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mouse ngf prongf neutralizing antibodies  (Alomone Labs)


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    Structured Review

    Alomone Labs mouse ngf prongf neutralizing antibodies
    Mouse Ngf Prongf Neutralizing Antibodies, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+ngf+prongf/Mouse+NGF%2FproNGF+Neutralizing+Antibody/pm39378286-197-13-19
    Average 94 stars, based on 35 article reviews
    mouse ngf prongf neutralizing antibodies - by Bioz Stars, 2026-11
    94/100 stars

    Images

    Related Articles

    Expressing:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.

    Western Blot:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.

    Labeling:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.

    In Situ Hybridization:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.

    Cell Culture:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.

    In Vitro:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.

    Real-time Polymerase Chain Reaction:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.

    Immunofluorescence:

    Article Title: RIP2 Gates TRAF6 Interaction with Death Receptor p75 NTR to Regulate Cerebellar Granule Neuron Survival.
    Article Snippet: Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.Mouse IgG1 isotype control (MAB002) and anti-mature NGF (mNGF and MAB256) were obtained from R&D Systems.. Mature NGF (N-100), brain-derived neurotrophic factor (BDNF) (B-250), and anti-NGF/ proNGF (total NGF) neutralizing antibody (ALM-006) were obtained from Alomone.. TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.TRAF6 inhibitor (NBP2-26506) was obtained from Novus Biologicals.



