human pgp 9 5 protein  (Alomone Labs)


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    Alomone Labs human pgp 9 5 protein
    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all <t>PGP-9.5-IR</t> nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
    Human Pgp 9 5 Protein, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    Images

    1) Product Images from "Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve"

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-8-1

    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
    Figure Legend Snippet: Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Techniques Used: Staining, Immunostaining

    anti prongf  (Alomone Labs)


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    Alomone Labs anti prongf
    Anti Prongf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti prongf/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
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    anti prongf - by Bioz Stars, 2023-01
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    human pgp 9 5 protein  (Alomone Labs)


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    Alomone Labs human pgp 9 5 protein
    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all <t>PGP-9.5-IR</t> nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
    Human Pgp 9 5 Protein, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    Images

    1) Product Images from "Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve"

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-8-1

    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
    Figure Legend Snippet: Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Techniques Used: Staining, Immunostaining

    rabbit anti prongf  (Alomone Labs)


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    Alomone Labs rabbit anti prongf
    Distribution of <t>proNGF</t> immunoreactivity in naïve glabrous skin and following application of CCI . A) In sham operated controls, proNGF (brown precipitate) was found in the upper dermis, particularly in wall of blood vessels, and in small patches of keratinocytes (arrowhead). B) 1 week post-injury, proNGF immunolabeling was detected in mast cells (arrows; identified based on toluidine blue metachromatic counterstaining), in blood vessels in the upper dermis as well as in keratinocytes. C) At 2 weeks post-injury, note the intense immunostaining of keratinocytes, the labeling of some unidentified structures in dermis and a lower number of immunostained mast cells. D) At 4 weeks post-injury, note mast cell immunolabeling. E) Preincubation of antibody with control peptide abolished all specific staining. F) proNGF quantification was done by Western Blot analysis (n = 6) from sham, and animals 1 - 4 week post-injury. OD was normalized against β-actin loading controls. ***p < 0.001, **p < 0.01, *p < 0.05; +SEM.
    Rabbit Anti Prongf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti prongf/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    rabbit anti prongf - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve"

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-8-1

    Distribution of proNGF immunoreactivity in naïve glabrous skin and following application of CCI . A) In sham operated controls, proNGF (brown precipitate) was found in the upper dermis, particularly in wall of blood vessels, and in small patches of keratinocytes (arrowhead). B) 1 week post-injury, proNGF immunolabeling was detected in mast cells (arrows; identified based on toluidine blue metachromatic counterstaining), in blood vessels in the upper dermis as well as in keratinocytes. C) At 2 weeks post-injury, note the intense immunostaining of keratinocytes, the labeling of some unidentified structures in dermis and a lower number of immunostained mast cells. D) At 4 weeks post-injury, note mast cell immunolabeling. E) Preincubation of antibody with control peptide abolished all specific staining. F) proNGF quantification was done by Western Blot analysis (n = 6) from sham, and animals 1 - 4 week post-injury. OD was normalized against β-actin loading controls. ***p < 0.001, **p < 0.01, *p < 0.05; +SEM.
    Figure Legend Snippet: Distribution of proNGF immunoreactivity in naïve glabrous skin and following application of CCI . A) In sham operated controls, proNGF (brown precipitate) was found in the upper dermis, particularly in wall of blood vessels, and in small patches of keratinocytes (arrowhead). B) 1 week post-injury, proNGF immunolabeling was detected in mast cells (arrows; identified based on toluidine blue metachromatic counterstaining), in blood vessels in the upper dermis as well as in keratinocytes. C) At 2 weeks post-injury, note the intense immunostaining of keratinocytes, the labeling of some unidentified structures in dermis and a lower number of immunostained mast cells. D) At 4 weeks post-injury, note mast cell immunolabeling. E) Preincubation of antibody with control peptide abolished all specific staining. F) proNGF quantification was done by Western Blot analysis (n = 6) from sham, and animals 1 - 4 week post-injury. OD was normalized against β-actin loading controls. ***p < 0.001, **p < 0.01, *p < 0.05; +SEM.

    Techniques Used: Immunolabeling, Immunostaining, Labeling, Staining, Western Blot

