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  • The proapoptotic dp5 gene is a direct target of the MLK-JNK-c-Jun pathway in sympathetic neurons. 19304750

    The death of sympathetic neurons after nerve growth factor (NGF) withdrawal requires de novo gene expression. Dp5 was one of the first NGF withdrawal-induced genes to be identified and it encodes a proapoptotic BH3-only member of the Bcl-2 family. To study how dp5 transcription is regulated by NGF withdrawal we cloned the regulatory regions of the rat dp5 gene and constructed a series of dp5-luciferase reporter plasmids. In microinjection experiments with sympathetic neurons we found that three regions of dp5 contribute to its induction after NGF withdrawal: the promoter, a conserved region in the single intron, and sequences in the 3' untranslated region of the dp5 mRNA. A construct containing all three regions is efficiently activated by NGF withdrawal and, like the endogenous dp5, its induction requires mixed-lineage kinase (MLK) and c-Jun N-terminal kinase (JNK) activity. JNKs phosphorylate the AP-1 transcription factor c-Jun, and thereby increase its activity. We identified a conserved ATF site in the dp5 promoter that binds c-Jun and ATF2, which is critical for dp5 promoter induction after NGF withdrawal. These results suggest that part of the mechanism by which the MLK-JNK-c-Jun pathway promotes neuronal apoptosis is by activating the transcription of the dp5 gene.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB17003
    Nombre del producto:
    Anti-Bim Antibody, internal epitope, pan-Bim isoforms

  • Mkp1 is a c-Jun target gene that antagonizes JNK-dependent apoptosis in sympathetic neurons. 20702711

    Developing sympathetic neurons depend on NGF for survival. When sympathetic neurons are deprived of NGF in vitro, a well documented series of events, including c-Jun N-terminal kinase (JNK) pathway activation, release of cytochrome c from the mitochondria, and caspase activation, culminates in the death of the neuron by apoptosis within 24-48 h. This process requires de novo gene expression, suggesting that increased expression of specific genes activates the cell death program. Using rat gene microarrays, we found that NGF withdrawal induces the expression of many genes, including mkp1, which encodes a MAPK phosphatase that can dephosphorylate JNKs. The increase in mkp1 mRNA level requires the MLK-JNK-c-Jun pathway, and we show that Mkp1 is an important regulator of JNK-dependent apoptosis in sympathetic neurons. In microinjection experiments, Mkp1 overexpression can inhibit JNK-mediated phosphorylation of c-Jun and protect sympathetic neurons from apoptosis, while Mkp1 knockdown accelerates NGF withdrawal-induced death. Accordingly, the number of superior cervical ganglion (SCG) neurons is reduced in mkp1-/- mice at P1 during the period of developmental sympathetic neuron death. We also show that c-Jun and ATF2 bind to two conserved ATF binding sites in the mkp1 promoter in vitro and in chromatin. Both of these ATF sites contribute to basal promoter activity and are required for mkp1 promoter induction after NGF withdrawal. These results demonstrate that Mkp1 is part of a negative feedback loop induced by the MLK-JNK-c-Jun signaling pathway that modulates JNK activity and the rate of neuronal death in rat sympathetic neurons following NGF withdrawal.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB17003
    Nombre del producto:
    Anti-Bim Antibody, internal epitope, pan-Bim isoforms

  • Transactivation of Trk neurotrophin receptors by G-protein-coupled receptor ligands occurs on intracellular membranes. 15282267

    Neurotrophins, such as NGF and BDNF, activate Trk receptor tyrosine kinases through receptor dimerization at the cell surface followed by autophosphorylation and intracellular signaling. It has been shown that activation of Trk receptor tyrosine kinases can also occur via a G-protein-coupled receptor (GPCR) mechanism, without involvement of neurotrophins. Two GPCR ligands, adenosine and pituitary adenylate cyclase-activating polypeptide (PACAP), can activate Trk receptor activity to increase the survival of neural cells through stimulation of Akt activity. To investigate the mechanism of Trk receptor transactivation, we have examined the localization of Trk receptors in PC12 cells and primary neurons after treatment with adenosine agonists and PACAP. In contrast to neurotrophin treatment, Trk receptors were sensitive to transcriptional and translational inhibitors, and they were found predominantly in intracellular locations particularly associated with Golgi membranes. Biotinylation and immunostaining experiments confirm that most of the transactivated Trk receptors are found in intracellular membranes. These results indicate that there are alternative modes of activating Trk receptor tyrosine kinases in the absence of neurotrophin binding at the cell surface and that receptor signaling may occur and persist inside of neuronal cells.
    Tipo de documento:
    Referencia
    Referencia del producto:
    ABN1383
    Nombre del producto:
    Anti-phospho-TrkA (Tyr794) Antibody

  • Site-specific labeling of neurotrophins and their receptors via short and versatile peptide tags. 25426999

