ngf  (Alomone Labs)


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    Structured Review

    Alomone Labs ngf
    PI3K activity regulates the constitutive levels of ApoER2 CTF but is not involved in ApoER2 shedding induced by <t>NGF.</t> (A) PC12-ApoER2 cells were serum-starved and pre-treated with 10 μM DAPT and 50 μM LY294002 or 5 μM <t>ZSTK474</t> for 1 h. Then, the cells were incubated with 100 ng/mL NGF for 2 h. ApoER2 and p75 NTR were recognized using antibodies directed against their intracellular regions. The activation of PI3K, induced by NGF, was determined by detection of phospho-AKT. α-tubulin is shown as a loading control. The blot levels of ApoER2 CTF (B and C) and of p75 NTR CTF (D and E) were normalized to the loading control α-tubulin and plotted as the average ± SD of three independent experiments. One way ANOVA, Holm-Sidak post-hoc test, * P
    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
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    Average 93 stars, based on 1 article reviews
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    Images

    1) Product Images from "Neurotrophins regulate ApoER2 proteolysis through activation of the Trk signaling pathway"

    Article Title: Neurotrophins regulate ApoER2 proteolysis through activation of the Trk signaling pathway

    Journal: BMC Neuroscience

    doi: 10.1186/1471-2202-15-108

    PI3K activity regulates the constitutive levels of ApoER2 CTF but is not involved in ApoER2 shedding induced by NGF. (A) PC12-ApoER2 cells were serum-starved and pre-treated with 10 μM DAPT and 50 μM LY294002 or 5 μM ZSTK474 for 1 h. Then, the cells were incubated with 100 ng/mL NGF for 2 h. ApoER2 and p75 NTR were recognized using antibodies directed against their intracellular regions. The activation of PI3K, induced by NGF, was determined by detection of phospho-AKT. α-tubulin is shown as a loading control. The blot levels of ApoER2 CTF (B and C) and of p75 NTR CTF (D and E) were normalized to the loading control α-tubulin and plotted as the average ± SD of three independent experiments. One way ANOVA, Holm-Sidak post-hoc test, * P
    Figure Legend Snippet: PI3K activity regulates the constitutive levels of ApoER2 CTF but is not involved in ApoER2 shedding induced by NGF. (A) PC12-ApoER2 cells were serum-starved and pre-treated with 10 μM DAPT and 50 μM LY294002 or 5 μM ZSTK474 for 1 h. Then, the cells were incubated with 100 ng/mL NGF for 2 h. ApoER2 and p75 NTR were recognized using antibodies directed against their intracellular regions. The activation of PI3K, induced by NGF, was determined by detection of phospho-AKT. α-tubulin is shown as a loading control. The blot levels of ApoER2 CTF (B and C) and of p75 NTR CTF (D and E) were normalized to the loading control α-tubulin and plotted as the average ± SD of three independent experiments. One way ANOVA, Holm-Sidak post-hoc test, * P

    Techniques Used: Activity Assay, Incubation, Activation Assay

    2) Product Images from "Regulation of BDNF Release by ARMS/Kidins220 through Modulation of Synaptotagmin-IV Levels"

    Article Title: Regulation of BDNF Release by ARMS/Kidins220 through Modulation of Synaptotagmin-IV Levels

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1653-17.2018

    ARMS regulates BDNF release in DRG and cortical neurons. A , ARMS depletion in cultured DRG neurons. Cultured DRG neurons were infected at DIV 4 with control (shControl), ARMS shRNA-1 (shARMS-1), or ARMS shRNA-2 (shARMS-2) lentiviruses and lysates were obtained at DIV 11. Western blot analyses were performed. A representative blot is shown ( n = 4). B , BDNF secretion in response to NGF is enhanced in ARMS-depleted DRG neurons. BDNF ELISA was performed using the supernatant of DRG neurons from A that were nonstimulated (basal) and then stimulated with NGF for 30 min at DIV 11. Cell lysates were collected to assess BDNF levels ( n = 4). Paired Student's t test, mean ± SEM. shControl versus shARMS-1, t = 3.745, df = 3; shControl versus shARMS-2, t = 3.638, df = 3. C , ARMS knockdown in cultured cortical neurons. Cultured cortical neurons were infected with shControl, shARMS-1, or shARMS-2 lentiviruses at DIV 2 and with lentiviruses expressing BDNF at DIV 7. Cell lysates were obtained at DIV 10. Western blot analyses were performed. A representative blot is shown ( n = 4). D , ARMS knockdown potentiates BDNF release in response to different stimuli in cortical neurons. BDNF ELISA was performed using the supernatant of cortical neurons from C that were nonstimulated (basal) and then stimulated with KCl, NT-3, or NT-4 for 30 min at DIV 10 ( n = 9, n = 5, and n = 4 for shControl, shARMS-1, and shARMS-2, respectively). Unpaired Student's t test, mean ± SEM. K + Depol: shControl versus shARMS-1, t = 2.846, df = 12; shControl versus shARMS-2, t = 5.923, df = 11; NT-3: shControl versus shARMS-1, t = 3.917, df = 12; shControl versus shARMS-2, t = 10.03, df = 11; NT-4: shControl versus shARMS-1, t = 3.742, df = 12; shControl versus shARMS-2, t .
    Figure Legend Snippet: ARMS regulates BDNF release in DRG and cortical neurons. A , ARMS depletion in cultured DRG neurons. Cultured DRG neurons were infected at DIV 4 with control (shControl), ARMS shRNA-1 (shARMS-1), or ARMS shRNA-2 (shARMS-2) lentiviruses and lysates were obtained at DIV 11. Western blot analyses were performed. A representative blot is shown ( n = 4). B , BDNF secretion in response to NGF is enhanced in ARMS-depleted DRG neurons. BDNF ELISA was performed using the supernatant of DRG neurons from A that were nonstimulated (basal) and then stimulated with NGF for 30 min at DIV 11. Cell lysates were collected to assess BDNF levels ( n = 4). Paired Student's t test, mean ± SEM. shControl versus shARMS-1, t = 3.745, df = 3; shControl versus shARMS-2, t = 3.638, df = 3. C , ARMS knockdown in cultured cortical neurons. Cultured cortical neurons were infected with shControl, shARMS-1, or shARMS-2 lentiviruses at DIV 2 and with lentiviruses expressing BDNF at DIV 7. Cell lysates were obtained at DIV 10. Western blot analyses were performed. A representative blot is shown ( n = 4). D , ARMS knockdown potentiates BDNF release in response to different stimuli in cortical neurons. BDNF ELISA was performed using the supernatant of cortical neurons from C that were nonstimulated (basal) and then stimulated with KCl, NT-3, or NT-4 for 30 min at DIV 10 ( n = 9, n = 5, and n = 4 for shControl, shARMS-1, and shARMS-2, respectively). Unpaired Student's t test, mean ± SEM. K + Depol: shControl versus shARMS-1, t = 2.846, df = 12; shControl versus shARMS-2, t = 5.923, df = 11; NT-3: shControl versus shARMS-1, t = 3.917, df = 12; shControl versus shARMS-2, t = 10.03, df = 11; NT-4: shControl versus shARMS-1, t = 3.742, df = 12; shControl versus shARMS-2, t .

