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recombinant murine klotho  (R&D Systems)


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    R&D Systems recombinant murine klotho
    Recombinant Murine Klotho, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 57 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/recombinant+klotho+protein/Recombinant+Mouse+Klotho+(aa+35-982)+Protein%2C+CF/10__1161_slash_jaha__125__045175-59-13-23
    Average 94 stars, based on 57 article reviews
    recombinant murine klotho - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Recombinant:

    Article Title: Aging Impairs the Capacity of Cardiac Functional Recovery Following Endotoxemia: Modulation of Myocardial Klotho Level for Remedy.
    Article Snippet: Introduction: Endotoxemic/septic cardiac dysfunction occurs frequently in elderly patients undergoing major surgery and contributes to postsurgery morbidity and mortality.. This study evaluated the effect of aging on cardiac functional recovery following endotoxemia and explored therapeutic approaches for promotion of the recovery.. Methods: A small dose of endotoxin (0.5 mg/kg, iv) was administered to young adult (3-4 mo) and old (18-22 mo) mice with or without subsequent treatment with recombinant interleukin-37 (IL-37, 50 mg/kg, iv) or recombinant Klotho (10 mg/kg, iv).

    Article Title: Klotho Improves Cardiac Function by Suppressing Reactive Oxygen Species (ROS) Mediated Apoptosis by Modulating Mapks/Nrf2 Signaling in Doxorubicin-Induced Cardiotoxicity
    Article Snippet: Several rats were exposed to DOX (3 mg/kg, Sigma-Aldrich) by intraperitoneal injections (single dose of DOX every another day for total three injections) [ ]. .. Recombinant klotho protein (0.01 mg/kg, R&D) was administrated to rats by intraperitoneal injections every another day for total two injections [ ]. .. The JNK inhibitor SP600125 (15 mg/kg, Tocris Bioscience), ERK1/2 inhibitor U0126 (0.22 μg/kg, Sigma-Aldrich) and p38 inhibitor SB203580 (1 mg/kg, Selleck Chemicals,) were administrated to rats by intraperitoneal injections daily for consecutive four days [ – ].

    Article Title: Klotho relieves inflammation and exerts a cardioprotective effect during renal ischemia/reperfusion-induced cardiorenal syndrome.
    Article Snippet: .. As previously performed, we treated animals with recombinant Klotho protein (R&D Systems, Minnesota, USA). ..

    Article Title: Klotho mitigates diquat-induced myocardial injury in rats by activating Nrf2/ARE-mediated suppression of oxidative stress
    Article Snippet: H9c2 cardiomyocytes were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA) and cultured in Dulbecco’s Modified Eagle Medium (DEME; 11965175, Gibco, USA) containing 10% fetal bovine serum (A3382101, Gibco, USA) and 1% penicillin-streptomycin (15140148, Gibco, USA) at 37°C in a humidified atmosphere containing 5% CO 2 . .. To induce oxidative injury, cells were treated with 50 μM DQ (45422, Sigma-Aldrich, USA) for 24 h. For Klotho intervention, cells were treated with 1 μg/mL recombinant Klotho protein (1819-KL, R&D Systems, USA) [ 19 , 20 ]. .. H9c2 cells were seeded in 96-well plates at a density of 5×10 3 /well and incubated at 37°C for 24 h. Cell viability was assessed using the CCK-8 (C0040; Beyotime, Shanghai, China) according to the manufacturer’s instructions.

    Article Title: Klotho Reduces Necroptosis by Targeting Oxidative Stress Involved in Renal Ischemic-Reperfusion Injury.
    Article Snippet: .. For the therapeutic investigation, a single dose of recombinant Klotho protein (360 ng/25 g body weight; R&D Systems, Inc., Minneapolis, MN) or nec-1 (1.65 mg/kg body weight; Sigma-Aldrich, St. Louis, MO) was intraperitoneally applied at 30 min or 0 min of reperfusion, respectively. .. Cell culture The TCMK-1 (murine tubular epithelial cells) and human kidney 2 (HK2) (proximal tubular cells) cell lines were obtained from the American Type Culture Collection (ATCC; Manassas, VA).