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    Fig. 6 Immunofluorescence study <t>of</t> <t>p75NTR</t> and <t>proNGF</t> in the bladder mucosa and detrusor at baseline (a–d), 2 weeks of treatment (e–l) and 4 weeks of treatment (m–t). proNGF (green fluorescence) is mainly localised to the urothelial layer (UT) with low to absent signal in the lamina propria (LP) in the control mice, while in Dm and THX-B-treated mice the signal can also be detected in the LP. The proNGF signal in the detrusor muscle fibres (white arrow) does not show a specific change across groups and different time points. The p75NTR signal (red fluorescence) in the control mice is expressed in the LP and around the muscle bundles (in detrusor). In Dm, p75NTR shows expression mainly in the UT layer at baseline. This pattern changes with time to show more expression in the UT and LP, which is co-expressed with proNGF. In proNGF mAb- treated mice the p75NTR
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    Fig. 2. Signaling through <t>proNGF–p75NTR,</t> but not mNGF–TrkA, is required for Gb3- induced mechanical sensitization. (A) Experimental timeline of the von Frey tests and the i.pl. injection of Gb3 and anti body/antiserum or antibody/antiserum alone. (B, C) The antiserum (1 μl/paw, i.pl.) containing anti-proNGF antibody effectively recovered the Gb3-induced decrease of the 50% paw withdrawal threshold (PWT; 1 h: H = 9.40, P = 0.009; 3 h: H = 9.13, P = 0.010; 6 h: H = 6.79, P = 0.034; 24 h: H = 6.24, P = 0.044) and its area under the curve (AUC; H = 10.1, P = 0.006). n = 8 per group. The injection volume was 10 μl. (D, E) The anti-NGF antibody (1 μg/paw and 10 μg/ paw, i.pl.) failed to significantly alleviate reductions in the pain threshold and its AUC (H = 10.5, P = 0.015) in Gb3-injected mice. Vehicle, n = 7; Gb3 + Control IgG, n = 8; Gb3 + Anti-NGF antibody (1 μg), n = 9; Gb3 + Anti-NGF antibody (10 μg), n = 6. The injection volume was 10 or 20 μl. (F, G) Administration of an anti-p75NTR antibody (1 μg/paw, i.pl.) almost completely reversed the Gb3-induced decline of the 50% PWT (24 h: H = 8.44, P = 0.015) and its AUC (H = 9.16, P = 0.010) to the level of the vehicle control. Vehicle, n = 11; Gb3 + Control IgG, n = 15; Gb3 + Anti-p75NTR antibody, n = 14. The injection volume was 10 or 20 μl. (H, I) Inhibition of TrkA activity with the neutral izing antibody (1 μg/paw and 10 μg/paw, i. pl.) gave minimal influence on the Gb3- induced mechanical allodynia (AUC: H = 9.80, P = 0.020). Vehicle, n = 11; Gb3 + Control IgG, n = 11; Gb3 + Anti-TrkA anti body (1 μg), n = 7; Gb3 + Anti-TrkA anti body (10 μg), n = 7. The injection volume was 20 μl. *P < 0.05, **P < 0.01 vs the Vehicle group, #P < 0.05, ##P < 0.01 vs the Gb3 + Normal serum or Control IgG group by Dunn’s test with Holm adjustment.
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    Fig. 2. Signaling through <t>proNGF–p75NTR,</t> but not mNGF–TrkA, is required for Gb3- induced mechanical sensitization. (A) Experimental timeline of the von Frey tests and the i.pl. injection of Gb3 and anti body/antiserum or antibody/antiserum alone. (B, C) The antiserum (1 μl/paw, i.pl.) containing anti-proNGF antibody effectively recovered the Gb3-induced decrease of the 50% paw withdrawal threshold (PWT; 1 h: H = 9.40, P = 0.009; 3 h: H = 9.13, P = 0.010; 6 h: H = 6.79, P = 0.034; 24 h: H = 6.24, P = 0.044) and its area under the curve (AUC; H = 10.1, P = 0.006). n = 8 per group. The injection volume was 10 μl. (D, E) The anti-NGF antibody (1 μg/paw and 10 μg/ paw, i.pl.) failed to significantly alleviate reductions in the pain threshold and its AUC (H = 10.5, P = 0.015) in Gb3-injected mice. Vehicle, n = 7; Gb3 + Control IgG, n = 8; Gb3 + Anti-NGF antibody (1 μg), n = 9; Gb3 + Anti-NGF antibody (10 μg), n = 6. The injection volume was 10 or 20 μl. (F, G) Administration of an anti-p75NTR antibody (1 μg/paw, i.pl.) almost completely reversed the Gb3-induced decline of the 50% PWT (24 h: H = 8.44, P = 0.015) and its AUC (H = 9.16, P = 0.010) to the level of the vehicle control. Vehicle, n = 11; Gb3 + Control IgG, n = 15; Gb3 + Anti-p75NTR antibody, n = 14. The injection volume was 10 or 20 μl. (H, I) Inhibition of TrkA activity with the neutral izing antibody (1 μg/paw and 10 μg/paw, i. pl.) gave minimal influence on the Gb3- induced mechanical allodynia (AUC: H = 9.80, P = 0.020). Vehicle, n = 11; Gb3 + Control IgG, n = 11; Gb3 + Anti-TrkA anti body (1 μg), n = 7; Gb3 + Anti-TrkA anti body (10 μg), n = 7. The injection volume was 20 μl. *P < 0.05, **P < 0.01 vs the Vehicle group, #P < 0.05, ##P < 0.01 vs the Gb3 + Normal serum or Control IgG group by Dunn’s test with Holm adjustment.
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    Fig. 2. Signaling through <t>proNGF–p75NTR,</t> but not mNGF–TrkA, is required for Gb3- induced mechanical sensitization. (A) Experimental timeline of the von Frey tests and the i.pl. injection of Gb3 and anti body/antiserum or antibody/antiserum alone. (B, C) The antiserum (1 μl/paw, i.pl.) containing anti-proNGF antibody effectively recovered the Gb3-induced decrease of the 50% paw withdrawal threshold (PWT; 1 h: H = 9.40, P = 0.009; 3 h: H = 9.13, P = 0.010; 6 h: H = 6.79, P = 0.034; 24 h: H = 6.24, P = 0.044) and its area under the curve (AUC; H = 10.1, P = 0.006). n = 8 per group. The injection volume was 10 μl. (D, E) The anti-NGF antibody (1 μg/paw and 10 μg/ paw, i.pl.) failed to significantly alleviate reductions in the pain threshold and its AUC (H = 10.5, P = 0.015) in Gb3-injected mice. Vehicle, n = 7; Gb3 + Control IgG, n = 8; Gb3 + Anti-NGF antibody (1 μg), n = 9; Gb3 + Anti-NGF antibody (10 μg), n = 6. The injection volume was 10 or 20 μl. (F, G) Administration of an anti-p75NTR antibody (1 μg/paw, i.pl.) almost completely reversed the Gb3-induced decline of the 50% PWT (24 h: H = 8.44, P = 0.015) and its AUC (H = 9.16, P = 0.010) to the level of the vehicle control. Vehicle, n = 11; Gb3 + Control IgG, n = 15; Gb3 + Anti-p75NTR antibody, n = 14. The injection volume was 10 or 20 μl. (H, I) Inhibition of TrkA activity with the neutral izing antibody (1 μg/paw and 10 μg/paw, i. pl.) gave minimal influence on the Gb3- induced mechanical allodynia (AUC: H = 9.80, P = 0.020). Vehicle, n = 11; Gb3 + Control IgG, n = 11; Gb3 + Anti-TrkA anti body (1 μg), n = 7; Gb3 + Anti-TrkA anti body (10 μg), n = 7. The injection volume was 20 μl. *P < 0.05, **P < 0.01 vs the Vehicle group, #P < 0.05, ##P < 0.01 vs the Gb3 + Normal serum or Control IgG group by Dunn’s test with Holm adjustment.
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    Image Search Results


    Fig. 6 Immunofluorescence study of p75NTR and proNGF in the bladder mucosa and detrusor at baseline (a–d), 2 weeks of treatment (e–l) and 4 weeks of treatment (m–t). proNGF (green fluorescence) is mainly localised to the urothelial layer (UT) with low to absent signal in the lamina propria (LP) in the control mice, while in Dm and THX-B-treated mice the signal can also be detected in the LP. The proNGF signal in the detrusor muscle fibres (white arrow) does not show a specific change across groups and different time points. The p75NTR signal (red fluorescence) in the control mice is expressed in the LP and around the muscle bundles (in detrusor). In Dm, p75NTR shows expression mainly in the UT layer at baseline. This pattern changes with time to show more expression in the UT and LP, which is co-expressed with proNGF. In proNGF mAb- treated mice the p75NTR

    Journal: Diabetologia

    Article Title: Antagonism of proNGF or its receptor p75 NTR reverses remodelling and improves bladder function in a mouse model of diabetic voiding dysfunction.

    doi: 10.1007/s00125-020-05222-4

    Figure Lengend Snippet: Fig. 6 Immunofluorescence study of p75NTR and proNGF in the bladder mucosa and detrusor at baseline (a–d), 2 weeks of treatment (e–l) and 4 weeks of treatment (m–t). proNGF (green fluorescence) is mainly localised to the urothelial layer (UT) with low to absent signal in the lamina propria (LP) in the control mice, while in Dm and THX-B-treated mice the signal can also be detected in the LP. The proNGF signal in the detrusor muscle fibres (white arrow) does not show a specific change across groups and different time points. The p75NTR signal (red fluorescence) in the control mice is expressed in the LP and around the muscle bundles (in detrusor). In Dm, p75NTR shows expression mainly in the UT layer at baseline. This pattern changes with time to show more expression in the UT and LP, which is co-expressed with proNGF. In proNGF mAb- treated mice the p75NTR

    Article Snippet: For immunofluorescence, tissue sections were blocked (0.6% BSA in PBS, 0.3% Triton, 10% goat serum) for 30 min, then placed with the primary antibody p75NTR ECD (1:500, MC192, Osenses, CA, USA), and proNGF (1:500, OriGene Tech.

    Techniques: Immunofluorescence, Fluorescence, Control, Expressing

    The list of primary and secondary antibodies used in Western blot and fluorescence microscopy techniques.

    Journal: International Journal of Molecular Sciences

    Article Title: The Slow-Releasing and Mitochondria-Targeted Hydrogen Sulfide (H 2 S) Delivery Molecule AP39 Induces Brain Tolerance to Ischemia

    doi: 10.3390/ijms22157816

    Figure Lengend Snippet: The list of primary and secondary antibodies used in Western blot and fluorescence microscopy techniques.

    Article Snippet: pro-NGF , Alomone , AGP-031 , 1:300.