    Changes in p75 expression on S100-IR Schwann cells . A) In sham-operated rats Schwann cells (green) were detected by means of S100 immunoreactivity in small nerves, with immunoreactivity of varying intensity from bright (arrow), lower in the dermis, to dim, along the dermo-epidermal junction. P75 immunoreactivity (red) was evident surrounding all S100-IR Schwann cells. B) One week following nerve injury, p75 immunostaining was dramatically upregulated in Schwann cells; the intense red color masked the mixture of red and green stainings which could be detected by analysing the separately the S100 and p75 stainings (not shown). C-D) 2 & 4 weeks post-injury a decrease in p75 intensity was observed in that the yellow indicative of S100 co-labelling was able to be visualized. E) proNGF (red) S100 (green) and p75 (blue) triple labelling to demonstrate the relative distribution of Schwann cells with respect to proNGF; note a limited distribution of Schwann cells with proNGF and faint immunoreactivity for p75 in sham-operated controls. F) 2 weeks post-injury, the clear upregulation of p75 immunoreactivity associated with S100 (arrow) was observed, which wrapped around proNGF-IR blood vessels.
    Figure Legend Snippet: Changes in p75 expression on S100-IR Schwann cells . A) In sham-operated rats Schwann cells (green) were detected by means of S100 immunoreactivity in small nerves, with immunoreactivity of varying intensity from bright (arrow), lower in the dermis, to dim, along the dermo-epidermal junction. P75 immunoreactivity (red) was evident surrounding all S100-IR Schwann cells. B) One week following nerve injury, p75 immunostaining was dramatically upregulated in Schwann cells; the intense red color masked the mixture of red and green stainings which could be detected by analysing the separately the S100 and p75 stainings (not shown). C-D) 2 & 4 weeks post-injury a decrease in p75 intensity was observed in that the yellow indicative of S100 co-labelling was able to be visualized. E) proNGF (red) S100 (green) and p75 (blue) triple labelling to demonstrate the relative distribution of Schwann cells with respect to proNGF; note a limited distribution of Schwann cells with proNGF and faint immunoreactivity for p75 in sham-operated controls. F) 2 weeks post-injury, the clear upregulation of p75 immunoreactivity associated with S100 (arrow) was observed, which wrapped around proNGF-IR blood vessels.

    Techniques Used: Expressing, Immunostaining

    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
    Figure Legend Snippet: Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Techniques Used: Staining, Immunostaining

    anti prongf antibody  (Alomone Labs)


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    Alomone Labs anti prongf antibody
    Anti Prongf Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti prongf antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti prongf antibody - by Bioz Stars, 2023-01
    94/100 stars

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    rabbit anti prongf antibody  (Alomone Labs)


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    Alomone Labs rabbit anti prongf antibody
    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and <t>proNGF</t> . A) In sham-operated animals, p75 was distributed (red) around and <t>with</t> <t>PGP</t> 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
    Rabbit Anti Prongf Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti prongf antibody/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti prongf antibody - by Bioz Stars, 2023-01
    86/100 stars

    Images

    1) Product Images from "Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve"

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-8-1

    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
    Figure Legend Snippet: Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Techniques Used: Staining, Immunostaining

    polyclonal rabbit anti prongf  (Alomone Labs)


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    Alomone Labs polyclonal rabbit anti prongf
    Polyclonal Rabbit Anti Prongf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    polyclonal rabbit anti prongf - by Bioz Stars, 2023-01
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    prongf  (Alomone Labs)


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    Alomone Labs prongf
    Overexpression of <t>proNGF</t> <t>reduced</t> <t>NGF</t> and induced expression of TrkA and p75 NTR , but not sortilin. A , B : Western blot (WB) analysis of rat retinal lysate showed significant (1.5-fold) increase in expression of TrkA and p75 NTR in rats electroporated with pGFP-proNGF123 as compared with those electroporated with pGFP (n=4). C : WB analysis showed that overexpression of pGFP-proNGF123 in rat retinas did not affect sortilin protein expression level as compared with the control rats (n=4). D : WB analysis showed that overexpression of pGFP-proNGF123 significantly reduced NGF expression (n=5) compared with GFP controls. The asterisk represents significant difference as compared with control group at p<0.05. ROD, relative optical density.
    Prongf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Electroporation-mediated gene delivery of cleavage-resistant pro–nerve growth factor causes retinal neuro- and vascular degeneration"

    Article Title: Electroporation-mediated gene delivery of cleavage-resistant pro–nerve growth factor causes retinal neuro- and vascular degeneration

    Journal: Molecular Vision

    doi:

    Overexpression of proNGF reduced NGF and induced expression of TrkA and p75 NTR , but not sortilin. A , B : Western blot (WB) analysis of rat retinal lysate showed significant (1.5-fold) increase in expression of TrkA and p75 NTR in rats electroporated with pGFP-proNGF123 as compared with those electroporated with pGFP (n=4). C : WB analysis showed that overexpression of pGFP-proNGF123 in rat retinas did not affect sortilin protein expression level as compared with the control rats (n=4). D : WB analysis showed that overexpression of pGFP-proNGF123 significantly reduced NGF expression (n=5) compared with GFP controls. The asterisk represents significant difference as compared with control group at p<0.05. ROD, relative optical density.
    Figure Legend Snippet: Overexpression of proNGF reduced NGF and induced expression of TrkA and p75 NTR , but not sortilin. A , B : Western blot (WB) analysis of rat retinal lysate showed significant (1.5-fold) increase in expression of TrkA and p75 NTR in rats electroporated with pGFP-proNGF123 as compared with those electroporated with pGFP (n=4). C : WB analysis showed that overexpression of pGFP-proNGF123 in rat retinas did not affect sortilin protein expression level as compared with the control rats (n=4). D : WB analysis showed that overexpression of pGFP-proNGF123 significantly reduced NGF expression (n=5) compared with GFP controls. The asterisk represents significant difference as compared with control group at p<0.05. ROD, relative optical density.