    Techniques Used: Cell Culture, Infection, shRNA, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing

    3) Product Images from "TrkA In Vivo Function Is Negatively Regulated by Ubiquitination"

    Article Title: TrkA In Vivo Function Is Negatively Regulated by Ubiquitination

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4294-13.2014

    NGF leads to increased TrkA activation and higher AKT and MEK phosphorylation in TrkAΔKFG mutant neurons. A , DRG neurons were isolated from E13.5 WT (+/+), heterozygous (+/−), or TrkAΔKFG mutant (−/−) embryos (6–8
    Figure Legend Snippet: NGF leads to increased TrkA activation and higher AKT and MEK phosphorylation in TrkAΔKFG mutant neurons. A , DRG neurons were isolated from E13.5 WT (+/+), heterozygous (+/−), or TrkAΔKFG mutant (−/−) embryos (6–8

    Techniques Used: Activation Assay, Mutagenesis, Isolation

    Lys 450 in the KFG motif is important for the ubiquitination of TrkA receptors in response to NGF. A–C , HEK293T cell lines stably expressing a single copy of WT, KFG deleted (ΔKFG), AFG (single lysine to alanine mutation), or KAA (phenylalanine
    Figure Legend Snippet: Lys 450 in the KFG motif is important for the ubiquitination of TrkA receptors in response to NGF. A–C , HEK293T cell lines stably expressing a single copy of WT, KFG deleted (ΔKFG), AFG (single lysine to alanine mutation), or KAA (phenylalanine

    Techniques Used: Stable Transfection, Expressing, Mutagenesis

    Deletion of the KFG domain from TrkA alters NGF-induced trafficking of TrkA. A , HEK293T cells stably expressing WT or KFG deleted TrkA as in were treated with 100 ng/ml NGF for the indicated time (1–6 h) followed by biotinylation. Cell
    Figure Legend Snippet: Deletion of the KFG domain from TrkA alters NGF-induced trafficking of TrkA. A , HEK293T cells stably expressing WT or KFG deleted TrkA as in were treated with 100 ng/ml NGF for the indicated time (1–6 h) followed by biotinylation. Cell

    Techniques Used: Stable Transfection, Expressing

    4) Product Images from "B-RAF kinase drives developmental axon growth and promotes axon regeneration in the injured mature CNS"

    Article Title: B-RAF kinase drives developmental axon growth and promotes axon regeneration in the injured mature CNS

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20131780

    Expression of kaB-RAF substantially rescues sensory afferent growth in the absence of TrkA/NGF signaling. (A, left) Normal sensory cutaneous innervation at E16.5. (middle) Sensory cutaneous innervation is lost in embryos lacking the NGF receptor TrkA. (right) Expression of kaB-RAF restores cutaneous innervation. Arrowheads label the blue β-gal–positive (presumptive TrkA + ) sensory trajectories. (B) Visualization of axon growth patterns after tissue clearing. The thoracic somatosensory innervation driven by kaB-RAF in a TrkA −/− embryo (bottom; compare with middle for TrkA −/− alone) is similar to that seen in a control TrkA WT/− littermate (top). White arrowheads indicate the normal pathways of peripheral axons extending from thoracic DRGs. Red arrowheads indicate sensory projections rescued by kaB-RAF in the TrkA −/− background. (C) Expression of kaB-RAF substantially rescues trigeminal TrkA + afferent growth in the absence of TrkA/NGF signaling. Presumptive TrkA + trigeminal axon projections (top) are lost in TrkA-deficient mice (middle) and are rescued by kaB-RAF (bottom). Ga, great auricular nerve; Go, greater occipital nerve; Mn, mandibular branch; Mx, maxillary branch; Op, ophthalmical branch. Images show littermates and are representative of three embryos per genotype. Bars: (A) 2 mm; (B and C) 1 mm.
    Figure Legend Snippet: Expression of kaB-RAF substantially rescues sensory afferent growth in the absence of TrkA/NGF signaling. (A, left) Normal sensory cutaneous innervation at E16.5. (middle) Sensory cutaneous innervation is lost in embryos lacking the NGF receptor TrkA. (right) Expression of kaB-RAF restores cutaneous innervation. Arrowheads label the blue β-gal–positive (presumptive TrkA + ) sensory trajectories. (B) Visualization of axon growth patterns after tissue clearing. The thoracic somatosensory innervation driven by kaB-RAF in a TrkA −/− embryo (bottom; compare with middle for TrkA −/− alone) is similar to that seen in a control TrkA WT/− littermate (top). White arrowheads indicate the normal pathways of peripheral axons extending from thoracic DRGs. Red arrowheads indicate sensory projections rescued by kaB-RAF in the TrkA −/− background. (C) Expression of kaB-RAF substantially rescues trigeminal TrkA + afferent growth in the absence of TrkA/NGF signaling. Presumptive TrkA + trigeminal axon projections (top) are lost in TrkA-deficient mice (middle) and are rescued by kaB-RAF (bottom). Ga, great auricular nerve; Go, greater occipital nerve; Mn, mandibular branch; Mx, maxillary branch; Op, ophthalmical branch. Images show littermates and are representative of three embryos per genotype. Bars: (A) 2 mm; (B and C) 1 mm.