    Techniques: Western Blot, Fluorescence, Microscopy, Marker

    Fig. 2. Signaling through proNGF–p75NTR, but not mNGF–TrkA, is required for Gb3- induced mechanical sensitization. (A) Experimental timeline of the von Frey tests and the i.pl. injection of Gb3 and anti body/antiserum or antibody/antiserum alone. (B, C) The antiserum (1 μl/paw, i.pl.) containing anti-proNGF antibody effectively recovered the Gb3-induced decrease of the 50% paw withdrawal threshold (PWT; 1 h: H = 9.40, P = 0.009; 3 h: H = 9.13, P = 0.010; 6 h: H = 6.79, P = 0.034; 24 h: H = 6.24, P = 0.044) and its area under the curve (AUC; H = 10.1, P = 0.006). n = 8 per group. The injection volume was 10 μl. (D, E) The anti-NGF antibody (1 μg/paw and 10 μg/ paw, i.pl.) failed to significantly alleviate reductions in the pain threshold and its AUC (H = 10.5, P = 0.015) in Gb3-injected mice. Vehicle, n = 7; Gb3 + Control IgG, n = 8; Gb3 + Anti-NGF antibody (1 μg), n = 9; Gb3 + Anti-NGF antibody (10 μg), n = 6. The injection volume was 10 or 20 μl. (F, G) Administration of an anti-p75NTR antibody (1 μg/paw, i.pl.) almost completely reversed the Gb3-induced decline of the 50% PWT (24 h: H = 8.44, P = 0.015) and its AUC (H = 9.16, P = 0.010) to the level of the vehicle control. Vehicle, n = 11; Gb3 + Control IgG, n = 15; Gb3 + Anti-p75NTR antibody, n = 14. The injection volume was 10 or 20 μl. (H, I) Inhibition of TrkA activity with the neutral izing antibody (1 μg/paw and 10 μg/paw, i. pl.) gave minimal influence on the Gb3- induced mechanical allodynia (AUC: H = 9.80, P = 0.020). Vehicle, n = 11; Gb3 + Control IgG, n = 11; Gb3 + Anti-TrkA anti body (1 μg), n = 7; Gb3 + Anti-TrkA anti body (10 μg), n = 7. The injection volume was 20 μl. *P < 0.05, **P < 0.01 vs the Vehicle group, #P < 0.05, ##P < 0.01 vs the Gb3 + Normal serum or Control IgG group by Dunn’s test with Holm adjustment.

    Journal: European journal of pharmacology

    Article Title: Fabry disease-associated globotriaosylceramide induces mechanical allodynia via activation of signaling through proNGF-p75 NTR but not mature NGF-TrkA.

    doi: 10.1016/j.ejphar.2021.173882

    Figure Lengend Snippet: Fig. 2. Signaling through proNGF–p75NTR, but not mNGF–TrkA, is required for Gb3- induced mechanical sensitization. (A) Experimental timeline of the von Frey tests and the i.pl. injection of Gb3 and anti body/antiserum or antibody/antiserum alone. (B, C) The antiserum (1 μl/paw, i.pl.) containing anti-proNGF antibody effectively recovered the Gb3-induced decrease of the 50% paw withdrawal threshold (PWT; 1 h: H = 9.40, P = 0.009; 3 h: H = 9.13, P = 0.010; 6 h: H = 6.79, P = 0.034; 24 h: H = 6.24, P = 0.044) and its area under the curve (AUC; H = 10.1, P = 0.006). n = 8 per group. The injection volume was 10 μl. (D, E) The anti-NGF antibody (1 μg/paw and 10 μg/ paw, i.pl.) failed to significantly alleviate reductions in the pain threshold and its AUC (H = 10.5, P = 0.015) in Gb3-injected mice. Vehicle, n = 7; Gb3 + Control IgG, n = 8; Gb3 + Anti-NGF antibody (1 μg), n = 9; Gb3 + Anti-NGF antibody (10 μg), n = 6. The injection volume was 10 or 20 μl. (F, G) Administration of an anti-p75NTR antibody (1 μg/paw, i.pl.) almost completely reversed the Gb3-induced decline of the 50% PWT (24 h: H = 8.44, P = 0.015) and its AUC (H = 9.16, P = 0.010) to the level of the vehicle control. Vehicle, n = 11; Gb3 + Control IgG, n = 15; Gb3 + Anti-p75NTR antibody, n = 14. The injection volume was 10 or 20 μl. (H, I) Inhibition of TrkA activity with the neutral izing antibody (1 μg/paw and 10 μg/paw, i. pl.) gave minimal influence on the Gb3- induced mechanical allodynia (AUC: H = 9.80, P = 0.020). Vehicle, n = 11; Gb3 + Control IgG, n = 11; Gb3 + Anti-TrkA anti body (1 μg), n = 7; Gb3 + Anti-TrkA anti body (10 μg), n = 7. The injection volume was 20 μl. *P < 0.05, **P < 0.01 vs the Vehicle group, #P < 0.05, ##P < 0.01 vs the Gb3 + Normal serum or Control IgG group by Dunn’s test with Holm adjustment.