    Techniques Used: Over Expression, Expressing, Western Blot

    anti prongf antibody  (Alomone Labs)


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    Alomone Labs anti prongf antibody
    PDR-aqueous humor stimulates cell migration in a <t>proNGF-dependent</t> manner. HRE cells were grown to confluence and then scratched using a standard cell scrapper. Cells were switched to serum free medium and treated with aqueous humor samples (10 μ L/mL) in the presence or absence of either anti-proNGF antibody or <t>rabbit</t> <t>IgG</t> (1 μ g/mL). Representative micrographs for wounded HME cells are shown after 18 hours of various treatments. Statistical analysis showed that aqueous humor increased mean cell migration by 1.8-fold compared to the control group. Addition of anti-proNGF antibody to aqueous humor samples significantly reduced the mean percent of cell migration to the level of the control group whereas IgG did not significantly impact stimulatory effect of aqueous humor samples. Addition of anti-ProNGF antibody to control HRE cells did not significantly affect percent cell migration compared to control group ( ∗,‡ statistically significant compared to control and aqueous humor groups, resp., ( P < 0.05), n of aqueous humor samples = 7, n of cell cultures = 14–16).
    Anti Prongf Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Pronerve Growth Factor Induces Angiogenesis via Activation of TrkA: Possible Role in Proliferative Diabetic Retinopathy"

    Article Title: Pronerve Growth Factor Induces Angiogenesis via Activation of TrkA: Possible Role in Proliferative Diabetic Retinopathy

    Journal: Journal of Diabetes Research

    doi: 10.1155/2013/432659

    PDR-aqueous humor stimulates cell migration in a proNGF-dependent manner. HRE cells were grown to confluence and then scratched using a standard cell scrapper. Cells were switched to serum free medium and treated with aqueous humor samples (10 μ L/mL) in the presence or absence of either anti-proNGF antibody or rabbit IgG (1 μ g/mL). Representative micrographs for wounded HME cells are shown after 18 hours of various treatments. Statistical analysis showed that aqueous humor increased mean cell migration by 1.8-fold compared to the control group. Addition of anti-proNGF antibody to aqueous humor samples significantly reduced the mean percent of cell migration to the level of the control group whereas IgG did not significantly impact stimulatory effect of aqueous humor samples. Addition of anti-ProNGF antibody to control HRE cells did not significantly affect percent cell migration compared to control group ( ∗,‡ statistically significant compared to control and aqueous humor groups, resp., ( P < 0.05), n of aqueous humor samples = 7, n of cell cultures = 14–16).
    Figure Legend Snippet: PDR-aqueous humor stimulates cell migration in a proNGF-dependent manner. HRE cells were grown to confluence and then scratched using a standard cell scrapper. Cells were switched to serum free medium and treated with aqueous humor samples (10 μ L/mL) in the presence or absence of either anti-proNGF antibody or rabbit IgG (1 μ g/mL). Representative micrographs for wounded HME cells are shown after 18 hours of various treatments. Statistical analysis showed that aqueous humor increased mean cell migration by 1.8-fold compared to the control group. Addition of anti-proNGF antibody to aqueous humor samples significantly reduced the mean percent of cell migration to the level of the control group whereas IgG did not significantly impact stimulatory effect of aqueous humor samples. Addition of anti-ProNGF antibody to control HRE cells did not significantly affect percent cell migration compared to control group ( ∗,‡ statistically significant compared to control and aqueous humor groups, resp., ( P < 0.05), n of aqueous humor samples = 7, n of cell cultures = 14–16).

