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    Alomone Labs pro ngf
    Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml <t>NGF</t> or 20 ng/ml <t>pro-NGF</t> for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p
    Pro Ngf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    pro ngf - by Bioz Stars, 2022-11
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    1) Product Images from "Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells"

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-019-1758-z

    Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml NGF or 20 ng/ml pro-NGF for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p
    Figure Legend Snippet: Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml NGF or 20 ng/ml pro-NGF for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction

    Schematic view of the role of caspase-2 in p75NTR signaling and lipid metabolism. We propose the following scheme for the action of p75NTR and of caspase-2 in SREBP2 and associated gene regulation. Stimulation of p75NTR by NGF or pro-NGF activates the signaling protein p38 MAPK that can phosphorylate caspase-2 (CASP2) leading to the release of caspase-3 (CASP3) from its complex. CASP3, in turn, can cleave SREBP molecules to yield an active transcription factor. SREBP responsive genes include LDLR and other lipogenic genes but also CASP2 itself. Normally SREBP is processed by the enzymes S1P and S2P via a feedback inhibition determined by the cell cholesterol level. We hypothesize that the steroid-mediated and neurotrophin/p75NTR-induced SREBP pathways are distinct but functionally linked
    Figure Legend Snippet: Schematic view of the role of caspase-2 in p75NTR signaling and lipid metabolism. We propose the following scheme for the action of p75NTR and of caspase-2 in SREBP2 and associated gene regulation. Stimulation of p75NTR by NGF or pro-NGF activates the signaling protein p38 MAPK that can phosphorylate caspase-2 (CASP2) leading to the release of caspase-3 (CASP3) from its complex. CASP3, in turn, can cleave SREBP molecules to yield an active transcription factor. SREBP responsive genes include LDLR and other lipogenic genes but also CASP2 itself. Normally SREBP is processed by the enzymes S1P and S2P via a feedback inhibition determined by the cell cholesterol level. We hypothesize that the steroid-mediated and neurotrophin/p75NTR-induced SREBP pathways are distinct but functionally linked

    Techniques Used: Inhibition

    NGF is expressed in fatty liver of obese mice together with p75NTR. a NGF has increased in leptin-deficient ob/ob mouse livers compared with control, wild-type (wt) mice. b p75NTR was expressed in liver with no significant change between ob/ob and control mice. c , d The level of NGF has increased in leptin-receptor-deficient db/db mouse liver in comparison to controls, c immunoblot analysis and d quantification. ** p
    Figure Legend Snippet: NGF is expressed in fatty liver of obese mice together with p75NTR. a NGF has increased in leptin-deficient ob/ob mouse livers compared with control, wild-type (wt) mice. b p75NTR was expressed in liver with no significant change between ob/ob and control mice. c , d The level of NGF has increased in leptin-receptor-deficient db/db mouse liver in comparison to controls, c immunoblot analysis and d quantification. ** p

    Techniques Used: Mouse Assay

    p75NTR stimulation activated SREBP1 and SREBP2 in Huh7 hepatocyte cells. Human Huh7 cells were stimulated with 10 ng/ml pro-NGF or 50 ng/ml NGF for 16 h followed by immunoblotting using antibodies to detect the presence of cleaved/activated SREBP1 and SREBP2. a SREBP1, immunoblots and b quantification. Values are mean ± SD, n = 3. ** P
    Figure Legend Snippet: p75NTR stimulation activated SREBP1 and SREBP2 in Huh7 hepatocyte cells. Human Huh7 cells were stimulated with 10 ng/ml pro-NGF or 50 ng/ml NGF for 16 h followed by immunoblotting using antibodies to detect the presence of cleaved/activated SREBP1 and SREBP2. a SREBP1, immunoblots and b quantification. Values are mean ± SD, n = 3. ** P