    Techniques Used: Expressing, Mouse Assay

    Activation of B-RAF indirectly rescues CGRP expression in TrkA −/− nociceptive neurons. (A, left) Normal CGRP staining in the DRG and superficial dorsal horn. Arrowhead indicates CGRP-expressing spinal motoneurons. (middle) CGRP expression is completely abolished in the DRG and its projections in TrkA/Bax double-null mice. CGRP staining in spinal motoneurons is not affected by loss of TrkA signaling (arrowhead). (right) CGRP expression in DRG is rescued by expression of kaB-RAF, in the absence of TrkA signaling ( LSL-kaBraf:nes-Cre:TrkA −/− :Bax −/− ). Arrowhead indicates the CGRP + motor neurons. Dashed white lines outline the spinal cord and DRG. (B) The nociceptive projection into the dorsal horn (left) does not depend on TrkA (middle). Expression of kaB-RAF causes overgrowth and ectopic targeting of these fibers (right). (A and B) Images are representative of three embryos each. (C) Activation of B-RAF does not directly induce CGRP expression in cultured DRG neurons. (top) No CGRP is expressed in 7-d in vitro cultures of dissociated E12.5 LSL-kaBraf:Bax −/− :nes-Cre DRG neurons. (bottom) NGF and conditioned medium from skin cultures are necessary to induce CGRP expression in E12.5 LSL-kaBraf:Bax −/− :nes-Cre DRG neurons. Images are representative of three independent experiments. This experiment has been repeated three times. Each experiment used two embryos per genotype. Bars: (A and B) 100 µm; (C) 20 µm.
    Figure Legend Snippet: Activation of B-RAF indirectly rescues CGRP expression in TrkA −/− nociceptive neurons. (A, left) Normal CGRP staining in the DRG and superficial dorsal horn. Arrowhead indicates CGRP-expressing spinal motoneurons. (middle) CGRP expression is completely abolished in the DRG and its projections in TrkA/Bax double-null mice. CGRP staining in spinal motoneurons is not affected by loss of TrkA signaling (arrowhead). (right) CGRP expression in DRG is rescued by expression of kaB-RAF, in the absence of TrkA signaling ( LSL-kaBraf:nes-Cre:TrkA −/− :Bax −/− ). Arrowhead indicates the CGRP + motor neurons. Dashed white lines outline the spinal cord and DRG. (B) The nociceptive projection into the dorsal horn (left) does not depend on TrkA (middle). Expression of kaB-RAF causes overgrowth and ectopic targeting of these fibers (right). (A and B) Images are representative of three embryos each. (C) Activation of B-RAF does not directly induce CGRP expression in cultured DRG neurons. (top) No CGRP is expressed in 7-d in vitro cultures of dissociated E12.5 LSL-kaBraf:Bax −/− :nes-Cre DRG neurons. (bottom) NGF and conditioned medium from skin cultures are necessary to induce CGRP expression in E12.5 LSL-kaBraf:Bax −/− :nes-Cre DRG neurons. Images are representative of three independent experiments. This experiment has been repeated three times. Each experiment used two embryos per genotype. Bars: (A and B) 100 µm; (C) 20 µm.

    Techniques Used: Activation Assay, Expressing, Staining, Mouse Assay, Cell Culture, In Vitro

    5) Product Images from "Potentiation of Nerve Growth Factor-Induced Neurite Outgrowth in PC12 Cells by Ifenprodil: The Role of Sigma-1 and IP3 Receptors"

    Article Title: Potentiation of Nerve Growth Factor-Induced Neurite Outgrowth in PC12 Cells by Ifenprodil: The Role of Sigma-1 and IP3 Receptors

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0037989

    Effects of IP 3 receptor antagonists on NGF-induced neurite outgrowth in PC12 cells. (A): In the presence of NGF (2.5 ng/ml), vehicle, ifenprodil (10 µM), ifenprodil (10 µM)+xestospongin C (1.0 µM), xestospongin C (1.0 µM) were incubated with PC12 cells. (B): In the presence of NGF (2.5 ng/ml), vehicle, ifenprodil (10 µM), ifenprodil (10 µM)+2-APB (100 µM), or 2-APB (100 µM) were incubated in PC12 cells. Four days after incubation with test drugs, morphometric analysis was performed. The data show the mean ± SEM (n = 6). ***p
    Figure Legend Snippet: Effects of IP 3 receptor antagonists on NGF-induced neurite outgrowth in PC12 cells. (A): In the presence of NGF (2.5 ng/ml), vehicle, ifenprodil (10 µM), ifenprodil (10 µM)+xestospongin C (1.0 µM), xestospongin C (1.0 µM) were incubated with PC12 cells. (B): In the presence of NGF (2.5 ng/ml), vehicle, ifenprodil (10 µM), ifenprodil (10 µM)+2-APB (100 µM), or 2-APB (100 µM) were incubated in PC12 cells. Four days after incubation with test drugs, morphometric analysis was performed. The data show the mean ± SEM (n = 6). ***p

    Techniques Used: Incubation

    6) Product Images from "Phosphorylation of Serine 779 in Fibroblast Growth Factor Receptor 1 and 2 by Protein Kinase C? Regulates Ras/Mitogen-activated Protein Kinase Signaling and Neuronal Differentiation *"

    Article Title: Phosphorylation of Serine 779 in Fibroblast Growth Factor Receptor 1 and 2 by Protein Kinase C? Regulates Ras/Mitogen-activated Protein Kinase Signaling and Neuronal Differentiation *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M112.421669

    Ser 779 in the cytoplasmic tail of FGFR1 and FGFR2 is required for maximal ERK activation. A–D , PC12 cells expressing PFR1 or PFR1-S779G ( A ) or wt-FGFR2 or FGFR2-S779G ( B–D ) were stimulated with PDGF-BB ( A ), FGF9 ( B ), EGF ( C ), or NGF (
    Figure Legend Snippet: Ser 779 in the cytoplasmic tail of FGFR1 and FGFR2 is required for maximal ERK activation. A–D , PC12 cells expressing PFR1 or PFR1-S779G ( A ) or wt-FGFR2 or FGFR2-S779G ( B–D ) were stimulated with PDGF-BB ( A ), FGF9 ( B ), EGF ( C ), or NGF (