    Techniques Used: Migration

    PDR-aqueous humor stimulates tube-like structures in a proNGF-dependent manner. HRE cells were grown into confluence then trypsinized and mixed with reduced-growth factor Matrigel and treated with aqueous humor samples (10 μ L/mL) in the presence or absence of either anti-proNGF antibody or rabbit IgG (1 μ g/mL). Representative micrographs for alignment of HRE into tube-like structures are shown after 18 hrs of incubation. Statistical analysis of tube length showed that aqueous humor increased mean tube formation 1.7-fold compared to the control group. Addition of anti-proNGF antibodies to aqueous humor samples significantly reduced the relative mean tube length but did not affect control group. Prior treatment of humor samples with rabbit IgG did not significantly reduce relative mean length when compared to the untreated aq. humor group ( ∗,‡ statistically significant compared to control and aqueous humor groups, resp., ( P < 0.05), n of aqueous humor samples = 7, n of cell cultures = 14–16).
    Figure Legend Snippet: PDR-aqueous humor stimulates tube-like structures in a proNGF-dependent manner. HRE cells were grown into confluence then trypsinized and mixed with reduced-growth factor Matrigel and treated with aqueous humor samples (10 μ L/mL) in the presence or absence of either anti-proNGF antibody or rabbit IgG (1 μ g/mL). Representative micrographs for alignment of HRE into tube-like structures are shown after 18 hrs of incubation. Statistical analysis of tube length showed that aqueous humor increased mean tube formation 1.7-fold compared to the control group. Addition of anti-proNGF antibodies to aqueous humor samples significantly reduced the relative mean tube length but did not affect control group. Prior treatment of humor samples with rabbit IgG did not significantly reduce relative mean length when compared to the untreated aq. humor group ( ∗,‡ statistically significant compared to control and aqueous humor groups, resp., ( P < 0.05), n of aqueous humor samples = 7, n of cell cultures = 14–16).

    Techniques Used: Incubation

    ProNGF and aqueous humor from PDR patients stimulated cell proliferation. HRE cells were grown into confluence then trypsinized and plated as described in method section. Cells were switched to serum free medium and treated with aqueous humor samples (10 μ L/mL) in the presence or absence of either anti-proNGF antibody or rabbit IgG (1 μ g/mL) for 24 hours then cells were trypsinized and counted. Statistical analysis showed that aqueous humor from PDR patients stimulated cell proliferation by 1.8-fold compared to the control group. Adding anti-proNGF antibody to aqueous humor samples significantly reduced the relative number of proliferating cells while IgG did not. Addition of anti-proNGF antibody to HRE cells did not affect number of proliferating cells ( ∗,‡ statistically significant compared to control and aqueous humor groups, resp., ( P < 0.05), n of aqueous humor samples = 6, n of cell cultures = 12–14).
    Figure Legend Snippet: ProNGF and aqueous humor from PDR patients stimulated cell proliferation. HRE cells were grown into confluence then trypsinized and plated as described in method section. Cells were switched to serum free medium and treated with aqueous humor samples (10 μ L/mL) in the presence or absence of either anti-proNGF antibody or rabbit IgG (1 μ g/mL) for 24 hours then cells were trypsinized and counted. Statistical analysis showed that aqueous humor from PDR patients stimulated cell proliferation by 1.8-fold compared to the control group. Adding anti-proNGF antibody to aqueous humor samples significantly reduced the relative number of proliferating cells while IgG did not. Addition of anti-proNGF antibody to HRE cells did not affect number of proliferating cells ( ∗,‡ statistically significant compared to control and aqueous humor groups, resp., ( P < 0.05), n of aqueous humor samples = 6, n of cell cultures = 12–14).

    Techniques Used:

    anti prongf  (Alomone Labs)


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    Structured Review

    Alomone Labs anti prongf
    <t>ProNGF/NGF</t> ratio in vitreous correlated to proNGF/NGF ratio in serum. (a) In vitreous, the expression ratio of proNGF to NGF in individual diabetic participants was significantly higher than nondiabetic control participants ( N = 4–10, * P < 0.05). (b) In serum expression ratio of proNGF to NGF in individual diabetic participants was also significantly higher than nondiabetic control participants ( N = 6–11, * P < 0.05). (c) Deming linear regression of proNGF/NGF ratios in vitreous as a function of the ratio in serum of diabetic participants had a slope of 9.33 ± 3.33 and an intercept of 31.21 ± 27.65. The linear correlation was significant with a Pearson coefficient of R 2 = 0.567 ( N = 8, P < 0.05).
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    1) Product Images from "Imbalance of the Nerve Growth Factor and Its Precursor as a Potential Biomarker for Diabetic Retinopathy"

    Article Title: Imbalance of the Nerve Growth Factor and Its Precursor as a Potential Biomarker for Diabetic Retinopathy

    Journal: BioMed Research International

    doi: 10.1155/2015/571456

    ProNGF/NGF ratio in vitreous correlated to proNGF/NGF ratio in serum. (a) In vitreous, the expression ratio of proNGF to NGF in individual diabetic participants was significantly higher than nondiabetic control participants ( N = 4–10, * P < 0.05). (b) In serum expression ratio of proNGF to NGF in individual diabetic participants was also significantly higher than nondiabetic control participants ( N = 6–11, * P < 0.05). (c) Deming linear regression of proNGF/NGF ratios in vitreous as a function of the ratio in serum of diabetic participants had a slope of 9.33 ± 3.33 and an intercept of 31.21 ± 27.65. The linear correlation was significant with a Pearson coefficient of R 2 = 0.567 ( N = 8, P < 0.05).
    Figure Legend Snippet: ProNGF/NGF ratio in vitreous correlated to proNGF/NGF ratio in serum. (a) In vitreous, the expression ratio of proNGF to NGF in individual diabetic participants was significantly higher than nondiabetic control participants ( N = 4–10, * P < 0.05). (b) In serum expression ratio of proNGF to NGF in individual diabetic participants was also significantly higher than nondiabetic control participants ( N = 6–11, * P < 0.05). (c) Deming linear regression of proNGF/NGF ratios in vitreous as a function of the ratio in serum of diabetic participants had a slope of 9.33 ± 3.33 and an intercept of 31.21 ± 27.65. The linear correlation was significant with a Pearson coefficient of R 2 = 0.567 ( N = 8, P < 0.05).