    Techniques Used: Western Blot

    Role of Caspase-2 in p75NTR mediated regulation of SREBP. a Structure of human caspase-2 (CASP2) showing the CARD domain and the 18 and 13 kDa caspase subunits. p38 MAPK phosphorylation site at threonine (Thr)180 in CASP2 is conserved among species. The amino acid numbering underlying functional domains in CASP2 is shown. Boxes represent sequence homology among mammalian species. b Phosphoprotein retardation was performed as described in Materials and methods. A specific phospho-CASP2 antibody against Thr180 was used in conjunction with an antibody against CASP2, recognizing non-phosphorylated form of the enzyme. Phosphorylated CASP2 migrated slower in the Phos-Tag gel (right) as compared with the protein run on denaturating SDS-PAGE (left). c , d Huh7 hepatocyte cells were stimulated with 50 ng NGF ( c ) or 10 ng/ml pro-NGF ( d ) for different times followed by immunoblotting using phospho-CASP2 and anti-CASP2 antibodies. β-Actin was used as a control. e , f Cells were treated with pro-NGF for 6 h in the absence or presence 1 μM of the p38 MAPK inhibitor, SB203580 (SB). e Immunoblot and f quantification of p-CASP2 levels. SB reduced the increase in p-CASP2 by pro-NGF. Values are means ± SD, n = 4. * p
    Figure Legend Snippet: Role of Caspase-2 in p75NTR mediated regulation of SREBP. a Structure of human caspase-2 (CASP2) showing the CARD domain and the 18 and 13 kDa caspase subunits. p38 MAPK phosphorylation site at threonine (Thr)180 in CASP2 is conserved among species. The amino acid numbering underlying functional domains in CASP2 is shown. Boxes represent sequence homology among mammalian species. b Phosphoprotein retardation was performed as described in Materials and methods. A specific phospho-CASP2 antibody against Thr180 was used in conjunction with an antibody against CASP2, recognizing non-phosphorylated form of the enzyme. Phosphorylated CASP2 migrated slower in the Phos-Tag gel (right) as compared with the protein run on denaturating SDS-PAGE (left). c , d Huh7 hepatocyte cells were stimulated with 50 ng NGF ( c ) or 10 ng/ml pro-NGF ( d ) for different times followed by immunoblotting using phospho-CASP2 and anti-CASP2 antibodies. β-Actin was used as a control. e , f Cells were treated with pro-NGF for 6 h in the absence or presence 1 μM of the p38 MAPK inhibitor, SB203580 (SB). e Immunoblot and f quantification of p-CASP2 levels. SB reduced the increase in p-CASP2 by pro-NGF. Values are means ± SD, n = 4. * p

    Techniques Used: Functional Assay, Sequencing, SDS Page

    2) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    3) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    4) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    5) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    6) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    7) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    8) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    9) Product Images from "Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury"

    Article Title: Fluoxetine Prevents Oligodendrocyte Cell Death by Inhibiting Microglia Activation after Spinal Cord Injury

    Journal: Journal of Neurotrauma

    doi: 10.1089/neu.2014.3527

    section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p
    Figure Legend Snippet: section (n=3). ( A ) Presence of p-p38-MAPK–positive microglia in the ventral horn of gray matter at 5 days after injury. Representative images are from sections 1 mm rostral to the lesion epicenter. Scale bar, 50 μm. ( B ) Western blot of p-p38-MAPK at 3 and 5 days after injury. ( C ) Densitometric analysis of Western blot. Note that fluoxetine inhibits p38-MAPK activation after SCI, as compared to vehicle control. ( D ) Real-time reverse-transcriptase polymerase chain reaction of NGF at 3 days after injury. ( E ) Western blot of pro-NGF at 5 days after SCI. ( F ) Densitometric analysis of Western blot. Note that fluoxetine inhibits pro-NGF expression at 5 days after SCI. Values are presented as means±standard deviation. * p

    Techniques Used: Western Blot, Activation Assay, Polymerase Chain Reaction, Expressing, Standard Deviation

    10) Product Images from "The p75NTR SIGNALING CASCADE MEDIATES MECHANICAL HYPERALGESIA INDUCED BY NERVE GROWTH FACTOR INJECTED INTO THE RAT HIND PAW"

    Article Title: The p75NTR SIGNALING CASCADE MEDIATES MECHANICAL HYPERALGESIA INDUCED BY NERVE GROWTH FACTOR INJECTED INTO THE RAT HIND PAW

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2013.09.046

    Mechanical ipsilateral hyperalgesia is induced by mutated, protease-resistant Pro-NGF. Paw withdrawal frequency in response to stimulation with 10g and 15g VFH was enhanced following s.c. injection of mPro-NGF ( 500 ng/10 µL) into the rat plantar hind paw ( n =8). * P
    Figure Legend Snippet: Mechanical ipsilateral hyperalgesia is induced by mutated, protease-resistant Pro-NGF. Paw withdrawal frequency in response to stimulation with 10g and 15g VFH was enhanced following s.c. injection of mPro-NGF ( 500 ng/10 µL) into the rat plantar hind paw ( n =8). * P

    Techniques Used: Injection

    11) Product Images from "The p75NTR SIGNALING CASCADE MEDIATES MECHANICAL HYPERALGESIA INDUCED BY NERVE GROWTH FACTOR INJECTED INTO THE RAT HIND PAW"

    Article Title: The p75NTR SIGNALING CASCADE MEDIATES MECHANICAL HYPERALGESIA INDUCED BY NERVE GROWTH FACTOR INJECTED INTO THE RAT HIND PAW

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2013.09.046

    Local pre-treatment with myristoylated pseudosubstrate inhibitor of atypical PKCs decreased hyperalgesia from NGF and C2-ceramide. For all panels the inhibitor (40 µg /20 µl) was injected subcutaneously into the plantar hind paw 24h before the intraplantar injection of the algogens. ( A ) mPSI alone did not change the plantar hind paw responsiveness to mechanical stimulation, when tested at 24h after injection into naïve rats. ( B ) NGF injected into the plantar area after mPSI induced a much smaller than usual hyperalgesia ( n =16): significant changes in responses were found only for 15g force (p=0.0489, Friedman Test for 5 groups; no significance by Dunn's post hoc test). However, even for 15g, P > 0.05 was found when the test was applied to 4 same day-groups, excluding 24h time point responses. Analysis by Mann Whitney test revealed a significant difference for comparisons with corresponding baseline values only for 4g and 15g, at 3h and 24h time points, respectively. ( C ) Injection into the plantar hind paw of scrambled mPSI(40 µg /20 µl), which lacks inhibitory action on aPKCs, 24h before the intraplantar injection of NGF, neither prevented, nor decreased hyperalgesia from NGF (500 ng/10 µl) ( n =8). * P
    Figure Legend Snippet: Local pre-treatment with myristoylated pseudosubstrate inhibitor of atypical PKCs decreased hyperalgesia from NGF and C2-ceramide. For all panels the inhibitor (40 µg /20 µl) was injected subcutaneously into the plantar hind paw 24h before the intraplantar injection of the algogens. ( A ) mPSI alone did not change the plantar hind paw responsiveness to mechanical stimulation, when tested at 24h after injection into naïve rats. ( B ) NGF injected into the plantar area after mPSI induced a much smaller than usual hyperalgesia ( n =16): significant changes in responses were found only for 15g force (p=0.0489, Friedman Test for 5 groups; no significance by Dunn's post hoc test). However, even for 15g, P > 0.05 was found when the test was applied to 4 same day-groups, excluding 24h time point responses. Analysis by Mann Whitney test revealed a significant difference for comparisons with corresponding baseline values only for 4g and 15g, at 3h and 24h time points, respectively. ( C ) Injection into the plantar hind paw of scrambled mPSI(40 µg /20 µl), which lacks inhibitory action on aPKCs, 24h before the intraplantar injection of NGF, neither prevented, nor decreased hyperalgesia from NGF (500 ng/10 µl) ( n =8). * P

    Techniques Used: Injection, MANN-WHITNEY

    12) Product Images from "Chronic and Acute Models of Retinal Neurodegeneration TrkA Activity Are Neuroprotective whereas p75NTR Activity Is Neurotoxic through a Paracrine Mechanism"

    Article Title: Chronic and Acute Models of Retinal Neurodegeneration TrkA Activity Are Neuroprotective whereas p75NTR Activity Is Neurotoxic through a Paracrine Mechanism

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M110.147801

    Endogenous NGF-TrkA interactions are protective for RGCs during retinal degeneration. Quantification of surviving RGCs: A , at 14 days post-ON axotomy; B , at 42 days of chronic glaucoma. The density of RGCs in the untreated contralateral normal eye is
    Figure Legend Snippet: Endogenous NGF-TrkA interactions are protective for RGCs during retinal degeneration. Quantification of surviving RGCs: A , at 14 days post-ON axotomy; B , at 42 days of chronic glaucoma. The density of RGCs in the untreated contralateral normal eye is

    Techniques Used:

    NGF-p75 interactions are deleterious to RGC survival in normal eyes and during retinal degeneration. Quantification of surviving RGCs: A , normal eyes at 21 or 28 days post-treatment; B , at 7 or 14 days post-ON axotomy; C , at 42 days of chronic glaucoma.
    Figure Legend Snippet: NGF-p75 interactions are deleterious to RGC survival in normal eyes and during retinal degeneration. Quantification of surviving RGCs: A , normal eyes at 21 or 28 days post-treatment; B , at 7 or 14 days post-ON axotomy; C , at 42 days of chronic glaucoma.

    Techniques Used:

    13) Product Images from "Chronic and Acute Models of Retinal Neurodegeneration TrkA Activity Are Neuroprotective whereas p75NTR Activity Is Neurotoxic through a Paracrine Mechanism"

    Article Title: Chronic and Acute Models of Retinal Neurodegeneration TrkA Activity Are Neuroprotective whereas p75NTR Activity Is Neurotoxic through a Paracrine Mechanism

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M110.147801

    Restricting the Interactions of Endogenous NGF and Pro-NGF with p75NTR as a Strategy for Neuroprotection during Glaucoma and ON Axotomy
    Figure Legend Snippet: Restricting the Interactions of Endogenous NGF and Pro-NGF with p75NTR as a Strategy for Neuroprotection during Glaucoma and ON Axotomy

    Techniques Used:

    14) Product Images from "Chronic and Acute Models of Retinal Neurodegeneration TrkA Activity Are Neuroprotective whereas p75NTR Activity Is Neurotoxic through a Paracrine Mechanism"

    Article Title: Chronic and Acute Models of Retinal Neurodegeneration TrkA Activity Are Neuroprotective whereas p75NTR Activity Is Neurotoxic through a Paracrine Mechanism

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M110.147801

    THX-B and LM-24 inhibit NGF-p75 binding selectively, and during degeneration they protect retinal structure and delay RGC death. A , wild type NGF was immobilized on ELISA plates and binding of the indicated primary reagents (p75-Fc ( n = 5), TrkA-Fc (
    Figure Legend Snippet: THX-B and LM-24 inhibit NGF-p75 binding selectively, and during degeneration they protect retinal structure and delay RGC death. A , wild type NGF was immobilized on ELISA plates and binding of the indicated primary reagents (p75-Fc ( n = 5), TrkA-Fc (

    Techniques Used: Binding Assay, Enzyme-linked Immunosorbent Assay

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    Alomone Labs anti prongf antibody
    Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml <t>NGF</t> or 20 ng/ml <t>pro-NGF</t> for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p
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    Alomone Labs pro ngf
    Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml <t>NGF</t> or 20 ng/ml <t>pro-NGF</t> for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p
    Pro Ngf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pro ngf/product/Alomone Labs
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    Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml NGF or 20 ng/ml pro-NGF for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml NGF or 20 ng/ml pro-NGF for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p

    Article Snippet: Liver tissue was homogenized, and an equal amount of protein was subjected to immunoblotting using anti-NGF (1:1000; Alamone Labs, Jerusalem, Israel), anti-pro-NGF antibodies (1:300; Alamone Labs), and other antibodies as described below.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    Schematic view of the role of caspase-2 in p75NTR signaling and lipid metabolism. We propose the following scheme for the action of p75NTR and of caspase-2 in SREBP2 and associated gene regulation. Stimulation of p75NTR by NGF or pro-NGF activates the signaling protein p38 MAPK that can phosphorylate caspase-2 (CASP2) leading to the release of caspase-3 (CASP3) from its complex. CASP3, in turn, can cleave SREBP molecules to yield an active transcription factor. SREBP responsive genes include LDLR and other lipogenic genes but also CASP2 itself. Normally SREBP is processed by the enzymes S1P and S2P via a feedback inhibition determined by the cell cholesterol level. We hypothesize that the steroid-mediated and neurotrophin/p75NTR-induced SREBP pathways are distinct but functionally linked

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: Schematic view of the role of caspase-2 in p75NTR signaling and lipid metabolism. We propose the following scheme for the action of p75NTR and of caspase-2 in SREBP2 and associated gene regulation. Stimulation of p75NTR by NGF or pro-NGF activates the signaling protein p38 MAPK that can phosphorylate caspase-2 (CASP2) leading to the release of caspase-3 (CASP3) from its complex. CASP3, in turn, can cleave SREBP molecules to yield an active transcription factor. SREBP responsive genes include LDLR and other lipogenic genes but also CASP2 itself. Normally SREBP is processed by the enzymes S1P and S2P via a feedback inhibition determined by the cell cholesterol level. We hypothesize that the steroid-mediated and neurotrophin/p75NTR-induced SREBP pathways are distinct but functionally linked

    Article Snippet: Liver tissue was homogenized, and an equal amount of protein was subjected to immunoblotting using anti-NGF (1:1000; Alamone Labs, Jerusalem, Israel), anti-pro-NGF antibodies (1:300; Alamone Labs), and other antibodies as described below.