    Techniques Used: Activation Assay, Expressing

    7) Product Images from "Analysis of Ret knockin mice reveals a critical role for IKKs, but not PI 3-K, in neurotrophic factor-induced survival of sympathetic neurons"

    Article Title: Analysis of Ret knockin mice reveals a critical role for IKKs, but not PI 3-K, in neurotrophic factor-induced survival of sympathetic neurons

    Journal: Cell death and differentiation

    doi: 10.1038/cdd.2008.76

    IKKs are necessary for NGF- and GDNF-mediated survival of sympathetic neurons. (A and B) Neurons were infected with shRNAs to IKKs in combination (“α+ β”) or alone (“α” or “β”)
    Figure Legend Snippet: IKKs are necessary for NGF- and GDNF-mediated survival of sympathetic neurons. (A and B) Neurons were infected with shRNAs to IKKs in combination (“α+ β”) or alone (“α” or “β”)

    Techniques Used: Infection

    Neither PI 3-K/Akt nor ERK1/2 are necessary for GDNF-mediated survival. (A) Sympathetic neurons from wild type mice were cultured for five days in NGF and then switched to GDNF with or without the indicated doses of the PI 3-K inhibitor LY294002. Neuronal
    Figure Legend Snippet: Neither PI 3-K/Akt nor ERK1/2 are necessary for GDNF-mediated survival. (A) Sympathetic neurons from wild type mice were cultured for five days in NGF and then switched to GDNF with or without the indicated doses of the PI 3-K inhibitor LY294002. Neuronal

    Techniques Used: Mouse Assay, Cell Culture

    Knockdown of B-Raf, but not A-Raf or C-Raf, prevents GDNF-and NGF-mediated survival of wild type mouse sympathetic neurons. (A,B,C) Left panels, neurons were infected with lentiviruses expressing shRNAs to A-Raf (A1 and A2), B-Raf (B1 and B2) and C-Raf
    Figure Legend Snippet: Knockdown of B-Raf, but not A-Raf or C-Raf, prevents GDNF-and NGF-mediated survival of wild type mouse sympathetic neurons. (A,B,C) Left panels, neurons were infected with lentiviruses expressing shRNAs to A-Raf (A1 and A2), B-Raf (B1 and B2) and C-Raf

    Techniques Used: Infection, Expressing

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    Alomone Labs anti p75ntr
    Suggested model. In order to arrive at the cell body and subsequently the CNS, rabies virus hijacks a fast route using the <t>p75NTR</t> endosomal pathway. In a p75NTR dependent path, RABV manipulates the axonal transport machinery to migrate faster to the cell body. An alternative, slower path, may involve alternative RABV receptors.
    Anti P75ntr, 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/anti p75ntr/product/Alomone Labs
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    Alomone Labs anti p75ntr polyclonal antibody
    Process of differentiation of H-iris iPS cells to nervous system cells. Cells were pre-differentiated from ( a ) H-iris iPS cells to ( b ) neural stem/progenitor cells by adhesive culture. ( c ) Cells sorted with <t>p75NTR</t> were differentiated into neurons. By changing the medium condition, the nerve cells were differentiated into Recoverin-positive cells. ( d ) In contrast, after suspension culture, neurites were elongated by adhesive culture and differentiated into retinal ganglion cells. Bars: 100 μm.
    Anti P75ntr Polyclonal Antibody, 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
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    91
    Alomone Labs recombinant rat ngf
    <t>TGF-β1</t> promoted the mRNA expression of <t>NGF</t> in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Recombinant Rat Ngf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs pc12 cells
    Irradiation with 137 Cs γ-rays depresses NGF-induced neurite extension in <t>PC12</t> cells. (a) Phase-contrast micrographs, (b) lengths of neurites and (c) numbers of neurites in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation. Lengths or numbers of neurites are expressed as the relative ratio to the non-irradiated group. Data are presented as the mean ± standard error of triplicate samples. * P
    Pc12 Cells, 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
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    Suggested model. In order to arrive at the cell body and subsequently the CNS, rabies virus hijacks a fast route using the p75NTR endosomal pathway. In a p75NTR dependent path, RABV manipulates the axonal transport machinery to migrate faster to the cell body. An alternative, slower path, may involve alternative RABV receptors.

    Journal: PLoS Pathogens

    Article Title: Rabies Virus Hijacks and Accelerates the p75NTR Retrograde Axonal Transport Machinery

    doi: 10.1371/journal.ppat.1004348

    Figure Lengend Snippet: Suggested model. In order to arrive at the cell body and subsequently the CNS, rabies virus hijacks a fast route using the p75NTR endosomal pathway. In a p75NTR dependent path, RABV manipulates the axonal transport machinery to migrate faster to the cell body. An alternative, slower path, may involve alternative RABV receptors.

    Article Snippet: For RABV-p75 imaging, explant cultures were incubated with fluorescent anti-p75NTR (ANT-007-AO, Alomone Labs) for 10 minutes and washed 3 times in poor neurobasal medium prior to imaging.

    Techniques:

    RABV is retrogradely transported with neurotrophin receptors. ( A–D ), Retrograde transport of EGFP-RABV, added to the distal axon compartment of DRG explant previously treated with fluorescent antibodies against p75NTR and TrkA. Arrowheads: RABV puncta positive for p75NTR, arrows: RABV puncta positive for p75NTR and TrkA. Scale bar = 10 µm. ( E,F ) Co-localisation of RABV with p75NTR and TrkA calculated from two and one experiments, respectively. ( G ) Trajectories of RABV trafficked with neurotrophin receptors (NTFR, Blue) or without (Red), illustrating a more processive displacement over time of RABV with NTFR. ( H ) Merged kymographs of RABV (green) p75NTR (red) and TrkA (cyan), drawn for multi-channel time lapse. Vertical scale bar = 5 µm, horizontal scale bar = 40 seconds.

    Journal: PLoS Pathogens

    Article Title: Rabies Virus Hijacks and Accelerates the p75NTR Retrograde Axonal Transport Machinery

    doi: 10.1371/journal.ppat.1004348

    Figure Lengend Snippet: RABV is retrogradely transported with neurotrophin receptors. ( A–D ), Retrograde transport of EGFP-RABV, added to the distal axon compartment of DRG explant previously treated with fluorescent antibodies against p75NTR and TrkA. Arrowheads: RABV puncta positive for p75NTR, arrows: RABV puncta positive for p75NTR and TrkA. Scale bar = 10 µm. ( E,F ) Co-localisation of RABV with p75NTR and TrkA calculated from two and one experiments, respectively. ( G ) Trajectories of RABV trafficked with neurotrophin receptors (NTFR, Blue) or without (Red), illustrating a more processive displacement over time of RABV with NTFR. ( H ) Merged kymographs of RABV (green) p75NTR (red) and TrkA (cyan), drawn for multi-channel time lapse. Vertical scale bar = 5 µm, horizontal scale bar = 40 seconds.

    Article Snippet: For RABV-p75 imaging, explant cultures were incubated with fluorescent anti-p75NTR (ANT-007-AO, Alomone Labs) for 10 minutes and washed 3 times in poor neurobasal medium prior to imaging.

    Techniques:

    RABV binds and internalizes with p75NTR in DRG neuron tips. Co-localization of EGFP-RABV with p75NTR is shown by live TIRF imaging and sub-pixel localization algorithms. ( A ) RABV-p75 particles shift from the periphery to the center of the growth cone, where they are internalized into the cell. Lower panels zoom in on dashed square, showing co-localized puncta (left) shifting towards the center of the growth cone (middle) until finally internalized (right). ( B ) Presentation of six separate events of RABV and p75NTR binding and internalization on the surface of the growth cone shown in (A). Colored trajectories denote displacement from point of detection to point of disappearance. ( C ) RABV and p75NTR are internalized together, illustrated by corresponding plots of puncta intensity over time (normalized to background), calculated for co-localized particles shown in lower panels of (A). Scale bars = 5 µm. ( D ) Zoom-in on colocalized RABV and p75 spot, taken from panel (A), scale bar = 1 µm. ( E ) Overlay of 1D-Gaussian fits of p75 and RABV intensity profiles at the x-axis of the image in panel (D). ( F ) Representative overlay of radial symmetry fits of the x-y intensity profiles of p75 and RABV spots. σ is the standard deviation of each fitting function; distance between the two spot centers is 51.3 nm. ( G ) Knockdown of p75NTR decreases rabies virus infection for shorts time incubation. DRGs embryonic cells infected with lentiviral vectors (LV) containing 4 different EGFP-tagged shRNA's against p75NTR or LV-EGFP, were transfected with RABV for 30 or 120 minutes. Low levels of infected neurons were found in shRNA-p75-EGFP cells Average RABV infection rates were normalized to LV-EGFP controls (n = 4 experiments, error bars = SEM, *p

    Journal: PLoS Pathogens

    Article Title: Rabies Virus Hijacks and Accelerates the p75NTR Retrograde Axonal Transport Machinery

    doi: 10.1371/journal.ppat.1004348

    Figure Lengend Snippet: RABV binds and internalizes with p75NTR in DRG neuron tips. Co-localization of EGFP-RABV with p75NTR is shown by live TIRF imaging and sub-pixel localization algorithms. ( A ) RABV-p75 particles shift from the periphery to the center of the growth cone, where they are internalized into the cell. Lower panels zoom in on dashed square, showing co-localized puncta (left) shifting towards the center of the growth cone (middle) until finally internalized (right). ( B ) Presentation of six separate events of RABV and p75NTR binding and internalization on the surface of the growth cone shown in (A). Colored trajectories denote displacement from point of detection to point of disappearance. ( C ) RABV and p75NTR are internalized together, illustrated by corresponding plots of puncta intensity over time (normalized to background), calculated for co-localized particles shown in lower panels of (A). Scale bars = 5 µm. ( D ) Zoom-in on colocalized RABV and p75 spot, taken from panel (A), scale bar = 1 µm. ( E ) Overlay of 1D-Gaussian fits of p75 and RABV intensity profiles at the x-axis of the image in panel (D). ( F ) Representative overlay of radial symmetry fits of the x-y intensity profiles of p75 and RABV spots. σ is the standard deviation of each fitting function; distance between the two spot centers is 51.3 nm. ( G ) Knockdown of p75NTR decreases rabies virus infection for shorts time incubation. DRGs embryonic cells infected with lentiviral vectors (LV) containing 4 different EGFP-tagged shRNA's against p75NTR or LV-EGFP, were transfected with RABV for 30 or 120 minutes. Low levels of infected neurons were found in shRNA-p75-EGFP cells Average RABV infection rates were normalized to LV-EGFP controls (n = 4 experiments, error bars = SEM, *p

    Article Snippet: For RABV-p75 imaging, explant cultures were incubated with fluorescent anti-p75NTR (ANT-007-AO, Alomone Labs) for 10 minutes and washed 3 times in poor neurobasal medium prior to imaging.

    Techniques: Imaging, Binding Assay, Standard Deviation, Infection, Incubation, shRNA, Transfection

    RABV travels faster and is more directed when transported with p75NTR. ( A–C ) Multi-channel live imaging of EGFP-RABV 2 hours after addition to distal axon compartment of DRG explant previously treated with a fluorescent antibody against p75NTR. Arrowheads: p75NTR-positive RABV puncta, scale bar = 10 µm. ( D,E ) Kymographs of and P75NTR extracted from time lapse depicted in (A–C). ( F ) RABV-only tracks (green) are less directed than RABV-p75NTR tracks (yellow), as shown when overlaying corresponding kymographs. Vertical scale bar = 5 µm, horizontal scale bar = 40 seconds. ( G–O ) Characterization of directed RABV puncta, transported with and without p75NTR, n = 184 and n = 122, respectively. (G) RABV presents higher speeds when transported with p75NTR, due to less frequent (H) and shorter pauses (I). Overall RABV-p75NTR spent less time paused on average (J), Diameter and intensity measurements revealed that RABV puncta positive for p75NTR were larger ( K ) and had higher intensity levels ( L ) than p75NTR-negative puncta. ( M–O ) p75NTR positive puncta (blue) are faster, more directed and present higher displacements over time, compared to p75NTR negative puncta (red), illustrated by distribution of instantaneous velocities in (M) (RABV+p75: n = 8051 events; RABV-p75: n = 7423 events) displacement plotted over time (N) and mean square displacement (O). Data is pulled from two separate experiments, error bars represent SEM. *p