    Article Title: Klotho Regulates Retinal Pigment Epithelial Functions and Protects Against Oxidative Stress
    Article Snippet: RPE functional assays For the phagocytosis assays, the RPE cells were grown to confluency for 20 h on poly- d -lysine (2 μg/cm 2 , BD Biosciences) and laminin-coated (4 μg/ml, Sigma-Aldrich) 96-well plates (50,000 cells/well) in EpiCM medium without serum. .. Cultures were then incubated with recombinant Klotho protein (10 ng/ml; R&D Systems) for 30 min or 16 h. Phagocytosis was assayed by adding 200 μg of Alexa Fluor 488-conjugated zymosan (Invitrogen) for 1 h, and was quantified by fluorometry using the Vybrant Phagocytosis Assay (Invitrogen). .. RPE cell viability was measured with the PrestoBlue Cell Viability Reagent (Invitrogen) and quantified by fluorometry.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Aging Impairs the Capacity of Cardiac Functional Recovery Following Endotoxemia: Modulation of Myocardial Klotho Level for Remedy.
    Article Snippet: Introduction: Endotoxemic/septic cardiac dysfunction occurs frequently in elderly patients undergoing major surgery and contributes to postsurgery morbidity and mortality.. This study evaluated the effect of aging on cardiac functional recovery following endotoxemia and explored therapeutic approaches for promotion of the recovery.. Methods: A small dose of endotoxin (0.5 mg/kg, iv) was administered to young adult (3-4 mo) and old (18-22 mo) mice with or without subsequent treatment with recombinant interleukin-37 (IL-37, 50 mg/kg, iv) or recombinant Klotho (10 mg/kg, iv).

    Incubation:

    Article Title: Klotho inhibits angiotensin II-induced cardiomyocyte hypertrophy through suppression of the AT1R/beta catenin pathway.
    Article Snippet: Accepted Manuscript Klotho inhibits angiotensin II-induced cardiomyocyte hypertrophy through suppression of the AT1R/beta catenin pathway Liangzhu Yu, Wei Meng, Jieqiong Ding, Menglin Cheng PII: S0006-291X(16)30342-4 DOI: 10.1016/j.bbrc.2016.03.029 Reference: YBBRC 35461 To appear in: Biochemical and Biophysical Research Communications Received Date: 19 February 2016 Accepted Date: 8 March 2016 Please cite this article as: L. Yu, W. Meng, J. Ding, M. Cheng, Klotho inhibits angiotensin II-induced cardiomyocyte hypertrophy through suppression of the AT1R/beta catenin pathway, Biochemical and Biophysical Research Communications (2016), doi: 10.1016/j.bbrc.2016.03.029.. This is a PDF file of an unedited manuscript that has been accepted for publication.. As a service to our customers we are providing this early version of the manuscript.

    Article Title: Klotho Regulates Retinal Pigment Epithelial Functions and Protects Against Oxidative Stress
    Article Snippet: RPE functional assays For the phagocytosis assays, the RPE cells were grown to confluency for 20 h on poly- d -lysine (2 μg/cm 2 , BD Biosciences) and laminin-coated (4 μg/ml, Sigma-Aldrich) 96-well plates (50,000 cells/well) in EpiCM medium without serum. .. Cultures were then incubated with recombinant Klotho protein (10 ng/ml; R&D Systems) for 30 min or 16 h. Phagocytosis was assayed by adding 200 μg of Alexa Fluor 488-conjugated zymosan (Invitrogen) for 1 h, and was quantified by fluorometry using the Vybrant Phagocytosis Assay (Invitrogen). .. RPE cell viability was measured with the PrestoBlue Cell Viability Reagent (Invitrogen) and quantified by fluorometry.

    Phagocytosis Assay:

    Article Title: Klotho Regulates Retinal Pigment Epithelial Functions and Protects Against Oxidative Stress
    Article Snippet: RPE functional assays For the phagocytosis assays, the RPE cells were grown to confluency for 20 h on poly- d -lysine (2 μg/cm 2 , BD Biosciences) and laminin-coated (4 μg/ml, Sigma-Aldrich) 96-well plates (50,000 cells/well) in EpiCM medium without serum. .. Cultures were then incubated with recombinant Klotho protein (10 ng/ml; R&D Systems) for 30 min or 16 h. Phagocytosis was assayed by adding 200 μg of Alexa Fluor 488-conjugated zymosan (Invitrogen) for 1 h, and was quantified by fluorometry using the Vybrant Phagocytosis Assay (Invitrogen). .. RPE cell viability was measured with the PrestoBlue Cell Viability Reagent (Invitrogen) and quantified by fluorometry.



