primary abs against hmgb1 Search Results


rabbit anti-hmgb1  (GeneTex)
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GeneTex rabbit anti-hmgb1
Expression of RAGE and its ligands in control and ALS thoracic spinal cord tissue. (A) RAGE expression in control ( A , top), and in ALS tissue ( A , bottom). (B) S100B immunostaining in control tissue ( B , top) and in ALS tissue ( B , bottom). (C) <t>HMGB1</t> immunostaining in the control tissue ( C , top) and in ALS tissue ( C , bottom). (D) CML immunostaining in control spinal cord ( D , top) and in ALS spinal cord ( D , bottom). (E–G) Quantification of immunostaining intensity revealed that expression of all studied proteins was significantly increased in ALS thoracic spinal cord tissue compared to controls. S100B (E) was increased about 70%, HMGB1 (F) displayed almost threefold increase and CML (G) showed almost double level of increase in immunostaining between ALS and control subjects. Sections are representative of n = 6 control and n = 5 ALS tissue samples per condition. Error bars represent mean ± SEM, ∗ p < 0.05. Scale bar: 50 μm.
Rabbit Anti Hmgb1, supplied by GeneTex, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Expression of RAGE and its ligands in control and ALS thoracic spinal cord tissue. (A) RAGE expression in control ( A , top), and in ALS tissue ( A , bottom). (B) S100B immunostaining in control tissue ( B , top) and in ALS tissue ( B , bottom). (C) HMGB1 immunostaining in the control tissue ( C , top) and in ALS tissue ( C , bottom). (D) CML immunostaining in control spinal cord ( D , top) and in ALS spinal cord ( D , bottom). (E–G) Quantification of immunostaining intensity revealed that expression of all studied proteins was significantly increased in ALS thoracic spinal cord tissue compared to controls. S100B (E) was increased about 70%, HMGB1 (F) displayed almost threefold increase and CML (G) showed almost double level of increase in immunostaining between ALS and control subjects. Sections are representative of n = 6 control and n = 5 ALS tissue samples per condition. Error bars represent mean ± SEM, ∗ p < 0.05. Scale bar: 50 μm.

Journal: Frontiers in Cellular Neuroscience

Article Title: Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis

doi: 10.3389/fncel.2015.00485

Figure Lengend Snippet: Expression of RAGE and its ligands in control and ALS thoracic spinal cord tissue. (A) RAGE expression in control ( A , top), and in ALS tissue ( A , bottom). (B) S100B immunostaining in control tissue ( B , top) and in ALS tissue ( B , bottom). (C) HMGB1 immunostaining in the control tissue ( C , top) and in ALS tissue ( C , bottom). (D) CML immunostaining in control spinal cord ( D , top) and in ALS spinal cord ( D , bottom). (E–G) Quantification of immunostaining intensity revealed that expression of all studied proteins was significantly increased in ALS thoracic spinal cord tissue compared to controls. S100B (E) was increased about 70%, HMGB1 (F) displayed almost threefold increase and CML (G) showed almost double level of increase in immunostaining between ALS and control subjects. Sections are representative of n = 6 control and n = 5 ALS tissue samples per condition. Error bars represent mean ± SEM, ∗ p < 0.05. Scale bar: 50 μm.

Article Snippet: Tissue homogenates (30 μg) were subjected to electrophoresis using 4–12% SDS-PAGE gels and specific protein signals were detected using the following antibodies: mouse anti-β-actin (A1978, 1:4000, Sigma); rabbit anti-RAGE (GTX23611, 1:1000, GeneTex); rabbit anti-S100B (ab52642, 1:5000, Abcam); and rabbit anti-HMGB1 (GTX101277, 1:1000, GeneTex).

Techniques: Expressing, Immunostaining

High magnification images of immunostaining for RAGE and its ligands in the thoracic spinal cord. Increased immunostaining pattern on the border of gray (lamina IX) and white matter was observed for (A) RAGE, (B) S100B, (C) HMGB1 and (D) CML in ALS versus control samples. Scale bar: 50 μm.