    Techniques Used: Expressing

    anti prongf  (Alomone Labs)


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    Structured Review

    Alomone Labs anti prongf
    <t>proNGF</t> expression in nevi, primary melanoma and metastatic human tissues ( A – F ). Immunohistochemical detection of proNGF, representative pictures are shown for compound nevi ( A ), dysplastic nevi ( B ), thin primary melanomas ( C ), thick primary melanomas ( D ), lymph node metastases ( E ) and distant metastases ( F ). ( G ) Digital quantification of proNGF staining intensities according to grouped pathological subtypes: nevi (h-score = 156.2, IQR 138.9–176.1), primary melanomas (h-score = 129.0, IQR 111.8–1148.1) and metastases (h-score = 115.1, IQR 93.33–130.1). ( H ) proNGF staining intensities for individual pathological subtypes: CN = compound nevi (h-score = 143.4, IQR 126.1–176.0), DN = dysplastic nevi (h-score = 158.6, IQR 143.0–189.6), TnP = thin primary (h-score = 125.3, IQR 111.8–134.6), TkP = thick primary (h-score = 133.6, IQR 109.2–154.1), LNM = lymph node metastasis (h-score = 116.7, IQR 105.9–132.3), DM = distant metastasis (h-score = 101.8, IQR 91.64–129.7). ( I ) Correlation of proNGF <t>and</t> <t>NGF</t> stain intensities. Scale bar = 90 µm. Data are expressed as medians (horizontal line in the center of the box) and box limits indicate the interquartile range (IQR) with the whiskers extending 1.5 times the IQR from the 25th and 75th percentiles; outliers are represented by dots. H-score distributions were compared using the Wilcoxon rank-sum (dichotomous) or Kruskal–Wallis (multiple comparisons) tests ( p < 0.05).
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    1) Product Images from "Expression of NGF/proNGF and Their Receptors TrkA, p75 NTR and Sortilin in Melanoma"

    Article Title: Expression of NGF/proNGF and Their Receptors TrkA, p75 NTR and Sortilin in Melanoma

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23084260

    proNGF expression in nevi, primary melanoma and metastatic human tissues ( A – F ). Immunohistochemical detection of proNGF, representative pictures are shown for compound nevi ( A ), dysplastic nevi ( B ), thin primary melanomas ( C ), thick primary melanomas ( D ), lymph node metastases ( E ) and distant metastases ( F ). ( G ) Digital quantification of proNGF staining intensities according to grouped pathological subtypes: nevi (h-score = 156.2, IQR 138.9–176.1), primary melanomas (h-score = 129.0, IQR 111.8–1148.1) and metastases (h-score = 115.1, IQR 93.33–130.1). ( H ) proNGF staining intensities for individual pathological subtypes: CN = compound nevi (h-score = 143.4, IQR 126.1–176.0), DN = dysplastic nevi (h-score = 158.6, IQR 143.0–189.6), TnP = thin primary (h-score = 125.3, IQR 111.8–134.6), TkP = thick primary (h-score = 133.6, IQR 109.2–154.1), LNM = lymph node metastasis (h-score = 116.7, IQR 105.9–132.3), DM = distant metastasis (h-score = 101.8, IQR 91.64–129.7). ( I ) Correlation of proNGF and NGF stain intensities. Scale bar = 90 µm. Data are expressed as medians (horizontal line in the center of the box) and box limits indicate the interquartile range (IQR) with the whiskers extending 1.5 times the IQR from the 25th and 75th percentiles; outliers are represented by dots. H-score distributions were compared using the Wilcoxon rank-sum (dichotomous) or Kruskal–Wallis (multiple comparisons) tests ( p < 0.05).
    Figure Legend Snippet: proNGF expression in nevi, primary melanoma and metastatic human tissues ( A – F ). Immunohistochemical detection of proNGF, representative pictures are shown for compound nevi ( A ), dysplastic nevi ( B ), thin primary melanomas ( C ), thick primary melanomas ( D ), lymph node metastases ( E ) and distant metastases ( F ). ( G ) Digital quantification of proNGF staining intensities according to grouped pathological subtypes: nevi (h-score = 156.2, IQR 138.9–176.1), primary melanomas (h-score = 129.0, IQR 111.8–1148.1) and metastases (h-score = 115.1, IQR 93.33–130.1). ( H ) proNGF staining intensities for individual pathological subtypes: CN = compound nevi (h-score = 143.4, IQR 126.1–176.0), DN = dysplastic nevi (h-score = 158.6, IQR 143.0–189.6), TnP = thin primary (h-score = 125.3, IQR 111.8–134.6), TkP = thick primary (h-score = 133.6, IQR 109.2–154.1), LNM = lymph node metastasis (h-score = 116.7, IQR 105.9–132.3), DM = distant metastasis (h-score = 101.8, IQR 91.64–129.7). ( I ) Correlation of proNGF and NGF stain intensities. Scale bar = 90 µm. Data are expressed as medians (horizontal line in the center of the box) and box limits indicate the interquartile range (IQR) with the whiskers extending 1.5 times the IQR from the 25th and 75th percentiles; outliers are represented by dots. H-score distributions were compared using the Wilcoxon rank-sum (dichotomous) or Kruskal–Wallis (multiple comparisons) tests ( p < 0.05).