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    <t>Klotho</t> alleviated DQ-induced cardiomyocyte oxidative stress. (A, B) Cell viability was examined using Cell Counting Kit-8 (CCK-8) assay. (C) Klotho protein levels were examined using western blot analysis. (D) DQ-stimulated H9c2 cardiomyocytes were treated with <t>recombinant</t> Klotho protein, followed by viability assessment using CCK-8 assay. (E, F) Apoptosis was examined using flow cytometry. (G, H) ROS fluorescence signal, (I) MDA level, (J) GSH-ST, (K) GSH-PX, and (L) SOD activities in H9c2 cells were assessed using ELISA kits. (M, N) Nrf2, HO-1, and NQO1 protein levels were examined using western blot analysis. Data were presented as mean ± SD. * P <0.05, ** P <0.01, compared to control group. ## P <0.01, compared to DQ group.
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    <t>Klotho</t> alleviated DQ-induced cardiomyocyte oxidative stress. (A, B) Cell viability was examined using Cell Counting Kit-8 (CCK-8) assay. (C) Klotho protein levels were examined using western blot analysis. (D) DQ-stimulated H9c2 cardiomyocytes were treated with <t>recombinant</t> Klotho protein, followed by viability assessment using CCK-8 assay. (E, F) Apoptosis was examined using flow cytometry. (G, H) ROS fluorescence signal, (I) MDA level, (J) GSH-ST, (K) GSH-PX, and (L) SOD activities in H9c2 cells were assessed using ELISA kits. (M, N) Nrf2, HO-1, and NQO1 protein levels were examined using western blot analysis. Data were presented as mean ± SD. * P <0.05, ** P <0.01, compared to control group. ## P <0.01, compared to DQ group.
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    Klotho alleviated DQ-induced cardiomyocyte oxidative stress. (A, B) Cell viability was examined using Cell Counting Kit-8 (CCK-8) assay. (C) Klotho protein levels were examined using western blot analysis. (D) DQ-stimulated H9c2 cardiomyocytes were treated with recombinant Klotho protein, followed by viability assessment using CCK-8 assay. (E, F) Apoptosis was examined using flow cytometry. (G, H) ROS fluorescence signal, (I) MDA level, (J) GSH-ST, (K) GSH-PX, and (L) SOD activities in H9c2 cells were assessed using ELISA kits. (M, N) Nrf2, HO-1, and NQO1 protein levels were examined using western blot analysis. Data were presented as mean ± SD. * P <0.05, ** P <0.01, compared to control group. ## P <0.01, compared to DQ group.

    Journal: American Journal of Translational Research

    Article Title: Klotho mitigates diquat-induced myocardial injury in rats by activating Nrf2/ARE-mediated suppression of oxidative stress

    doi: 10.62347/SKBR3572

    Figure Lengend Snippet: Klotho alleviated DQ-induced cardiomyocyte oxidative stress. (A, B) Cell viability was examined using Cell Counting Kit-8 (CCK-8) assay. (C) Klotho protein levels were examined using western blot analysis. (D) DQ-stimulated H9c2 cardiomyocytes were treated with recombinant Klotho protein, followed by viability assessment using CCK-8 assay. (E, F) Apoptosis was examined using flow cytometry. (G, H) ROS fluorescence signal, (I) MDA level, (J) GSH-ST, (K) GSH-PX, and (L) SOD activities in H9c2 cells were assessed using ELISA kits. (M, N) Nrf2, HO-1, and NQO1 protein levels were examined using western blot analysis. Data were presented as mean ± SD. * P <0.05, ** P <0.01, compared to control group. ## P <0.01, compared to DQ group.

    Article Snippet: To induce oxidative injury, cells were treated with 50 μM DQ (45422, Sigma-Aldrich, USA) for 24 h. For Klotho intervention, cells were treated with 1 μg/mL recombinant Klotho protein (1819-KL, R&D Systems, USA) [ 19 , 20 ].