Journal: Frontiers in Cellular Neuroscience

Article Title: Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis

doi: 10.3389/fncel.2015.00485

Figure Lengend Snippet: High magnification images of immunostaining for RAGE and its ligands in the thoracic spinal cord. Increased immunostaining pattern on the border of gray (lamina IX) and white matter was observed for (A) RAGE, (B) S100B, (C) HMGB1 and (D) CML in ALS versus control samples. Scale bar: 50 μm.

Article Snippet: Tissue homogenates (30 μg) were subjected to electrophoresis using 4–12% SDS-PAGE gels and specific protein signals were detected using the following antibodies: mouse anti-β-actin (A1978, 1:4000, Sigma); rabbit anti-RAGE (GTX23611, 1:1000, GeneTex); rabbit anti-S100B (ab52642, 1:5000, Abcam); and rabbit anti-HMGB1 (GTX101277, 1:1000, GeneTex).

Techniques: Immunostaining

Co-expression of RAGE and RAGE ligands S100B, CML, and HMGB1 is higher in human ALS spinal cord. (A) Triple staining for RAGE (red), S100B (green), CML (blue) revealed increased immunoexpression of these proteins in the ALS spinal cord ( A , right) as compared to controls ( A , left) and a high degree of RAGE/ligand overlapping was observed in ALS samples (merged images). (B) Expression of RAGE (red) and its ligands, S100B (green) and HMGB1 (blue) was highly increased in the ALS ( B , right) spinal cord as compared to controls ( B , left) and a high degree of RAGE/ligand co-expression observed in ALS samples (merged images); control ( n = 6) vs. ALS samples ( n = 5). Scale bar: 100 μm. (C) A schematic diagram showing different regions of spinal cord; for the purpose of the study we examined thoracic motor spinal cord ventral horn lamina IX and surrounding white matter.

Journal: Frontiers in Cellular Neuroscience

Article Title: Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis

doi: 10.3389/fncel.2015.00485

Figure Lengend Snippet: Co-expression of RAGE and RAGE ligands S100B, CML, and HMGB1 is higher in human ALS spinal cord. (A) Triple staining for RAGE (red), S100B (green), CML (blue) revealed increased immunoexpression of these proteins in the ALS spinal cord ( A , right) as compared to controls ( A , left) and a high degree of RAGE/ligand overlapping was observed in ALS samples (merged images). (B) Expression of RAGE (red) and its ligands, S100B (green) and HMGB1 (blue) was highly increased in the ALS ( B , right) spinal cord as compared to controls ( B , left) and a high degree of RAGE/ligand co-expression observed in ALS samples (merged images); control ( n = 6) vs. ALS samples ( n = 5). Scale bar: 100 μm. (C) A schematic diagram showing different regions of spinal cord; for the purpose of the study we examined thoracic motor spinal cord ventral horn lamina IX and surrounding white matter.

Article Snippet: Tissue homogenates (30 μg) were subjected to electrophoresis using 4–12% SDS-PAGE gels and specific protein signals were detected using the following antibodies: mouse anti-β-actin (A1978, 1:4000, Sigma); rabbit anti-RAGE (GTX23611, 1:1000, GeneTex); rabbit anti-S100B (ab52642, 1:5000, Abcam); and rabbit anti-HMGB1 (GTX101277, 1:1000, GeneTex).

Techniques: Expressing, Staining

High magnification images of white/gray matter showing triple staining for RAGE and its ligands S100B, CML, and HMGB1. Immunostaining for RAGE (red) and its ligands S100B (green) and CML or HMGB1 (blue) revealed low immunoexpression in control tissue ( A and C ) and high immunoexpression in ALS tissue ( B and D ). Sections are representative of n = 6 control and n = 5 ALS tissue samples per condition. Scale bar: 100 μm.