    Techniques: Inhibition

    NGF is expressed in fatty liver of obese mice together with p75NTR. a NGF has increased in leptin-deficient ob/ob mouse livers compared with control, wild-type (wt) mice. b p75NTR was expressed in liver with no significant change between ob/ob and control mice. c , d The level of NGF has increased in leptin-receptor-deficient db/db mouse liver in comparison to controls, c immunoblot analysis and d quantification. ** p

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: NGF is expressed in fatty liver of obese mice together with p75NTR. a NGF has increased in leptin-deficient ob/ob mouse livers compared with control, wild-type (wt) mice. b p75NTR was expressed in liver with no significant change between ob/ob and control mice. c , d The level of NGF has increased in leptin-receptor-deficient db/db mouse liver in comparison to controls, c immunoblot analysis and d quantification. ** p

    Article Snippet: Liver tissue was homogenized, and an equal amount of protein was subjected to immunoblotting using anti-NGF (1:1000; Alamone Labs, Jerusalem, Israel), anti-pro-NGF antibodies (1:300; Alamone Labs), and other antibodies as described below.

    Techniques: Mouse Assay

    p75NTR stimulation activated SREBP1 and SREBP2 in Huh7 hepatocyte cells. Human Huh7 cells were stimulated with 10 ng/ml pro-NGF or 50 ng/ml NGF for 16 h followed by immunoblotting using antibodies to detect the presence of cleaved/activated SREBP1 and SREBP2. a SREBP1, immunoblots and b quantification. Values are mean ± SD, n = 3. ** P

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: p75NTR stimulation activated SREBP1 and SREBP2 in Huh7 hepatocyte cells. Human Huh7 cells were stimulated with 10 ng/ml pro-NGF or 50 ng/ml NGF for 16 h followed by immunoblotting using antibodies to detect the presence of cleaved/activated SREBP1 and SREBP2. a SREBP1, immunoblots and b quantification. Values are mean ± SD, n = 3. ** P

    Article Snippet: Liver tissue was homogenized, and an equal amount of protein was subjected to immunoblotting using anti-NGF (1:1000; Alamone Labs, Jerusalem, Israel), anti-pro-NGF antibodies (1:300; Alamone Labs), and other antibodies as described below.

    Techniques: Western Blot

    Role of Caspase-2 in p75NTR mediated regulation of SREBP. a Structure of human caspase-2 (CASP2) showing the CARD domain and the 18 and 13 kDa caspase subunits. p38 MAPK phosphorylation site at threonine (Thr)180 in CASP2 is conserved among species. The amino acid numbering underlying functional domains in CASP2 is shown. Boxes represent sequence homology among mammalian species. b Phosphoprotein retardation was performed as described in Materials and methods. A specific phospho-CASP2 antibody against Thr180 was used in conjunction with an antibody against CASP2, recognizing non-phosphorylated form of the enzyme. Phosphorylated CASP2 migrated slower in the Phos-Tag gel (right) as compared with the protein run on denaturating SDS-PAGE (left). c , d Huh7 hepatocyte cells were stimulated with 50 ng NGF ( c ) or 10 ng/ml pro-NGF ( d ) for different times followed by immunoblotting using phospho-CASP2 and anti-CASP2 antibodies. β-Actin was used as a control. e , f Cells were treated with pro-NGF for 6 h in the absence or presence 1 μM of the p38 MAPK inhibitor, SB203580 (SB). e Immunoblot and f quantification of p-CASP2 levels. SB reduced the increase in p-CASP2 by pro-NGF. Values are means ± SD, n = 4. * p

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: Role of Caspase-2 in p75NTR mediated regulation of SREBP. a Structure of human caspase-2 (CASP2) showing the CARD domain and the 18 and 13 kDa caspase subunits. p38 MAPK phosphorylation site at threonine (Thr)180 in CASP2 is conserved among species. The amino acid numbering underlying functional domains in CASP2 is shown. Boxes represent sequence homology among mammalian species. b Phosphoprotein retardation was performed as described in Materials and methods. A specific phospho-CASP2 antibody against Thr180 was used in conjunction with an antibody against CASP2, recognizing non-phosphorylated form of the enzyme. Phosphorylated CASP2 migrated slower in the Phos-Tag gel (right) as compared with the protein run on denaturating SDS-PAGE (left). c , d Huh7 hepatocyte cells were stimulated with 50 ng NGF ( c ) or 10 ng/ml pro-NGF ( d ) for different times followed by immunoblotting using phospho-CASP2 and anti-CASP2 antibodies. β-Actin was used as a control. e , f Cells were treated with pro-NGF for 6 h in the absence or presence 1 μM of the p38 MAPK inhibitor, SB203580 (SB). e Immunoblot and f quantification of p-CASP2 levels. SB reduced the increase in p-CASP2 by pro-NGF. Values are means ± SD, n = 4. * p

    Article Snippet: Liver tissue was homogenized, and an equal amount of protein was subjected to immunoblotting using anti-NGF (1:1000; Alamone Labs, Jerusalem, Israel), anti-pro-NGF antibodies (1:300; Alamone Labs), and other antibodies as described below.

    Techniques: Functional Assay, Sequencing, SDS Page

    Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml NGF or 20 ng/ml pro-NGF for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: Effect of p75NTR stimulation on lipid-associated genes in Huh7 cells. Huh7 cells were stimulated with 100 ng/ml NGF or 20 ng/ml pro-NGF for 48 h, and the expression of lipid-associated genes was analyzed by qPCR. Primers are shown in Table 2 . Results were normalized to GAPDH and controls set to 1. Values are mean ± SD, n = 3-4. *** p

    Article Snippet: Cells were stimulated with different concentrations of NGF or pro-NGF (cleavage-resistant, mutant protein) (Alamone Labs) for various periods of times.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    Schematic view of the role of caspase-2 in p75NTR signaling and lipid metabolism. We propose the following scheme for the action of p75NTR and of caspase-2 in SREBP2 and associated gene regulation. Stimulation of p75NTR by NGF or pro-NGF activates the signaling protein p38 MAPK that can phosphorylate caspase-2 (CASP2) leading to the release of caspase-3 (CASP3) from its complex. CASP3, in turn, can cleave SREBP molecules to yield an active transcription factor. SREBP responsive genes include LDLR and other lipogenic genes but also CASP2 itself. Normally SREBP is processed by the enzymes S1P and S2P via a feedback inhibition determined by the cell cholesterol level. We hypothesize that the steroid-mediated and neurotrophin/p75NTR-induced SREBP pathways are distinct but functionally linked

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: Schematic view of the role of caspase-2 in p75NTR signaling and lipid metabolism. We propose the following scheme for the action of p75NTR and of caspase-2 in SREBP2 and associated gene regulation. Stimulation of p75NTR by NGF or pro-NGF activates the signaling protein p38 MAPK that can phosphorylate caspase-2 (CASP2) leading to the release of caspase-3 (CASP3) from its complex. CASP3, in turn, can cleave SREBP molecules to yield an active transcription factor. SREBP responsive genes include LDLR and other lipogenic genes but also CASP2 itself. Normally SREBP is processed by the enzymes S1P and S2P via a feedback inhibition determined by the cell cholesterol level. We hypothesize that the steroid-mediated and neurotrophin/p75NTR-induced SREBP pathways are distinct but functionally linked

    Article Snippet: Cells were stimulated with different concentrations of NGF or pro-NGF (cleavage-resistant, mutant protein) (Alamone Labs) for various periods of times.

    Techniques: Inhibition

    NGF is expressed in fatty liver of obese mice together with p75NTR. a NGF has increased in leptin-deficient ob/ob mouse livers compared with control, wild-type (wt) mice. b p75NTR was expressed in liver with no significant change between ob/ob and control mice. c , d The level of NGF has increased in leptin-receptor-deficient db/db mouse liver in comparison to controls, c immunoblot analysis and d quantification. ** p

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: NGF is expressed in fatty liver of obese mice together with p75NTR. a NGF has increased in leptin-deficient ob/ob mouse livers compared with control, wild-type (wt) mice. b p75NTR was expressed in liver with no significant change between ob/ob and control mice. c , d The level of NGF has increased in leptin-receptor-deficient db/db mouse liver in comparison to controls, c immunoblot analysis and d quantification. ** p

    Article Snippet: Cells were stimulated with different concentrations of NGF or pro-NGF (cleavage-resistant, mutant protein) (Alamone Labs) for various periods of times.

