Recombinant human HMGB1 purchased from Sigma‐Aldrich (St. Louis, MO, USA) and specific chemical inhibitors including BAY87‐2243, U0126, SB203580 and SP600125 were purchased from Selleck (Houston, TX, USA). Antibodies for phospho‐Erk (Thr202/Tyr204,p‐ERK), total Erk, phospho‐p38 MAP kinase (Thr180/Tyr182,p‐p38), total P38 MAP kinase, phospho‐JNK (Thr183/Tyr185, p‐JNK) and total JNK were purchased from Cell Signaling Technology (Danvers, MA, USA). Antibodies for HMGB1 and HIF‐1α were purchased from Abcam (Cambridge, MA, USA). Antibodies for VEGF were obtained from Proteintech (Radnor, PA, USA).
Recombinant human hmgb1
Manufactured by Merck Group
Sourced in United States, China
Recombinant human HMGB1 is a protein product derived through recombinant DNA technology. It functions as a DNA-binding protein involved in various cellular processes.
Automatically generated - may contain errors
Lab products found in correlation
Total jnk, by Cell Signaling Technology (1 mentions)
Bay 87 2243, by Selleck Chemicals (1 mentions)
U0126, by Selleck Chemicals (1 mentions)
Sp600125, by Selleck Chemicals (1 mentions)
Sb203580, by Selleck Chemicals (1 mentions)
C57bl 6 mice, by Cyagen (1 mentions)
Non immune igg, by Merck Group (1 mentions)
Glycyrrhizin, by Merck Group (1 mentions)
Hmgb1, by Merck Group (1 mentions)
Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (1 mentions)
Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions)
Adenosine triphosphate (atp), by Merck Group (1 mentions)
Lipopolysaccharides (lps), by Merck Group (1 mentions)
4 protocols using recombinant human hmgb1
1
HMGB1 Signaling Pathway Modulation
2
Murine MSC Culture and Stimulation
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Primary bone marrow-derived MSCs of C57/BL6 mice were purchased from Cyagen Biosciences Inc. (Guangzhou, China). MSCs were cultured in Dulbecco’s modified Eagle’s medium/F12 (DMEM/F12) medium with 10% heat-inactivated fetal bovine serum. The present study used MSCs from 6th to 10th passages. Recombinant human HMGB1 was purchased from Sigma-Aldrich (Shanghai, China) and recombinant murine IFN-γ and TNF-α from PeproTech (Southfield, MI, USA). HMGB1 A and B box were synthesized as previously described. HMGB1 and cytokines were dissolved in PBS.
3
HMGB1 Modulation in Ischemia Pretreatment
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Mice received single intraperitoneal injections of recombinant human HMGB1 (10 μg per mouse; Sigma-Aldrich)14 (link) or anti-HMGB1 neutralizing polyclonal antibody (600 μg per mouse; Shino-Test Corporation)37 (link) at 1 h before ischemia induction, concurrent with the start of electroacupuncture pretreatment. Negative control mice were injected with saline instead of rhHMGB1 or with non-immune IgG (Sigma Aldrich) instead of anti-HMGB1 antibody.
4
Activation of VSMC NLRP3 Inflammasome
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Primary human VSMCs were isolated from walls of femoral artery tissues from healthy organ donors and the cells were identified by anti‐α‐SM actin staining, according to the protocols described previously.27 The cells were maintained in Dulbecco's modified Eagle’ medium (DMEM; Gibco, Karlsruhe, Germany) supplemented with 10% fetal bovine serum (FBS, Gibco), 100 units/mL penicillin and 100 μg/mL streptomycin at 37°C in a humidified incubator with 5% CO2. The cells at passages 3 to 9 were used for experiments.
To activate NLRP3 inflammasome, VSMCs were pretreated with, or without, different concentrations (100–1000 ng/mL) LPS for 16 hours and 5 mmol/L ATP (Sigma‐Aldrich, Missouri) for 1 hour. Furthermore, some cells were first treated with vehicle DMSO or 2 μmol/L Z‐YVAD‐FMK for 24 hours to inactivate caspase activity and then treated with LPS and/or ATP. Similarly, some cells were pretreated with vehicle PBS or 2 mmol/L glycyrrhizin (Sigma‐Aldrich, Missouri) for 24 hours to inhibit HMGB1 release and then stimulated with LPS and/or ATP. In addition, some cells were treated with different concentrations (0, 5, 10, 20, 50, 100 ng/mL) recombinant human HMGB1 (Sigma‐Aldrich) for 24 hours to determine the effect of extracellular HMGB1 on cell function.
To activate NLRP3 inflammasome, VSMCs were pretreated with, or without, different concentrations (100–1000 ng/mL) LPS for 16 hours and 5 mmol/L ATP (Sigma‐Aldrich, Missouri) for 1 hour. Furthermore, some cells were first treated with vehicle DMSO or 2 μmol/L Z‐YVAD‐FMK for 24 hours to inactivate caspase activity and then treated with LPS and/or ATP. Similarly, some cells were pretreated with vehicle PBS or 2 mmol/L glycyrrhizin (Sigma‐Aldrich, Missouri) for 24 hours to inhibit HMGB1 release and then stimulated with LPS and/or ATP. In addition, some cells were treated with different concentrations (0, 5, 10, 20, 50, 100 ng/mL) recombinant human HMGB1 (Sigma‐Aldrich) for 24 hours to determine the effect of extracellular HMGB1 on cell function.
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