Journal: Frontiers in Cellular Neuroscience

Article Title: Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis

doi: 10.3389/fncel.2015.00485

Figure Lengend Snippet: High magnification images of white/gray matter showing triple staining for RAGE and its ligands S100B, CML, and HMGB1. Immunostaining for RAGE (red) and its ligands S100B (green) and CML or HMGB1 (blue) revealed low immunoexpression in control tissue ( A and C ) and high immunoexpression in ALS tissue ( B and D ). Sections are representative of n = 6 control and n = 5 ALS tissue samples per condition. Scale bar: 100 μm.

Article Snippet: Tissue homogenates (30 μg) were subjected to electrophoresis using 4–12% SDS-PAGE gels and specific protein signals were detected using the following antibodies: mouse anti-β-actin (A1978, 1:4000, Sigma); rabbit anti-RAGE (GTX23611, 1:1000, GeneTex); rabbit anti-S100B (ab52642, 1:5000, Abcam); and rabbit anti-HMGB1 (GTX101277, 1:1000, GeneTex).

Techniques: Staining, Immunostaining

Protein levels of RAGE and its ligands S100B and HMGB1 are higher in human ALS spinal cord. Western blot analysis of RAGE (A) , RAGE ligands S100B (B) and HMGB1 (C) in control and ALS spinal cord tissue. The original blots were stripped followed by incubation with the other antigens under study. Signal for test antigen was then normalized to β-actin and the relative band densities were reported. n = 3 subjects/group. Error bars represent mean ± SEM, ∗ p < 0.05.

Journal: Frontiers in Cellular Neuroscience

Article Title: Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis

doi: 10.3389/fncel.2015.00485

Figure Lengend Snippet: Protein levels of RAGE and its ligands S100B and HMGB1 are higher in human ALS spinal cord. Western blot analysis of RAGE (A) , RAGE ligands S100B (B) and HMGB1 (C) in control and ALS spinal cord tissue. The original blots were stripped followed by incubation with the other antigens under study. Signal for test antigen was then normalized to β-actin and the relative band densities were reported. n = 3 subjects/group. Error bars represent mean ± SEM, ∗ p < 0.05.

Article Snippet: Tissue homogenates (30 μg) were subjected to electrophoresis using 4–12% SDS-PAGE gels and specific protein signals were detected using the following antibodies: mouse anti-β-actin (A1978, 1:4000, Sigma); rabbit anti-RAGE (GTX23611, 1:1000, GeneTex); rabbit anti-S100B (ab52642, 1:5000, Abcam); and rabbit anti-HMGB1 (GTX101277, 1:1000, GeneTex).

Techniques: Western Blot, Incubation

A proposed mechanism of RAGE action in ALS spinal cord. We propose that during pathological processes in ALS, neuronal and microglial RAGE becomes activated by RAGE ligands such as AGEs, S100B, and HMGB1. Once activated, RAGE triggers a cascade of metabolic changes, contributing to the release of reactive oxygen species (ROS) and inflammatory cytokines, subsequently resulting in altered protein structures and misfolded protein accumulation, impaired mitochondrial function and growing energy deficits ultimately leading to neuronal dysfunction and apoptosis.

Journal: Frontiers in Cellular Neuroscience

Article Title: Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis

doi: 10.3389/fncel.2015.00485

Figure Lengend Snippet: A proposed mechanism of RAGE action in ALS spinal cord. We propose that during pathological processes in ALS, neuronal and microglial RAGE becomes activated by RAGE ligands such as AGEs, S100B, and HMGB1. Once activated, RAGE triggers a cascade of metabolic changes, contributing to the release of reactive oxygen species (ROS) and inflammatory cytokines, subsequently resulting in altered protein structures and misfolded protein accumulation, impaired mitochondrial function and growing energy deficits ultimately leading to neuronal dysfunction and apoptosis.

Article Snippet: Tissue homogenates (30 μg) were subjected to electrophoresis using 4–12% SDS-PAGE gels and specific protein signals were detected using the following antibodies: mouse anti-β-actin (A1978, 1:4000, Sigma); rabbit anti-RAGE (GTX23611, 1:1000, GeneTex); rabbit anti-S100B (ab52642, 1:5000, Abcam); and rabbit anti-HMGB1 (GTX101277, 1:1000, GeneTex).

Techniques: