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  • 88
    Promega p75ntr
    P75ntr, supplied by Promega, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p75ntr/product/Promega
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p75ntr - by Bioz Stars, 2022-11
    88/100 stars
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    94
    Millipore p75ntr
    proNGF and NGF activated different intracellular pathways. (A) The neutralisation of <t>p75NTR</t> using either a specific anti-p75NTR antibody (a-p75; 2.5 µg/mL) or using the specific pharmacological inhibitor LM11A.31 (10 nM), decreased interleukin (IL)-6 release in LPS-activated SFMC of patients with JIA (n=16) treated with proNGF. On the contrary, the blocking of TrkA with a neutralising antibody (a-TrkA; 3 µg/mL) did not affect IL-6 release. (B) Western blot shows an increased phosphorylation of p38 and JNK after 5 minutes of proNGF stimulation in LPS-treated SFMC. mNGF treatment did not affect the phosphorylation of these downstream molecules. The result is representative of one out of three independent experiments. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). (C) In LPS-activated SFMC of three different patients with JIA, preincubation with the inhibitor LM11A-31 (10 nM), which blocks the binding of proNGF to p75NTR, abolished the phosphorylation of p38 and JNK induced after 5 minutes of proNGF addition. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). *p
    P75ntr, supplied by Millipore, 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/p75ntr/product/Millipore
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p75ntr - by Bioz Stars, 2022-11
    94/100 stars
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    96
    Cell Signaling Technology Inc p75ntr
    proNGF and NGF activated different intracellular pathways. (A) The neutralisation of <t>p75NTR</t> using either a specific anti-p75NTR antibody (a-p75; 2.5 µg/mL) or using the specific pharmacological inhibitor LM11A.31 (10 nM), decreased interleukin (IL)-6 release in LPS-activated SFMC of patients with JIA (n=16) treated with proNGF. On the contrary, the blocking of TrkA with a neutralising antibody (a-TrkA; 3 µg/mL) did not affect IL-6 release. (B) Western blot shows an increased phosphorylation of p38 and JNK after 5 minutes of proNGF stimulation in LPS-treated SFMC. mNGF treatment did not affect the phosphorylation of these downstream molecules. The result is representative of one out of three independent experiments. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). (C) In LPS-activated SFMC of three different patients with JIA, preincubation with the inhibitor LM11A-31 (10 nM), which blocks the binding of proNGF to p75NTR, abolished the phosphorylation of p38 and JNK induced after 5 minutes of proNGF addition. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). *p
    P75ntr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p75ntr/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p75ntr - by Bioz Stars, 2022-11
    96/100 stars
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    88
    Covance p75ntr
    Induction of <t>p75NTR</t> and proNGF in the white matter (corpus callosum) after CCI-TBI. ( A–D ) Immunoblot analysis showed that both p75NTR and proNGF protein levels are increased after TBI in the ipsilateral white matter as compared to uninjured (UN) and sham injured tissue. Two-way ANOVA, ( A ) for p75NTR: side, F (1,12) = 92.42, P
    P75ntr, supplied by Covance, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p75ntr/product/Covance
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p75ntr - by Bioz Stars, 2022-11
    88/100 stars
      Buy from Supplier

    Image Search Results


    proNGF and NGF activated different intracellular pathways. (A) The neutralisation of p75NTR using either a specific anti-p75NTR antibody (a-p75; 2.5 µg/mL) or using the specific pharmacological inhibitor LM11A.31 (10 nM), decreased interleukin (IL)-6 release in LPS-activated SFMC of patients with JIA (n=16) treated with proNGF. On the contrary, the blocking of TrkA with a neutralising antibody (a-TrkA; 3 µg/mL) did not affect IL-6 release. (B) Western blot shows an increased phosphorylation of p38 and JNK after 5 minutes of proNGF stimulation in LPS-treated SFMC. mNGF treatment did not affect the phosphorylation of these downstream molecules. The result is representative of one out of three independent experiments. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). (C) In LPS-activated SFMC of three different patients with JIA, preincubation with the inhibitor LM11A-31 (10 nM), which blocks the binding of proNGF to p75NTR, abolished the phosphorylation of p38 and JNK induced after 5 minutes of proNGF addition. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). *p