    Techniques: Cell Counting, CCK-8 Assay, Western Blot, Recombinant, Flow Cytometry, Fluorescence, Enzyme-linked Immunosorbent Assay, Control

    Nrf2 inhibition abrogated the protective effects of Klotho on DQ-induced oxidative stress. DQ-stimulated H9c2 cells received recombinant Klotho protein and Nrf2 inhibitor ML385. (A, B) Nrf2, HO-1, and NQO1 protein levels were examined using western blot analysis. (C) Cell viability was examined using CCK-8 assay. (D, E) Apoptosis was examined using flow cytometry. (F, G) ROS fluorescence signal, (H) MDA level, (I) GSH-ST, (J) GSH-PX, and (K) SOD activities in H9c2 cells were assessed using ELISA kits. Data were presented as mean ± SD. ** P <0.01, compared to control group. ## P <0.01, compared to DQ group. && P <0.01, compared to DQ+Klotho group.

    Journal: American Journal of Translational Research

    Article Title: Klotho mitigates diquat-induced myocardial injury in rats by activating Nrf2/ARE-mediated suppression of oxidative stress

    doi: 10.62347/SKBR3572

    Figure Lengend Snippet: Nrf2 inhibition abrogated the protective effects of Klotho on DQ-induced oxidative stress. DQ-stimulated H9c2 cells received recombinant Klotho protein and Nrf2 inhibitor ML385. (A, B) Nrf2, HO-1, and NQO1 protein levels were examined using western blot analysis. (C) Cell viability was examined using CCK-8 assay. (D, E) Apoptosis was examined using flow cytometry. (F, G) ROS fluorescence signal, (H) MDA level, (I) GSH-ST, (J) GSH-PX, and (K) SOD activities in H9c2 cells were assessed using ELISA kits. Data were presented as mean ± SD. ** P <0.01, compared to control group. ## P <0.01, compared to DQ group. && P <0.01, compared to DQ+Klotho group.

    Article Snippet: To induce oxidative injury, cells were treated with 50 μM DQ (45422, Sigma-Aldrich, USA) for 24 h. For Klotho intervention, cells were treated with 1 μg/mL recombinant Klotho protein (1819-KL, R&D Systems, USA) [ 19 , 20 ].

    Techniques: Inhibition, Recombinant, Western Blot, CCK-8 Assay, Flow Cytometry, Fluorescence, Enzyme-linked Immunosorbent Assay, Control

    Klotho alleviated DQ-induced acute myocardial injury in rats through Nrf2/ARE activation. Rats were intragastrically administered with DQ to induce acute myocardial injury and treated with recombinant Klotho protein for 5 days. (A, B) Klotho protein expression in myocardial tissues was assessed using immunohistochemistry. (C) H&E staining of myocardial tissue of rats in each group (D, E) ROS fluorescence signal, (F) MDA level, (G) GSH-ST, (H) GSH-PX, and (I) SOD activities in H9c2 cells were assessed using ELISA kits. (J, K) Nrf2, HO-1, and NQO1 protein levels in myocardial tissues was assessed using immunohistochemistry. ** P <0.01, compared to control group. ## P <0.01, compared to DQ group.

    Journal: American Journal of Translational Research

    Article Title: Klotho mitigates diquat-induced myocardial injury in rats by activating Nrf2/ARE-mediated suppression of oxidative stress

    doi: 10.62347/SKBR3572

    Figure Lengend Snippet: Klotho alleviated DQ-induced acute myocardial injury in rats through Nrf2/ARE activation. Rats were intragastrically administered with DQ to induce acute myocardial injury and treated with recombinant Klotho protein for 5 days. (A, B) Klotho protein expression in myocardial tissues was assessed using immunohistochemistry. (C) H&E staining of myocardial tissue of rats in each group (D, E) ROS fluorescence signal, (F) MDA level, (G) GSH-ST, (H) GSH-PX, and (I) SOD activities in H9c2 cells were assessed using ELISA kits. (J, K) Nrf2, HO-1, and NQO1 protein levels in myocardial tissues was assessed using immunohistochemistry. ** P <0.01, compared to control group. ## P <0.01, compared to DQ group.

    Article Snippet: To induce oxidative injury, cells were treated with 50 μM DQ (45422, Sigma-Aldrich, USA) for 24 h. For Klotho intervention, cells were treated with 1 μg/mL recombinant Klotho protein (1819-KL, R&D Systems, USA) [ 19 , 20 ].

    Techniques: Activation Assay, Recombinant, Expressing, Immunohistochemistry, Staining, Fluorescence, Enzyme-linked Immunosorbent Assay, Control