    Techniques Used: Expressing, Immunohistochemical staining, Staining

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    Alomone Labs human pgp 9 5 protein
    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all <t>PGP-9.5-IR</t> nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
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    Alomone Labs anti prongf
    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all <t>PGP-9.5-IR</t> nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
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    Alomone Labs rabbit anti prongf
    Distribution of <t>proNGF</t> immunoreactivity in naïve glabrous skin and following application of CCI . A) In sham operated controls, proNGF (brown precipitate) was found in the upper dermis, particularly in wall of blood vessels, and in small patches of keratinocytes (arrowhead). B) 1 week post-injury, proNGF immunolabeling was detected in mast cells (arrows; identified based on toluidine blue metachromatic counterstaining), in blood vessels in the upper dermis as well as in keratinocytes. C) At 2 weeks post-injury, note the intense immunostaining of keratinocytes, the labeling of some unidentified structures in dermis and a lower number of immunostained mast cells. D) At 4 weeks post-injury, note mast cell immunolabeling. E) Preincubation of antibody with control peptide abolished all specific staining. F) proNGF quantification was done by Western Blot analysis (n = 6) from sham, and animals 1 - 4 week post-injury. OD was normalized against β-actin loading controls. ***p < 0.001, **p < 0.01, *p < 0.05; +SEM.
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    Alomone Labs anti prongf antibody
    Distribution of <t>proNGF</t> immunoreactivity in naïve glabrous skin and following application of CCI . A) In sham operated controls, proNGF (brown precipitate) was found in the upper dermis, particularly in wall of blood vessels, and in small patches of keratinocytes (arrowhead). B) 1 week post-injury, proNGF immunolabeling was detected in mast cells (arrows; identified based on toluidine blue metachromatic counterstaining), in blood vessels in the upper dermis as well as in keratinocytes. C) At 2 weeks post-injury, note the intense immunostaining of keratinocytes, the labeling of some unidentified structures in dermis and a lower number of immunostained mast cells. D) At 4 weeks post-injury, note mast cell immunolabeling. E) Preincubation of antibody with control peptide abolished all specific staining. F) proNGF quantification was done by Western Blot analysis (n = 6) from sham, and animals 1 - 4 week post-injury. OD was normalized against β-actin loading controls. ***p < 0.001, **p < 0.01, *p < 0.05; +SEM.
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    Alomone Labs rabbit anti prongf antibody
    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and <t>proNGF</t> . A) In sham-operated animals, p75 was distributed (red) around and <t>with</t> <t>PGP</t> 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
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    Alomone Labs polyclonal rabbit anti prongf
    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and <t>proNGF</t> . A) In sham-operated animals, p75 was distributed (red) around and <t>with</t> <t>PGP</t> 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).
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    Alomone Labs prongf
    Overexpression of <t>proNGF</t> <t>reduced</t> <t>NGF</t> and induced expression of TrkA and p75 NTR , but not sortilin. A , B : Western blot (WB) analysis of rat retinal lysate showed significant (1.5-fold) increase in expression of TrkA and p75 NTR in rats electroporated with pGFP-proNGF123 as compared with those electroporated with pGFP (n=4). C : WB analysis showed that overexpression of pGFP-proNGF123 in rat retinas did not affect sortilin protein expression level as compared with the control rats (n=4). D : WB analysis showed that overexpression of pGFP-proNGF123 significantly reduced NGF expression (n=5) compared with GFP controls. The asterisk represents significant difference as compared with control group at p<0.05. ROD, relative optical density.
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    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Journal: Molecular Pain

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    doi: 10.1186/1744-8069-8-1

    Figure Lengend Snippet: Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Article Snippet: Immunohistochemical staining with this antibody in either rat or human skin was absent following preadsorption with purified human PGP 9.5 protein [ , ]. proNGF: The rabbit anti-proNGF antibody (Alomone #ANT-005 Lot#AN-03) was generated by injection of a synthetic peptide corresponding to a.a. 84-104 of the precursor form of rat NGF.