    Journal: PLoS Pathogens

    Article Title: Rabies Virus Hijacks and Accelerates the p75NTR Retrograde Axonal Transport Machinery

    doi: 10.1371/journal.ppat.1004348

    Figure Lengend Snippet: RABV travels faster and is more directed when transported with p75NTR. ( A–C ) Multi-channel live imaging of EGFP-RABV 2 hours after addition to distal axon compartment of DRG explant previously treated with a fluorescent antibody against p75NTR. Arrowheads: p75NTR-positive RABV puncta, scale bar = 10 µm. ( D,E ) Kymographs of and P75NTR extracted from time lapse depicted in (A–C). ( F ) RABV-only tracks (green) are less directed than RABV-p75NTR tracks (yellow), as shown when overlaying corresponding kymographs. Vertical scale bar = 5 µm, horizontal scale bar = 40 seconds. ( G–O ) Characterization of directed RABV puncta, transported with and without p75NTR, n = 184 and n = 122, respectively. (G) RABV presents higher speeds when transported with p75NTR, due to less frequent (H) and shorter pauses (I). Overall RABV-p75NTR spent less time paused on average (J), Diameter and intensity measurements revealed that RABV puncta positive for p75NTR were larger ( K ) and had higher intensity levels ( L ) than p75NTR-negative puncta. ( M–O ) p75NTR positive puncta (blue) are faster, more directed and present higher displacements over time, compared to p75NTR negative puncta (red), illustrated by distribution of instantaneous velocities in (M) (RABV+p75: n = 8051 events; RABV-p75: n = 7423 events) displacement plotted over time (N) and mean square displacement (O). Data is pulled from two separate experiments, error bars represent SEM. *p

    Article Snippet: For RABV-p75 imaging, explant cultures were incubated with fluorescent anti-p75NTR (ANT-007-AO, Alomone Labs) for 10 minutes and washed 3 times in poor neurobasal medium prior to imaging.

    Techniques: Imaging

    Process of differentiation of H-iris iPS cells to nervous system cells. Cells were pre-differentiated from ( a ) H-iris iPS cells to ( b ) neural stem/progenitor cells by adhesive culture. ( c ) Cells sorted with p75NTR were differentiated into neurons. By changing the medium condition, the nerve cells were differentiated into Recoverin-positive cells. ( d ) In contrast, after suspension culture, neurites were elongated by adhesive culture and differentiated into retinal ganglion cells. Bars: 100 μm.

    Journal: Cells

    Article Title: Novel Technique for Retinal Nerve Cell Regeneration with Electrophysiological Functions Using Human Iris-Derived iPS Cells

    doi: 10.3390/cells10040743

    Figure Lengend Snippet: Process of differentiation of H-iris iPS cells to nervous system cells. Cells were pre-differentiated from ( a ) H-iris iPS cells to ( b ) neural stem/progenitor cells by adhesive culture. ( c ) Cells sorted with p75NTR were differentiated into neurons. By changing the medium condition, the nerve cells were differentiated into Recoverin-positive cells. ( d ) In contrast, after suspension culture, neurites were elongated by adhesive culture and differentiated into retinal ganglion cells. Bars: 100 μm.

    Article Snippet: Paraffin sections were prepared from the fixed human iris tissue in the usual manner and incubated with anti-p75NTR polyclonal antibody (1:200; Alomone Labs, Jerusalem, Israel) for 1 h at 37 °C.

    Techniques:

    Cells sorted with p75NTR can concentrate Recoverin-positive cells. ( a ) Before p75NTR sorting, cells with large cytoplasms ( arrowheads ) were mixed. ( b ) Fixed cells were analyzed for p75NTR and Nestin by FCM. Most of the cells sorted in the strong positive region of p75NTR were double-positive for ( c ) p75NTR and ( d ) Nestin. ( e , f ) The morphology of cells sorted by their strong positivity for ( e ) p75NTR or ( f ) their weak positivity or negativity for p75NTR. ( g ) Relative semi-quantitative analysis of Recoverin gene expression in cells selected by p75NTR, and pre/post-differentiated cells. ( h ) Fluorescent immunostaining of Recoverin in differentiated cells. Bar in panel ( a ): 50 μm, bars in panels ( c , d ): 20 μm, bars in panels ( e , f , h ): 100 μm.

    Journal: Cells

    Article Title: Novel Technique for Retinal Nerve Cell Regeneration with Electrophysiological Functions Using Human Iris-Derived iPS Cells

    doi: 10.3390/cells10040743

    Figure Lengend Snippet: Cells sorted with p75NTR can concentrate Recoverin-positive cells. ( a ) Before p75NTR sorting, cells with large cytoplasms ( arrowheads ) were mixed. ( b ) Fixed cells were analyzed for p75NTR and Nestin by FCM. Most of the cells sorted in the strong positive region of p75NTR were double-positive for ( c ) p75NTR and ( d ) Nestin. ( e , f ) The morphology of cells sorted by their strong positivity for ( e ) p75NTR or ( f ) their weak positivity or negativity for p75NTR. ( g ) Relative semi-quantitative analysis of Recoverin gene expression in cells selected by p75NTR, and pre/post-differentiated cells. ( h ) Fluorescent immunostaining of Recoverin in differentiated cells. Bar in panel ( a ): 50 μm, bars in panels ( c , d ): 20 μm, bars in panels ( e , f , h ): 100 μm.

    Article Snippet: Paraffin sections were prepared from the fixed human iris tissue in the usual manner and incubated with anti-p75NTR polyclonal antibody (1:200; Alomone Labs, Jerusalem, Israel) for 1 h at 37 °C.

