Hemoglobin Antibody [Unconjugated]

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Hemoglobin localization in control and ALS spinal cord. Immunohistochemical staining of hemoglobin extravasation in cervical white matter from control (a–c) or ALS (d–f) spinal cord. Hemoglobin immunoreactivity (red) and lectin-positive vessels (green) are shown with a Hoechst nuclear counterstain (blue). Scale bars = 50 µm. Representative images of full spinal cord sections from the cervical level of a control case with no hemoglobin leakage (g), the thoracic level of an ALS case with white matter hemoglobin leakage (h), and the lumbar level of an ALS case with gray matter hemoglobin leakage (i) are shown. Dashed lines show gray matter boundary; scale bar = 1 mm. Occasional hemoglobin staining of SMI-32-positive anterior horn motor neurons was also observed (j–m). White arrowhead indicates a SMI-32-positive hemoglobin-positive motor neuron, where the red arrow indicates an SMI-32-positive hemoglobin-negative motor neuron. Scale bars = 50 µm Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Hemoglobin localization in control and ALS spinal cord. Immunohistochemical staining of hemoglobin extravasation in cervical white matter from control (a–c) or ALS (d–f) spinal cord. Hemoglobin immunoreactivity (red) and lectin-positive vessels (green) are shown with a Hoechst nuclear counterstain (blue). Scale bars = 50 µm. Representative images of full spinal cord sections from the cervical level of a control case with no hemoglobin leakage (g), the thoracic level of an ALS case with white matter hemoglobin leakage (h), and the lumbar level of an ALS case with gray matter hemoglobin leakage (i) are shown. Dashed lines show gray matter boundary; scale bar = 1 mm. Occasional hemoglobin staining of SMI-32-positive anterior horn motor neurons was also observed (j–m). White arrowhead indicates a SMI-32-positive hemoglobin-positive motor neuron, where the red arrow indicates an SMI-32-positive hemoglobin-negative motor neuron. Scale bars = 50 µm Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Hemoglobin localization in control and ALS spinal cord. Immunohistochemical staining of hemoglobin extravasation in cervical white matter from control (a–c) or ALS (d–f) spinal cord. Hemoglobin immunoreactivity (red) and lectin-positive vessels (green) are shown with a Hoechst nuclear counterstain (blue). Scale bars = 50 µm. Representative images of full spinal cord sections from the cervical level of a control case with no hemoglobin leakage (g), the thoracic level of an ALS case with white matter hemoglobin leakage (h), and the lumbar level of an ALS case with gray matter hemoglobin leakage (i) are shown. Dashed lines show gray matter boundary; scale bar = 1 mm. Occasional hemoglobin staining of SMI-32-positive anterior horn motor neurons was also observed (j–m). White arrowhead indicates a SMI-32-positive hemoglobin-positive motor neuron, where the red arrow indicates an SMI-32-positive hemoglobin-negative motor neuron. Scale bars = 50 µm Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Neurovascular unit component expression in leaked versus non-leaked vessels along the spinal cord axis. Immunohistochemical labelling of neurovascular unit markers in ALS spinal cord (a–l); tight junctions claudin-5 (a, g) and ZO-1 (b, h), efflux pump P-glycoprotein (c, i), basement membrane marker collagen IV (d, j), and astrocyte markers aquaporin 4 (e, k) and GFAP (f, l), in spinal cord vessels with or without hemoglobin leakage. Scale bar = 50 µm. Automated quantification of average intensity staining of neurovascular unit markers was carried out in all ALS cases (n = 13) or in a subset of ALS cases with high hemoglobin leakage (n = 5) in leaked and non-leaked areas of the white and gray matter of the spinal cord (m–r). Composite of original images showing anti-hemoglobin immunoreactivity (red) and lectin-positive vessels (green) (m) and overlays of hemoglobin leakage analysis output (white, partly transparent) over anti-hemoglobin (red) (n). Segmentation of vessels inside (magenta) or outside (white) areas of hemoglobin leakage in the white matter (o) or gray matter (p). Dashed lines show boundaries. Scale bar = 1 mm. Perivascular astrocyte endfeet staining (green) around lectin-positive vessels (white) in (q) was isolated using an automated mask of the glia limitans (r). Scale bar = 50 µm. The average intensities of marker staining were measured in leaked and non-leaked vessels of the gray and white matter (s–x). Data shown as mean ± SD (n = 5 or 13) with statistical significance determined with a two-way repeated-measures ANOVA with Sidak’s post-test. ns = not significant Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