    Journal: RMD Open

    Article Title: ProNGF-p75NTR axis plays a proinflammatory role in inflamed joints: a novel pathogenic mechanism in chronic arthritis

    doi: 10.1136/rmdopen-2017-000441

    Figure Lengend Snippet: proNGF and NGF activated different intracellular pathways. (A) The neutralisation of p75NTR using either a specific anti-p75NTR antibody (a-p75; 2.5 µg/mL) or using the specific pharmacological inhibitor LM11A.31 (10 nM), decreased interleukin (IL)-6 release in LPS-activated SFMC of patients with JIA (n=16) treated with proNGF. On the contrary, the blocking of TrkA with a neutralising antibody (a-TrkA; 3 µg/mL) did not affect IL-6 release. (B) Western blot shows an increased phosphorylation of p38 and JNK after 5 minutes of proNGF stimulation in LPS-treated SFMC. mNGF treatment did not affect the phosphorylation of these downstream molecules. The result is representative of one out of three independent experiments. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). (C) In LPS-activated SFMC of three different patients with JIA, preincubation with the inhibitor LM11A-31 (10 nM), which blocks the binding of proNGF to p75NTR, abolished the phosphorylation of p38 and JNK induced after 5 minutes of proNGF addition. Results of the densitometric analysis of all experiments are expressed as arbitrary units (AU). *p

    Article Snippet: In a study using the PC12 neuronal cell line, it was shown that proNGF can have neurotrophic activity in primed PC12 or apoptotic activity in unprimed PC12, two cell conditions characterised by a different ratio of TrkA and p75NTR, further suggesting that the biological activity of proNGF is dependent on the relative expression levels of TrkA and p75NTR.

    Techniques: Blocking Assay, Western Blot, Binding Assay

    p75NTR, TrkA and sortilin expression levels in patients with JIA. (A) mRNA expression levels of TrkA, p75NTR and sortilin in freshly isolated mononuclear cells from peripheral blood of healthy children (CTRL PBMC) and in mononuclear cells from peripheral blood or from synovial fluids of patients with JIA (respectively, JIA PBMC and JIA SFMC) were quantified by real-time PCR analysis. JIA PBMC (n=34) and JIA SFMC (n=66) express low TrkA and high p75NTR mRNA levels compared with CTRL PBMC (n=10). Sortilin, a coreceptor for p75NTR essential for proNGF binding, is highly expressed in JIA SFMC (n=19) and expressed in JIA PBMC (n=13) and in CTRL PBMC (n=7). The results are expressed as arbitrary units (AU) after normalisation with the housekeeping gene GAPDH. (B) p75NTR mRNA levels are higher in SFMC than in PBMC of matched patients with JIA (n=18). (C) Sortilin mRNA levels are higher in SFMC than in PBMC of matched patients with JIA (n=11). (D) Western blot and densitometric analysis of three independent experiments confirmed that p75NTR was the prevalent NGF receptor in JIA mononuclear cells, while TrkA was the most expressed NGF receptor in CTRL PBMC. Sortilin is also highly expressed in JIA mononuclear cells. *p

    Journal: RMD Open

    Article Title: ProNGF-p75NTR axis plays a proinflammatory role in inflamed joints: a novel pathogenic mechanism in chronic arthritis

    doi: 10.1136/rmdopen-2017-000441

    Figure Lengend Snippet: p75NTR, TrkA and sortilin expression levels in patients with JIA. (A) mRNA expression levels of TrkA, p75NTR and sortilin in freshly isolated mononuclear cells from peripheral blood of healthy children (CTRL PBMC) and in mononuclear cells from peripheral blood or from synovial fluids of patients with JIA (respectively, JIA PBMC and JIA SFMC) were quantified by real-time PCR analysis. JIA PBMC (n=34) and JIA SFMC (n=66) express low TrkA and high p75NTR mRNA levels compared with CTRL PBMC (n=10). Sortilin, a coreceptor for p75NTR essential for proNGF binding, is highly expressed in JIA SFMC (n=19) and expressed in JIA PBMC (n=13) and in CTRL PBMC (n=7). The results are expressed as arbitrary units (AU) after normalisation with the housekeeping gene GAPDH. (B) p75NTR mRNA levels are higher in SFMC than in PBMC of matched patients with JIA (n=18). (C) Sortilin mRNA levels are higher in SFMC than in PBMC of matched patients with JIA (n=11). (D) Western blot and densitometric analysis of three independent experiments confirmed that p75NTR was the prevalent NGF receptor in JIA mononuclear cells, while TrkA was the most expressed NGF receptor in CTRL PBMC. Sortilin is also highly expressed in JIA mononuclear cells. *p

    Article Snippet: In a study using the PC12 neuronal cell line, it was shown that proNGF can have neurotrophic activity in primed PC12 or apoptotic activity in unprimed PC12, two cell conditions characterised by a different ratio of TrkA and p75NTR, further suggesting that the biological activity of proNGF is dependent on the relative expression levels of TrkA and p75NTR.