    Techniques: Staining, Immunostaining

    Distribution of proNGF immunoreactivity in naïve glabrous skin and following application of CCI . A) In sham operated controls, proNGF (brown precipitate) was found in the upper dermis, particularly in wall of blood vessels, and in small patches of keratinocytes (arrowhead). B) 1 week post-injury, proNGF immunolabeling was detected in mast cells (arrows; identified based on toluidine blue metachromatic counterstaining), in blood vessels in the upper dermis as well as in keratinocytes. C) At 2 weeks post-injury, note the intense immunostaining of keratinocytes, the labeling of some unidentified structures in dermis and a lower number of immunostained mast cells. D) At 4 weeks post-injury, note mast cell immunolabeling. E) Preincubation of antibody with control peptide abolished all specific staining. F) proNGF quantification was done by Western Blot analysis (n = 6) from sham, and animals 1 - 4 week post-injury. OD was normalized against β-actin loading controls. ***p < 0.001, **p < 0.01, *p < 0.05; +SEM.

    Journal: Molecular Pain

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    doi: 10.1186/1744-8069-8-1

    Figure Lengend Snippet: Distribution of proNGF immunoreactivity in naïve glabrous skin and following application of CCI . A) In sham operated controls, proNGF (brown precipitate) was found in the upper dermis, particularly in wall of blood vessels, and in small patches of keratinocytes (arrowhead). B) 1 week post-injury, proNGF immunolabeling was detected in mast cells (arrows; identified based on toluidine blue metachromatic counterstaining), in blood vessels in the upper dermis as well as in keratinocytes. C) At 2 weeks post-injury, note the intense immunostaining of keratinocytes, the labeling of some unidentified structures in dermis and a lower number of immunostained mast cells. D) At 4 weeks post-injury, note mast cell immunolabeling. E) Preincubation of antibody with control peptide abolished all specific staining. F) proNGF quantification was done by Western Blot analysis (n = 6) from sham, and animals 1 - 4 week post-injury. OD was normalized against β-actin loading controls. ***p < 0.001, **p < 0.01, *p < 0.05; +SEM.

    Article Snippet: Primary antibodies such as mouse anti-TrkA (1:500, MAB1056, R&D Systems, Minneapolis, MN), rabbit anti-proNGF (1:500, ANT-005, Alomone Labs, Isreal), or mouse anti-p75 (1:200, MC192, Novus Biologicals) were incubated overnight in blocking buffer at 4°C.

    Techniques: Immunolabeling, Immunostaining, Labeling, Staining, Western Blot

    Changes in p75 expression on S100-IR Schwann cells . A) In sham-operated rats Schwann cells (green) were detected by means of S100 immunoreactivity in small nerves, with immunoreactivity of varying intensity from bright (arrow), lower in the dermis, to dim, along the dermo-epidermal junction. P75 immunoreactivity (red) was evident surrounding all S100-IR Schwann cells. B) One week following nerve injury, p75 immunostaining was dramatically upregulated in Schwann cells; the intense red color masked the mixture of red and green stainings which could be detected by analysing the separately the S100 and p75 stainings (not shown). C-D) 2 & 4 weeks post-injury a decrease in p75 intensity was observed in that the yellow indicative of S100 co-labelling was able to be visualized. E) proNGF (red) S100 (green) and p75 (blue) triple labelling to demonstrate the relative distribution of Schwann cells with respect to proNGF; note a limited distribution of Schwann cells with proNGF and faint immunoreactivity for p75 in sham-operated controls. F) 2 weeks post-injury, the clear upregulation of p75 immunoreactivity associated with S100 (arrow) was observed, which wrapped around proNGF-IR blood vessels.

    Journal: Molecular Pain

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    doi: 10.1186/1744-8069-8-1

    Figure Lengend Snippet: Changes in p75 expression on S100-IR Schwann cells . A) In sham-operated rats Schwann cells (green) were detected by means of S100 immunoreactivity in small nerves, with immunoreactivity of varying intensity from bright (arrow), lower in the dermis, to dim, along the dermo-epidermal junction. P75 immunoreactivity (red) was evident surrounding all S100-IR Schwann cells. B) One week following nerve injury, p75 immunostaining was dramatically upregulated in Schwann cells; the intense red color masked the mixture of red and green stainings which could be detected by analysing the separately the S100 and p75 stainings (not shown). C-D) 2 & 4 weeks post-injury a decrease in p75 intensity was observed in that the yellow indicative of S100 co-labelling was able to be visualized. E) proNGF (red) S100 (green) and p75 (blue) triple labelling to demonstrate the relative distribution of Schwann cells with respect to proNGF; note a limited distribution of Schwann cells with proNGF and faint immunoreactivity for p75 in sham-operated controls. F) 2 weeks post-injury, the clear upregulation of p75 immunoreactivity associated with S100 (arrow) was observed, which wrapped around proNGF-IR blood vessels.