Hemoglobin localization in control and ALS spinal cord. Immunohistochemical staining of hemoglobin extravasation in cervical white matter from control (a–c) or ALS (d–f) spinal cord. Hemoglobin immunoreactivity (red) and lectin-positive vessels (green) are shown with a Hoechst nuclear counterstain (blue). Scale bars = 50 µm. Representative images of full spinal cord sections from the cervical level of a control case with no hemoglobin leakage (g), the thoracic level of an ALS case with white matter hemoglobin leakage (h), and the lumbar level of an ALS case with gray matter hemoglobin leakage (i) are shown. Dashed lines show gray matter boundary; scale bar = 1 mm. Occasional hemoglobin staining of SMI-32-positive anterior horn motor neurons was also observed (j–m). White arrowhead indicates a SMI-32-positive hemoglobin-positive motor neuron, where the red arrow indicates an SMI-32-positive hemoglobin-negative motor neuron. Scale bars = 50 µm Image collected and cropped by CiteAb from the following open publication (//pubmed.ncbi.nlm.nih.gov/34446086), licensed under a CC-BY license. Not internally tested by R&D Systems.

• Reactivity: Hu
• Clonality: Polyclonal
• Host: Goat
• Conjugate: Unconjugated
• Concentration: LYOPH

Hemoglobin Antibody [Unconjugated] Summary

• Immunogen: Human Hemoglobin
• Source: N/A
• Isotype: IgG
• Clonality: Polyclonal
• Host: Goat
• Purity Statement: Antigen Affinity-purified

Applications/Dilutions

Publications

Read Publications using G-134-C in the following applications: IHC 1 publication IHC-P 1 publication

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 6 months, -20 to -70 °C under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in NaH₂PO₄, NaCl and Sodium Azide with Trehalose.
• Preservative: No Preservative
• Concentration: LYOPH
• Reconstitution Instructions: Reconstitute with sterile PBS. If 0.5 mL of PBS is used, the antibody concentration will be 0.2 mg/mL.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Hemoglobin Antibody [Unconjugated]

• alpha one globin;alpha-1 globin;alpha-1-globin;alpha-2 globin chain;Alpha-globin;ALPHA-GLOBIN GENE;delta globin;Haemoglobin;Hb;HbA1c;hemoglobin alpha 1 globin chain;Hemoglobin alpha chain;Hemoglobin subunit alpha;hemoglobin, alpha 1
• Hemoglobin

Background

Hemoglobin is a tetrameric heme-containing protein that is responsible for the transport of oxygen by red blood cells in the circulation. For most of fetal development and adulthood, hemoglobin consists of two alpha chains and two beta chains. Hemoglobin zeta (HBZ) is an approximately 15 kDa alpha chain-like protein that is produced during the first few weeks of embryogenesis until the onset of alpha chain expression. Its expression is prolonged in a0-thalassemia which is characterized by deficient alpha chain production. The Gower-1, Portland-1, and Portland-2 forms of hemoglobin consist of two zeta chains in association with either two epsilon, gamma, or beta chains, respectively. Human Hemoglobin zeta shares 79% amino acid sequence identity with mouse and rat Hemoglobin zeta.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Publications for Hemoglobin Antibody (G-134-C)(2)

Publications using G-134-C

• S Waters, MEV Swanson, BV Dieriks, YB Zhang, NL Grimsey, HC Murray, C Turner, HJ Waldvogel, RLM Faull, J An, R Bowser, MA Curtis, M Dragunow, E Scotter Blood-spinal cord barrier leakage is independent of motor neuron pathology in ALS Acta neuropathologica communications, 2021-08-26;9(1):144. 2021-08-26 [PMID: 34446086] (IHC, Human)
• EA Winkler, H Birk, JK Burkhardt, X Chen, JK Yue, D Guo, WC Rutledge, GF Lasker, C Partow, T Tihan, EF Chang, H Su, H Kim, BP Walcott, MT Lawton Reductions in brain pericytes are associated with arteriovenous malformation vascular instability J. Neurosurg., 2018-12-01;0(0):1-11. 2018-12-01 [PMID: 29303444] (IHC-P, Human)