of RAW264.7 treated with RANKL, SB203580 and CM from CST6 -knockdown or control SCP4 cells. * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Techniques: Phospho-proteomics, Transfection, Over Expression, Knockdown, Expressing, Recombinant, Control

CST6 recombinant protein effectively inhibits bone metastasis of breast cancer in mice. ( A ) Representative BLI, micro-CT, H&E and TRAP staining images of SCP2 bone metastases at week 5 after treatment of 1 mg/kg/day wild type or mutant CST6 proteins (n = 10 mice per group). Scale bar, 200 μm. ( B, C ) BLI ( B ) and osteoclast ( C ) quantitation of the metastasis. ( D ) Survival analysis of the mice. * P < 0.05, ** P < 0.01; ns, not significant.

Journal: Theranostics

Article Title: CST6 protein and peptides inhibit breast cancer bone metastasis by suppressing CTSB activity and osteoclastogenesis

doi: 10.7150/thno.62187

Figure Lengend Snippet: CST6 recombinant protein effectively inhibits bone metastasis of breast cancer in mice. ( A ) Representative BLI, micro-CT, H&E and TRAP staining images of SCP2 bone metastases at week 5 after treatment of 1 mg/kg/day wild type or mutant CST6 proteins (n = 10 mice per group). Scale bar, 200 μm. ( B, C ) BLI ( B ) and osteoclast ( C ) quantitation of the metastasis. ( D ) Survival analysis of the mice. * P < 0.05, ** P < 0.01; ns, not significant.

Techniques: Recombinant, Micro-CT, Staining, Mutagenesis, Quantitation Assay

CST6 peptides inhibit osteoclastogenesis and bone metastasis of breast cancer. ( A ) The effects of CST6 peptides to inhibit CTSB activity of RAW264.7 lysate (n = 3 independent experiments). ( B ) Osteoclastogenesis of primary bone marrow (n = 3 independent experiments) treated CST6 peptides or Zoledronic Acid (ZA). Scale bar, 150 μm. Asterisks indicate significance compared to the control. ( C-G ) The effects of CST6 peptides to inhibit SCP2 bone metastasis in mice after treatment of 1 mg/kg/day CST6 peptides (n = 10 mice per group). Shown are representative BLI, micro-CT, H&E and TRAP staining images of bone metastases in hind legs at week 5 ( C ), BLI quantitation of metastasis ( D ), TRAP + cell quantitation in metastases ( E ), body weights ( F ) and survival analysis ( G ) of the mice. Scale bar, 200 μm. ( H, I ) SCP2 bone metastasis in nude mice ( H ) and animal survival ( I ) with treatment of 1 mg/kg/day CST6 peptides, 1 mg/kg/day Zoledronic Acid (ZA) or 1 mg/kg/day Bortezomib (BO). * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Journal: Theranostics

Article Title: CST6 protein and peptides inhibit breast cancer bone metastasis by suppressing CTSB activity and osteoclastogenesis

doi: 10.7150/thno.62187

Figure Lengend Snippet: CST6 peptides inhibit osteoclastogenesis and bone metastasis of breast cancer. ( A ) The effects of CST6 peptides to inhibit CTSB activity of RAW264.7 lysate (n = 3 independent experiments). ( B ) Osteoclastogenesis of primary bone marrow (n = 3 independent experiments) treated CST6 peptides or Zoledronic Acid (ZA). Scale bar, 150 μm. Asterisks indicate significance compared to the control. ( C-G ) The effects of CST6 peptides to inhibit SCP2 bone metastasis in mice after treatment of 1 mg/kg/day CST6 peptides (n = 10 mice per group). Shown are representative BLI, micro-CT, H&E and TRAP staining images of bone metastases in hind legs at week 5 ( C ), BLI quantitation of metastasis ( D ), TRAP + cell quantitation in metastases ( E ), body weights ( F ) and survival analysis ( G ) of the mice. Scale bar, 200 μm. ( H, I ) SCP2 bone metastasis in nude mice ( H ) and animal survival ( I ) with treatment of 1 mg/kg/day CST6 peptides, 1 mg/kg/day Zoledronic Acid (ZA) or 1 mg/kg/day Bortezomib (BO). * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Techniques: Activity Assay, Control, Micro-CT, Staining, Quantitation Assay

Half-life and toxicity analysis of CST6 protein and peptides in mice. ( A ) Half-life analysis of CST6 protein and peptides in the blood of mice. ( B ) Body weights of mice 4 weeks after daily treatment of 1 mg/kg/day CST6 protein and peptides (n = 4 mice per group). ( C ) H&E staining of various organs in mice 4 weeks after daily treatment of 1 mg/kg/day CST6 protein and peptides. Scale bar, 200 μm.

Journal: Theranostics

Article Title: CST6 protein and peptides inhibit breast cancer bone metastasis by suppressing CTSB activity and osteoclastogenesis

doi: 10.7150/thno.62187

Figure Lengend Snippet: Half-life and toxicity analysis of CST6 protein and peptides in mice. ( A ) Half-life analysis of CST6 protein and peptides in the blood of mice. ( B ) Body weights of mice 4 weeks after daily treatment of 1 mg/kg/day CST6 protein and peptides (n = 4 mice per group). ( C ) H&E staining of various organs in mice 4 weeks after daily treatment of 1 mg/kg/day CST6 protein and peptides. Scale bar, 200 μm.

Techniques: Staining

Hematological analysis of mice after treatment of CST6 protein or peptides. Shown are the hematological results after intravenous treatment of 1 mg/kg/day CST6 protein and peptides for 4 weeks. WBC, white blood cell; RBC, red blood cell; MCV, erythrocyte mean corpuscular volume; HGB, hemoglobin; MCH, mean corpuscular hemoglobin; HCT, red blood cell specific volume; MCHC, mean corpuscular hemoglobin concentration.

Journal: Theranostics

Article Title: CST6 protein and peptides inhibit breast cancer bone metastasis by suppressing CTSB activity and osteoclastogenesis

doi: 10.7150/thno.62187

Figure Lengend Snippet: Hematological analysis of mice after treatment of CST6 protein or peptides. Shown are the hematological results after intravenous treatment of 1 mg/kg/day CST6 protein and peptides for 4 weeks. WBC, white blood cell; RBC, red blood cell; MCV, erythrocyte mean corpuscular volume; HGB, hemoglobin; MCH, mean corpuscular hemoglobin; HCT, red blood cell specific volume; MCHC, mean corpuscular hemoglobin concentration.

Techniques: Concentration Assay

Journal: The FASEB Journal

Article Title: Cathepsin B as a potential cystatin M/E target in the mouse hair follicle

doi: 10.1096/fj.201700267R

Figure Lengend Snippet: Regulation of epidermal protease activity by CST6. Model of the regulatory role of CST6 in processes that control epidermal cornification, desquamation and HF maintenance. 1 ) Inhibition of CTSL activity by CST6 is important in the cornification process, as CTSL is the elusive processing and activating enzyme for (TGM)-3. CTSL is also able to process CTSD, which in turn can activate TGM-1. 2 ) Inhibition of CTSV regulates desquamation, as CTSV is able to degrade desmosomal and corneodesmosomal proteins, such as desmoglein-1, desmocollin-1, and corneodesmosin. As CTSV is expressed only in humans, murine CTSL probably controls the specific functional enzymatic activities of both human CTSL and CTSV. 3 ) The findings in the present study suggest that inhibition of CtsB by Cst6 protects HF maintenance in mice. 4 ) Inhibition of human LGMN regulates the processing of (pro)-cathepsins; however mouse LGMN is not inhibited by mouse Cst6.

Article Snippet: Protease inhibitor activity of recombinant mouse Cst6 (R&D Systems) against recombinant mouse CtsB (R&D Systems) was determined by measuring the hydrolysis of the fluorescent Z-Leu-Arg-AMC substrate (R&D Systems) ( ).

Techniques: Activity Assay, Inhibition, Functional Assay

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1) Product Images from "Cathepsin B as a potential cystatin M/E target in the mouse hair follicle"

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