    Techniques: Expressing, Immunostaining

    p75NTR-positive cells observed in human iris tissue and cultured cells: ( a ) HE-stained human iris tissue; * The lens side of the iris. ( b ) Differential interference contrast image of iris tissue. ( c ) Fluorescent immunostaining of p75NTR; arrowheads = p75NTR-positive cells. ( d ) Iris-derived cells were cultured for 10 days; the inset shows cells growing from around the pigmented cells on the third day of culture. ( e ) p75NTR-positive cells (region of Gate 1, G1) were isolated with a cell sorter; the blue line represents the histogram of negative cells. ( f ) Morphology of p75NTR-positive sorted cells. Bars in panels ( a – c ), 50 μm; bars in panel ( d )’s inset and panel ( f ), 100 μm; bar in panel ( d ), 200 μm.

    Journal: Cells

    Article Title: Novel Technique for Retinal Nerve Cell Regeneration with Electrophysiological Functions Using Human Iris-Derived iPS Cells

    doi: 10.3390/cells10040743

    Figure Lengend Snippet: p75NTR-positive cells observed in human iris tissue and cultured cells: ( a ) HE-stained human iris tissue; * The lens side of the iris. ( b ) Differential interference contrast image of iris tissue. ( c ) Fluorescent immunostaining of p75NTR; arrowheads = p75NTR-positive cells. ( d ) Iris-derived cells were cultured for 10 days; the inset shows cells growing from around the pigmented cells on the third day of culture. ( e ) p75NTR-positive cells (region of Gate 1, G1) were isolated with a cell sorter; the blue line represents the histogram of negative cells. ( f ) Morphology of p75NTR-positive sorted cells. Bars in panels ( a – c ), 50 μm; bars in panel ( d )’s inset and panel ( f ), 100 μm; bar in panel ( d ), 200 μm.

    Article Snippet: Paraffin sections were prepared from the fixed human iris tissue in the usual manner and incubated with anti-p75NTR polyclonal antibody (1:200; Alomone Labs, Jerusalem, Israel) for 1 h at 37 °C.

    Techniques: Cell Culture, Staining, Immunostaining, Derivative Assay, Isolation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

    IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Quantitative RT-PCR, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Standard Deviation

    Irradiation with 137 Cs γ-rays depresses NGF-induced neurite extension in PC12 cells. (a) Phase-contrast micrographs, (b) lengths of neurites and (c) numbers of neurites in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation. Lengths or numbers of neurites are expressed as the relative ratio to the non-irradiated group. Data are presented as the mean ± standard error of triplicate samples. * P

    Journal: Journal of Radiation Research

    Article Title: Chronic irradiation with low-dose-rate 137Cs-γ rays inhibits NGF-induced neurite extension of PC12 cells via Ca2+/calmodulin-dependent kinase II activation

    doi: 10.1093/jrr/rrx032

    Figure Lengend Snippet: Irradiation with 137 Cs γ-rays depresses NGF-induced neurite extension in PC12 cells. (a) Phase-contrast micrographs, (b) lengths of neurites and (c) numbers of neurites in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation. Lengths or numbers of neurites are expressed as the relative ratio to the non-irradiated group. Data are presented as the mean ± standard error of triplicate samples. * P

    Article Snippet: Reagents We utilized the following reagents to investigate the effects of chronic, low-dose-rate 137 Cs-γ radiation on NGF-induced neurite extension in PC12 cells: NGF 2.5S (N-100, Alomone Labs, Jerusalem, Israel); anti-ERK1/ERK2 mouse-monoclonal antibody (MAB1576) and anti-phosphorylated ERK1/ERK2 rabbit-polyclonal antibody (MAB1018, both R & D systems, Minneapolis, MN, USA); anti-Trk A rabbit polyclonal antibody (sc-118) and anti-phosphorylated Trk A mouse-monoclonal antibody (sc-8058, both Santa Cruz Biotechnology, Dallas, TX, USA)—Trk A is a high-affinity nerve growth factor receptor; anti-tyrosine hydroxylase rabbit-monoclonal antibody (ab137869); anti-Akt rabbit polyclonal antibody (ab8805) and anti-phosphorylated Akt rabbit monoclonal antibody (ab81283); anti-Ca2+/calmodulin-dependent kinase II (CaMKII) rabbit polyclonal antibody (ab131468) and anti-phosphorylated CaMKII rabbit polyclonal antibody (ab5683, all Abcam plc, Cambridge, UK); KN-62 (I2142, Sigma-Aldrich, St Louis, MO, USA).

    Techniques: Irradiation

    Western blot analysis of NGF stimulation–related proteins in PC12 cells. Immunoblot showing varying levels of (a) phosphorylated NGF receptor (P-NGFR, upper) and NGF receptor (NGFR, lower), (b) phosphorylated ERK (P-ERK, upper) and ERK (lower), (c) tyrosine hydroxylase (TH) observed in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation. Similar results were obtained in three separate experiments. NGF = nerve growth factor, ERK = extracellular signal–regulated kinase.

    Journal: Journal of Radiation Research

    Article Title: Chronic irradiation with low-dose-rate 137Cs-γ rays inhibits NGF-induced neurite extension of PC12 cells via Ca2+/calmodulin-dependent kinase II activation

    doi: 10.1093/jrr/rrx032

    Figure Lengend Snippet: Western blot analysis of NGF stimulation–related proteins in PC12 cells. Immunoblot showing varying levels of (a) phosphorylated NGF receptor (P-NGFR, upper) and NGF receptor (NGFR, lower), (b) phosphorylated ERK (P-ERK, upper) and ERK (lower), (c) tyrosine hydroxylase (TH) observed in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation. Similar results were obtained in three separate experiments. NGF = nerve growth factor, ERK = extracellular signal–regulated kinase.