    Article Snippet: The details of the NGF-related antibodies/antiserum and their control IgG/serum were as follows: mouse monoclonal anti-NGF antibody (L148M, Exalpha Biologicals, Shirley, MA, USA; 1 μg and 10 μg, Shutov et al., 2016); sheep polyclonal anti-proNGF antibody (S-080-100, Biosensis, Thebarton, Australia; 1 μl J. Sugimoto et al. European Journal of Pharmacology 895 (2021) 173882 antiserum); mouse monoclonal anti-TrkA antibody (Ab00439-1.4, Absolute Antibody, Redcar, UK; 1 μg and 10 μg, Ugolini et al., 2007); rabbit polyclonal anti-p75NTR antibody (AB-N01AP, Advanced Targeting Systems, San Diego, CA, USA; 1 μg, Watanabe et al., 2008); normal mouse IgG as a control of anti-NGF or anti-TrkA antibody (0G11, Exalpha Biologicals; Ab00178-1.4, Absolute Antibody); normal rabbit IgG as a control of anti-p75NTR antibody (PM035, MBL, Nagoya, Japan); and normal sheep serum as a control of anti-proNGF antibody (S3772, Sigma-Aldrich).

    Techniques: Injection, Control, Inhibition, Activity Assay

    Fig. 3. Gb3 injection did not lead to elevation of proNGF and mNGF or their receptor expression in either plantar skin or dorsal root ganglia. There were no changes in proNGF (A, C) nor mNGF (B, D) content in the plantar skin (A, B) and dorsal root ganglia (DRG; C, D) in mice that were 1 h or 24 h post-Gb3 treatment. n = 9 per group. The injection volume was 10 or 20 μl. Gb3 injection did not modify the expression levels of p75NTR in the plantar skin (E, 1 h: n = 6 per group; 24 h: n = 7 per group) or the DRG (F, n = 7 per group). The injection volume was 10 μl. The Vehicle (Veh) group, open circles; the Gb3 group, closed circles; MW, molecular weight.

    Journal: European journal of pharmacology

    Article Title: Fabry disease-associated globotriaosylceramide induces mechanical allodynia via activation of signaling through proNGF-p75 NTR but not mature NGF-TrkA.

    doi: 10.1016/j.ejphar.2021.173882

    Figure Lengend Snippet: Fig. 3. Gb3 injection did not lead to elevation of proNGF and mNGF or their receptor expression in either plantar skin or dorsal root ganglia. There were no changes in proNGF (A, C) nor mNGF (B, D) content in the plantar skin (A, B) and dorsal root ganglia (DRG; C, D) in mice that were 1 h or 24 h post-Gb3 treatment. n = 9 per group. The injection volume was 10 or 20 μl. Gb3 injection did not modify the expression levels of p75NTR in the plantar skin (E, 1 h: n = 6 per group; 24 h: n = 7 per group) or the DRG (F, n = 7 per group). The injection volume was 10 μl. The Vehicle (Veh) group, open circles; the Gb3 group, closed circles; MW, molecular weight.

    Article Snippet: The details of the NGF-related antibodies/antiserum and their control IgG/serum were as follows: mouse monoclonal anti-NGF antibody (L148M, Exalpha Biologicals, Shirley, MA, USA; 1 μg and 10 μg, Shutov et al., 2016); sheep polyclonal anti-proNGF antibody (S-080-100, Biosensis, Thebarton, Australia; 1 μl J. Sugimoto et al. European Journal of Pharmacology 895 (2021) 173882 antiserum); mouse monoclonal anti-TrkA antibody (Ab00439-1.4, Absolute Antibody, Redcar, UK; 1 μg and 10 μg, Ugolini et al., 2007); rabbit polyclonal anti-p75NTR antibody (AB-N01AP, Advanced Targeting Systems, San Diego, CA, USA; 1 μg, Watanabe et al., 2008); normal mouse IgG as a control of anti-NGF or anti-TrkA antibody (0G11, Exalpha Biologicals; Ab00178-1.4, Absolute Antibody); normal rabbit IgG as a control of anti-p75NTR antibody (PM035, MBL, Nagoya, Japan); and normal sheep serum as a control of anti-proNGF antibody (S3772, Sigma-Aldrich).

    Techniques: Injection, Expressing, Molecular Weight