    Techniques: Expressing, Isolation, Real-time Polymerase Chain Reaction, Binding Assay, Western Blot

    p75NTR and disease severity (A) in persistent oligoarticular (n=29), extended oligoarticular (n=16) and polyarticular (n=13) patients p75NTR mRNA expression levels are higher in patients with JIA with the highest number of inflamed joints (**p

    Journal: RMD Open

    Article Title: ProNGF-p75NTR axis plays a proinflammatory role in inflamed joints: a novel pathogenic mechanism in chronic arthritis

    doi: 10.1136/rmdopen-2017-000441

    Figure Lengend Snippet: p75NTR and disease severity (A) in persistent oligoarticular (n=29), extended oligoarticular (n=16) and polyarticular (n=13) patients p75NTR mRNA expression levels are higher in patients with JIA with the highest number of inflamed joints (**p

    Article Snippet: In a study using the PC12 neuronal cell line, it was shown that proNGF can have neurotrophic activity in primed PC12 or apoptotic activity in unprimed PC12, two cell conditions characterised by a different ratio of TrkA and p75NTR, further suggesting that the biological activity of proNGF is dependent on the relative expression levels of TrkA and p75NTR.

    Techniques: Expressing

    Induction of p75NTR and proNGF in the white matter (corpus callosum) after CCI-TBI. ( A–D ) Immunoblot analysis showed that both p75NTR and proNGF protein levels are increased after TBI in the ipsilateral white matter as compared to uninjured (UN) and sham injured tissue. Two-way ANOVA, ( A ) for p75NTR: side, F (1,12) = 92.42, P

    Journal: Brain

    Article Title: A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury

    doi: 10.1093/brain/aww074

    Figure Lengend Snippet: Induction of p75NTR and proNGF in the white matter (corpus callosum) after CCI-TBI. ( A–D ) Immunoblot analysis showed that both p75NTR and proNGF protein levels are increased after TBI in the ipsilateral white matter as compared to uninjured (UN) and sham injured tissue. Two-way ANOVA, ( A ) for p75NTR: side, F (1,12) = 92.42, P

    Article Snippet: While the precise binding site of both neurotoxic peptides on p75NTR has not been determined, our results suggest that their functional epitopes may be different from that of these neurotrophins and are probably located at the level of CRD1.

    Techniques:

    Acute expression of p75NTR after FPI-TBI and reduction of neurodegeneration with EVT901 in vivo . ( A ) Immunohistochemical expression of p75NTR at 1–2 days in the dentate gyrus of TBI rats using specific anti-p75NTR antibody. ( B ) Representative photomicrographs (original magnification ×10) of Fluoro-Jade® staining of damaged neurons in the granular layer of the dentate gyrus in FPI-TBI rats 1 week post-injury. ( C ) Representative photomicrographs of Fluoro-Jade®-stained sections from the thalamus 14-days post-trauma (ipsilateral versus contralateral to the injury). ( D ) Quantification of Fluoro-Jade® B-positive degenerating cells in the thalamus of FPI-TBI rats after EVT901 treatment. Following Fluoro-Jade staining, the digital images were collected and the damaged cells were quantified using Explora Nova Software. Three mg/kg/day of EVT901 protected neurons in the thalamus after TBI [one-way ANOVA, EVT901 effect, F (3,18) = 8.46, P = 0.001]. # P

    Journal: Brain

    Article Title: A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury

    doi: 10.1093/brain/aww074

    Figure Lengend Snippet: Acute expression of p75NTR after FPI-TBI and reduction of neurodegeneration with EVT901 in vivo . ( A ) Immunohistochemical expression of p75NTR at 1–2 days in the dentate gyrus of TBI rats using specific anti-p75NTR antibody. ( B ) Representative photomicrographs (original magnification ×10) of Fluoro-Jade® staining of damaged neurons in the granular layer of the dentate gyrus in FPI-TBI rats 1 week post-injury. ( C ) Representative photomicrographs of Fluoro-Jade®-stained sections from the thalamus 14-days post-trauma (ipsilateral versus contralateral to the injury). ( D ) Quantification of Fluoro-Jade® B-positive degenerating cells in the thalamus of FPI-TBI rats after EVT901 treatment. Following Fluoro-Jade staining, the digital images were collected and the damaged cells were quantified using Explora Nova Software. Three mg/kg/day of EVT901 protected neurons in the thalamus after TBI [one-way ANOVA, EVT901 effect, F (3,18) = 8.46, P = 0.001]. # P

    Article Snippet: While the precise binding site of both neurotoxic peptides on p75NTR has not been determined, our results suggest that their functional epitopes may be different from that of these neurotrophins and are probably located at the level of CRD1.