    Techniques: Mouse Assay

    p75NTR stimulation activated SREBP1 and SREBP2 in Huh7 hepatocyte cells. Human Huh7 cells were stimulated with 10 ng/ml pro-NGF or 50 ng/ml NGF for 16 h followed by immunoblotting using antibodies to detect the presence of cleaved/activated SREBP1 and SREBP2. a SREBP1, immunoblots and b quantification. Values are mean ± SD, n = 3. ** P

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: p75NTR stimulation activated SREBP1 and SREBP2 in Huh7 hepatocyte cells. Human Huh7 cells were stimulated with 10 ng/ml pro-NGF or 50 ng/ml NGF for 16 h followed by immunoblotting using antibodies to detect the presence of cleaved/activated SREBP1 and SREBP2. a SREBP1, immunoblots and b quantification. Values are mean ± SD, n = 3. ** P

    Article Snippet: Cells were stimulated with different concentrations of NGF or pro-NGF (cleavage-resistant, mutant protein) (Alamone Labs) for various periods of times.

    Techniques: Western Blot

    Role of Caspase-2 in p75NTR mediated regulation of SREBP. a Structure of human caspase-2 (CASP2) showing the CARD domain and the 18 and 13 kDa caspase subunits. p38 MAPK phosphorylation site at threonine (Thr)180 in CASP2 is conserved among species. The amino acid numbering underlying functional domains in CASP2 is shown. Boxes represent sequence homology among mammalian species. b Phosphoprotein retardation was performed as described in Materials and methods. A specific phospho-CASP2 antibody against Thr180 was used in conjunction with an antibody against CASP2, recognizing non-phosphorylated form of the enzyme. Phosphorylated CASP2 migrated slower in the Phos-Tag gel (right) as compared with the protein run on denaturating SDS-PAGE (left). c , d Huh7 hepatocyte cells were stimulated with 50 ng NGF ( c ) or 10 ng/ml pro-NGF ( d ) for different times followed by immunoblotting using phospho-CASP2 and anti-CASP2 antibodies. β-Actin was used as a control. e , f Cells were treated with pro-NGF for 6 h in the absence or presence 1 μM of the p38 MAPK inhibitor, SB203580 (SB). e Immunoblot and f quantification of p-CASP2 levels. SB reduced the increase in p-CASP2 by pro-NGF. Values are means ± SD, n = 4. * p

    Journal: Cell Death & Disease

    Article Title: Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells

    doi: 10.1038/s41419-019-1758-z

    Figure Lengend Snippet: Role of Caspase-2 in p75NTR mediated regulation of SREBP. a Structure of human caspase-2 (CASP2) showing the CARD domain and the 18 and 13 kDa caspase subunits. p38 MAPK phosphorylation site at threonine (Thr)180 in CASP2 is conserved among species. The amino acid numbering underlying functional domains in CASP2 is shown. Boxes represent sequence homology among mammalian species. b Phosphoprotein retardation was performed as described in Materials and methods. A specific phospho-CASP2 antibody against Thr180 was used in conjunction with an antibody against CASP2, recognizing non-phosphorylated form of the enzyme. Phosphorylated CASP2 migrated slower in the Phos-Tag gel (right) as compared with the protein run on denaturating SDS-PAGE (left). c , d Huh7 hepatocyte cells were stimulated with 50 ng NGF ( c ) or 10 ng/ml pro-NGF ( d ) for different times followed by immunoblotting using phospho-CASP2 and anti-CASP2 antibodies. β-Actin was used as a control. e , f Cells were treated with pro-NGF for 6 h in the absence or presence 1 μM of the p38 MAPK inhibitor, SB203580 (SB). e Immunoblot and f quantification of p-CASP2 levels. SB reduced the increase in p-CASP2 by pro-NGF. Values are means ± SD, n = 4. * p

    Article Snippet: Cells were stimulated with different concentrations of NGF or pro-NGF (cleavage-resistant, mutant protein) (Alamone Labs) for various periods of times.

    Techniques: Functional Assay, Sequencing, SDS Page