    Article Snippet: Reagents We utilized the following reagents to investigate the effects of chronic, low-dose-rate 137 Cs-γ radiation on NGF-induced neurite extension in PC12 cells: NGF 2.5S (N-100, Alomone Labs, Jerusalem, Israel); anti-ERK1/ERK2 mouse-monoclonal antibody (MAB1576) and anti-phosphorylated ERK1/ERK2 rabbit-polyclonal antibody (MAB1018, both R & D systems, Minneapolis, MN, USA); anti-Trk A rabbit polyclonal antibody (sc-118) and anti-phosphorylated Trk A mouse-monoclonal antibody (sc-8058, both Santa Cruz Biotechnology, Dallas, TX, USA)—Trk A is a high-affinity nerve growth factor receptor; anti-tyrosine hydroxylase rabbit-monoclonal antibody (ab137869); anti-Akt rabbit polyclonal antibody (ab8805) and anti-phosphorylated Akt rabbit monoclonal antibody (ab81283); anti-Ca2+/calmodulin-dependent kinase II (CaMKII) rabbit polyclonal antibody (ab131468) and anti-phosphorylated CaMKII rabbit polyclonal antibody (ab5683, all Abcam plc, Cambridge, UK); KN-62 (I2142, Sigma-Aldrich, St Louis, MO, USA).

    Techniques: Western Blot, Irradiation

    Inhibition of CaMKII activity results in 137 Csγ-ray irradiation-induced depression of NGF-induced neurite extension in PC12 cells. (a) Immunoblot showing varying levels of phosphorylated CaMKII (P-CaMKII, upper) and CaMKII (lower) observed in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation in the presence or absence of KN-62. Similar results were obtained in three separate experiments. (b) Lengths and (c) numbers of neurites in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation in the presence or absence of KN-62. Lengths or numbers of neurites are expressed as the relative ratio to the non-irradiated group. Data are presented as the mean ± standard error of triplicate samples. * P

    Journal: Journal of Radiation Research

    Article Title: Chronic irradiation with low-dose-rate 137Cs-γ rays inhibits NGF-induced neurite extension of PC12 cells via Ca2+/calmodulin-dependent kinase II activation

    doi: 10.1093/jrr/rrx032

    Figure Lengend Snippet: Inhibition of CaMKII activity results in 137 Csγ-ray irradiation-induced depression of NGF-induced neurite extension in PC12 cells. (a) Immunoblot showing varying levels of phosphorylated CaMKII (P-CaMKII, upper) and CaMKII (lower) observed in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation in the presence or absence of KN-62. Similar results were obtained in three separate experiments. (b) Lengths and (c) numbers of neurites in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation in the presence or absence of KN-62. Lengths or numbers of neurites are expressed as the relative ratio to the non-irradiated group. Data are presented as the mean ± standard error of triplicate samples. * P

    Article Snippet: Reagents We utilized the following reagents to investigate the effects of chronic, low-dose-rate 137 Cs-γ radiation on NGF-induced neurite extension in PC12 cells: NGF 2.5S (N-100, Alomone Labs, Jerusalem, Israel); anti-ERK1/ERK2 mouse-monoclonal antibody (MAB1576) and anti-phosphorylated ERK1/ERK2 rabbit-polyclonal antibody (MAB1018, both R & D systems, Minneapolis, MN, USA); anti-Trk A rabbit polyclonal antibody (sc-118) and anti-phosphorylated Trk A mouse-monoclonal antibody (sc-8058, both Santa Cruz Biotechnology, Dallas, TX, USA)—Trk A is a high-affinity nerve growth factor receptor; anti-tyrosine hydroxylase rabbit-monoclonal antibody (ab137869); anti-Akt rabbit polyclonal antibody (ab8805) and anti-phosphorylated Akt rabbit monoclonal antibody (ab81283); anti-Ca2+/calmodulin-dependent kinase II (CaMKII) rabbit polyclonal antibody (ab131468) and anti-phosphorylated CaMKII rabbit polyclonal antibody (ab5683, all Abcam plc, Cambridge, UK); KN-62 (I2142, Sigma-Aldrich, St Louis, MO, USA).

    Techniques: Inhibition, Activity Assay, Irradiation

    Irradiation with 137 Cs γ-rays attenuates NGF-induced Rac1 activation without increasing phosphorylation of Akt in PC12 cells. (a) The activity of Rac1 in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation. Rac1 activity is expressed as the relative ratio to the NGF non-stimulated group without irradiation. Data are presented as the mean ± standard error of triplicate samples. ** P

    Journal: Journal of Radiation Research

    Article Title: Chronic irradiation with low-dose-rate 137Cs-γ rays inhibits NGF-induced neurite extension of PC12 cells via Ca2+/calmodulin-dependent kinase II activation

    doi: 10.1093/jrr/rrx032

    Figure Lengend Snippet: Irradiation with 137 Cs γ-rays attenuates NGF-induced Rac1 activation without increasing phosphorylation of Akt in PC12 cells. (a) The activity of Rac1 in PC12 cells after 5 days of NGF stimulation or non-stimulation, with or without 137 Csγ-ray irradiation. Rac1 activity is expressed as the relative ratio to the NGF non-stimulated group without irradiation. Data are presented as the mean ± standard error of triplicate samples. ** P

    Article Snippet: Reagents We utilized the following reagents to investigate the effects of chronic, low-dose-rate 137 Cs-γ radiation on NGF-induced neurite extension in PC12 cells: NGF 2.5S (N-100, Alomone Labs, Jerusalem, Israel); anti-ERK1/ERK2 mouse-monoclonal antibody (MAB1576) and anti-phosphorylated ERK1/ERK2 rabbit-polyclonal antibody (MAB1018, both R & D systems, Minneapolis, MN, USA); anti-Trk A rabbit polyclonal antibody (sc-118) and anti-phosphorylated Trk A mouse-monoclonal antibody (sc-8058, both Santa Cruz Biotechnology, Dallas, TX, USA)—Trk A is a high-affinity nerve growth factor receptor; anti-tyrosine hydroxylase rabbit-monoclonal antibody (ab137869); anti-Akt rabbit polyclonal antibody (ab8805) and anti-phosphorylated Akt rabbit monoclonal antibody (ab81283); anti-Ca2+/calmodulin-dependent kinase II (CaMKII) rabbit polyclonal antibody (ab131468) and anti-phosphorylated CaMKII rabbit polyclonal antibody (ab5683, all Abcam plc, Cambridge, UK); KN-62 (I2142, Sigma-Aldrich, St Louis, MO, USA).

    Techniques: Irradiation, Activation Assay, Activity Assay