    Techniques: Expressing, In Vivo, Immunohistochemistry, Staining, Software

    Mechanism of action through the CRD1 domain of p75NTR: cellular response and induction of neuritogenesis. ( A ) EVT901 inhibits the binding of AP-p75NTR to the receptor p75NTR. Binding experiments on SKN-BE-p75NTR with soluble AP-p75NTR (10 nM) in the presence of increasing concentrations of EVT901. Data are reported as mean % inhibition of binding, representative of three independent experiments. ( B ) Competition of 125 I-NGF binding with EVT901. Binding of 125 I-NGF (0.3 nM) to SKNBE-p75NTR in the presence of increasing concentrations of EVT901. Results are mean % inhibition of specific binding, representative of three independent experiments. ( C ) HEK293T cells transiently co-transfected with the same amount of DNA originating from the p75NTR full-length tagged either in C-terminal with HA (HA- p75NTR) or in N-terminal with Flag (Flag-p75NTR) and then treated or not with the compound EVT901 at 100 nM for 24 h. Oligomerization evaluated using an ELISA assay with flag-coated plates and anti-HA-HRP antibody [two-way ANOVA, EVT901 dose effect, F( 4,94) = 46.85, P

    Journal: Brain

    Article Title: A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury

    doi: 10.1093/brain/aww074

    Figure Lengend Snippet: Mechanism of action through the CRD1 domain of p75NTR: cellular response and induction of neuritogenesis. ( A ) EVT901 inhibits the binding of AP-p75NTR to the receptor p75NTR. Binding experiments on SKN-BE-p75NTR with soluble AP-p75NTR (10 nM) in the presence of increasing concentrations of EVT901. Data are reported as mean % inhibition of binding, representative of three independent experiments. ( B ) Competition of 125 I-NGF binding with EVT901. Binding of 125 I-NGF (0.3 nM) to SKNBE-p75NTR in the presence of increasing concentrations of EVT901. Results are mean % inhibition of specific binding, representative of three independent experiments. ( C ) HEK293T cells transiently co-transfected with the same amount of DNA originating from the p75NTR full-length tagged either in C-terminal with HA (HA- p75NTR) or in N-terminal with Flag (Flag-p75NTR) and then treated or not with the compound EVT901 at 100 nM for 24 h. Oligomerization evaluated using an ELISA assay with flag-coated plates and anti-HA-HRP antibody [two-way ANOVA, EVT901 dose effect, F( 4,94) = 46.85, P

    Article Snippet: While the precise binding site of both neurotoxic peptides on p75NTR has not been determined, our results suggest that their functional epitopes may be different from that of these neurotrophins and are probably located at the level of CRD1.

    Techniques: Binding Assay, Inhibition, Transfection, Enzyme-linked Immunosorbent Assay

    EVT901 blocks proNGF-mediated caspase activity and p75NTR expression in OPCs and oligodendrocytes in vitro and reduces proNGF-induced cell death. ( A ) Immunostaining showed that treatment with pro-NGF (50 ng/ml) induced caspase-3 activity in OPCs in vitro . ( B and C ) Caspase activity was measured by counting positive cells using the FLICA assay. Pro-NGF (50 ng/ml) increased caspase activity in cultured OPCs and oligodendrocytes. However, EVT901 added to the medium reduced the percentage of caspase-positive cells in a dose-dependent manner for OPCs and oligodendrocytes [one-way ANOVA, F (7,67) = 10.02, P

    Journal: Brain

    Article Title: A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury

    doi: 10.1093/brain/aww074

    Figure Lengend Snippet: EVT901 blocks proNGF-mediated caspase activity and p75NTR expression in OPCs and oligodendrocytes in vitro and reduces proNGF-induced cell death. ( A ) Immunostaining showed that treatment with pro-NGF (50 ng/ml) induced caspase-3 activity in OPCs in vitro . ( B and C ) Caspase activity was measured by counting positive cells using the FLICA assay. Pro-NGF (50 ng/ml) increased caspase activity in cultured OPCs and oligodendrocytes. However, EVT901 added to the medium reduced the percentage of caspase-positive cells in a dose-dependent manner for OPCs and oligodendrocytes [one-way ANOVA, F (7,67) = 10.02, P

    Article Snippet: While the precise binding site of both neurotoxic peptides on p75NTR has not been determined, our results suggest that their functional epitopes may be different from that of these neurotrophins and are probably located at the level of CRD1.

    Techniques: Activity Assay, Expressing, In Vitro, Immunostaining, Cell Culture