    Article Snippet: Primary antibodies such as mouse anti-TrkA (1:500, MAB1056, R&D Systems, Minneapolis, MN), rabbit anti-proNGF (1:500, ANT-005, Alomone Labs, Isreal), or mouse anti-p75 (1:200, MC192, Novus Biologicals) were incubated overnight in blocking buffer at 4°C.

    Techniques: Expressing, Immunostaining

    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Journal: Molecular Pain

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    doi: 10.1186/1744-8069-8-1

    Figure Lengend Snippet: Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Article Snippet: Primary antibodies such as mouse anti-TrkA (1:500, MAB1056, R&D Systems, Minneapolis, MN), rabbit anti-proNGF (1:500, ANT-005, Alomone Labs, Isreal), or mouse anti-p75 (1:200, MC192, Novus Biologicals) were incubated overnight in blocking buffer at 4°C.

    Techniques: Staining, Immunostaining

    Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Journal: Molecular Pain

    Article Title: Neurotrophic factor changes in the rat thick skin following chronic constriction injury of the sciatic nerve

    doi: 10.1186/1744-8069-8-1

    Figure Lengend Snippet: Distribution of p75 immunoreactivity following nerve injury and relationship to nerve fibers and proNGF . A) In sham-operated animals, p75 was distributed (red) around and with PGP 9.5-IR nerve fibers (green). P75 staining was found more clearly around large cutaneous PGP 9.5-IR nerve fiber bundles and smaller fibers along the dermo-epidermal junction. Where nerve fibers crossed the dermo-epidermal junction into the epidermis, the yellow color representing p75 associating with nerve fibers was lost (arrow). B) At 1 week post-injury, virtually all PGP-9.5-IR nerve fibers disappeared from the upper dermis and epidermis; immunostaining in p75-IR Schwann was very intense. C) At 2 weeks post-injury, a low number of PGP-9.5-IR fibers were detected and were associated with p75 Schwann cells (yellow), however most of the PGP-9.5-IR was restricted to Langerhans cells in epidermis (arrow) D) At 4 weeks post-injury, p75 immunoreactivity decreased co-incidentally with the increase in PGP-9.5 immunoreactivityin the upper dermis (yellow). E-H) ProNGF and p75 association in sham-operated controls and in lesioned animals was loose in that most proNGF immunoreactivity was segregated from that for p75 and there was no obvious co-localization (arrows).

    Article Snippet: Immunohistochemical staining with this antibody in either rat or human skin was absent following preadsorption with purified human PGP 9.5 protein [ , ]. proNGF: The rabbit anti-proNGF antibody (Alomone #ANT-005 Lot#AN-03) was generated by injection of a synthetic peptide corresponding to a.a. 84-104 of the precursor form of rat NGF.

    Techniques: Staining, Immunostaining

    Overexpression of proNGF reduced NGF and induced expression of TrkA and p75 NTR , but not sortilin. A , B : Western blot (WB) analysis of rat retinal lysate showed significant (1.5-fold) increase in expression of TrkA and p75 NTR in rats electroporated with pGFP-proNGF123 as compared with those electroporated with pGFP (n=4). C : WB analysis showed that overexpression of pGFP-proNGF123 in rat retinas did not affect sortilin protein expression level as compared with the control rats (n=4). D : WB analysis showed that overexpression of pGFP-proNGF123 significantly reduced NGF expression (n=5) compared with GFP controls. The asterisk represents significant difference as compared with control group at p<0.05. ROD, relative optical density.

    Journal: Molecular Vision

    Article Title: Electroporation-mediated gene delivery of cleavage-resistant pro–nerve growth factor causes retinal neuro- and vascular degeneration

    doi:

    Figure Lengend Snippet: Overexpression of proNGF reduced NGF and induced expression of TrkA and p75 NTR , but not sortilin. A , B : Western blot (WB) analysis of rat retinal lysate showed significant (1.5-fold) increase in expression of TrkA and p75 NTR in rats electroporated with pGFP-proNGF123 as compared with those electroporated with pGFP (n=4). C : WB analysis showed that overexpression of pGFP-proNGF123 in rat retinas did not affect sortilin protein expression level as compared with the control rats (n=4). D : WB analysis showed that overexpression of pGFP-proNGF123 significantly reduced NGF expression (n=5) compared with GFP controls. The asterisk represents significant difference as compared with control group at p<0.05. ROD, relative optical density.

    Article Snippet: Antibodies for proNGF and NGF (Alomone Labs Ltd), p75 NTR , sortilin, and TrkA (Millipore) were used.

    Techniques: Over Expression, Expressing, Western Blot