    We present a toolbox for the study of molecular interactions occurring between NGF and its receptors. By means of a suitable insertional mutagenesis method we show the insertion of an 8 amino acid tag (A4) into the sequence of NGF and of 12 amino acid tags (A1 and S6) into the sequence of TrkA and P75NTR NGF-receptors. These tags are shortened versions of the acyl and peptidyl carrier proteins; they are here covalently conjugated to the biotin-substituted arm of a coenzyme A (coA) substrate by phosphopantetheinyl transferase enzymes (PPTases). We demonstrate site-specific biotinylation of the purified recombinant tagged neurotrophin, in both the immature proNGF and mature NGF forms. The resulting tagged NGF is fully functional: it can signal and promote PC12 cells differentiation similarly to recombinant wild-type NGF. Furthermore, we show that the insertion of A1 and S6 tags into human TrkA and P75NTR sequences leads to the site-specific biotinylation of these receptors at the cell surface of living cells. Crucially, the two tags are labeled selectively by two different PPTases: this is exploited to reach orthogonal fluorolabeling of the two receptors co-expressed at low density in living cells. We describe the protocols to obtain the enzymatic, site-specific biotinylation of neurotrophins and their receptors as an alternative to their chemical, nonspecific biotinylation. The present strategy has three main advantages: i) it yields precise control of stoichiometry and site of biotin conjugation; ii) the tags used can be functionalized with virtually any small probe that can be carried by coA substrates, besides (and in addition to) biotin; iii) above all it makes possible to image and track interacting molecules at the single-molecule level in living systems.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Effects of nerve growth factor on expression of GAP-43 in right atria after sympathectomy in diabetic rats. 11703425

    AIM: The present study investigated the role of nerve growth factor (NGF) in the regeneration of noradrenergic nerves of right atria (following 6-hydroxydopamine; 6-OHDA, 100 mg/kg, i.p.) from non-diabetic and 8-week diabetic rats. RESULTS: In cryostat sections of the right atria, GAP-43 immunoreactivity was concentrated in nerve terminals, preterminal axons of the endocardium, epicardium and myocardium, as well as in nerve fibres innervating the blood vessels and ganglionic cells. In serial sections, all positive staining for GAP-43 showed immunoreactivity for the neuronal marker PGP-9.5. In untreated non-diabetic rats, the total GAP-43 immunoreactivity was reduced to 60% relative to pretreatment levels, at day 14 after 6-OHDA, as quantified by Western blotting. In diabetic rats, 6-OHDA treatment produced a marked increase in the levels of total GAP-43 at days 28 and 49. NGF treatment (1 mg/kg, s.c., 3 times/week, for 2 weeks) had no effect on the level of total GAP-43 in right atria from non-diabetic and diabetic rats before treatment with 6-OHDA. However, it normalized the reduced GAP-43 immunoreactivity observed in 6-OHDA-treated non-diabetic rats. Interestingly, NGF treatment alone produced an increase in GAP-43 phosphorylation relative to total GAP-43 in right atria from both non-diabetic (44%) and diabetic groups (42%). CONCLUSIONS: These findings suggest that nerve terminals of the right atria retain, in the mature adult, the capacity for structural and functional plasticity. The expression of GAP-43 in right atria of control and diabetic rats was differentially affected by 6-OHDA treatment. In injured noradrenergic neurones of the right atria, NGF modified the expression of GAP-43 only in non-diabetic rats and not in diabetic rats.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo

  • Delayed NGF infusion fails to reverse axotomy-induced degeneration of basal forebrain cholinergic neurons in adult p75(LNTR)-deficient mice. 11934472

    The p75 low-affinity neurotrophin receptor (p75(LNTR)) appears to have various functions that include enhancing nerve growth factor (NGF)-mediated survival by increasing TrkA (high-affinity NGF receptor) efficiency, and mediating apoptosis by acting as a ligand-regulated pro-apoptotic receptor. Here, we investigated the role of p75(LNTR) for adult cholinergic basal forebrain neurons by comparing neuronal responses to injury in control and p75(LNTR)-deficient mice. In both types of mice, approximately 70% of the cholinergic neurons in the ipsilateral medial septum had lost their markers choline acetyltransferase and tyrosine kinase A by 28 days following unilateral transection of the dorsal septohippocampal pathway (fimbria fornix). A 7-day delayed infusion of NGF that started 28 days after the injury resulted in reversal of choline acetyltransferase expression and cell atrophy in control, but not in p75(LNTR)-deficient, mice. This lack of response to delayed NGF treatment in p75(LNTR)-deficient mice was most likely not due to cell death, as all of the septohippocampal neurons, labeled with Fluorogold before the lesion, were present at 28 days post-lesion, similar to control mice. p75(LNTR)-deficient cholinergic neurons can respond to NGF as they were protected by NGF infusions that started immediately after the injury. These observations, the fact that lesioned p75(LNTR)-deficient neurons atrophy faster, and that non-lesioned neurons hypertrophy in response to NGF in control but not in p75(LNTR)-deficient mice, suggest that p75(LNTR) is needed for tyrosine kinase A and NGF signaling efficiency.In conclusion, during adulthood p75(LNTR) appears to play a beneficial role in the response of cholinergic neurons to injury, consistent with the proposed role of p75(LNTR) in the enhancement of TrkA signaling and the transport of neurotrophins by these neurons.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB143
    Nombre del producto:
    Anti-Choline Acetyltransferase (ChAT) Antibody

  • Localization of neurotrophin-3-like immunoreactivity in the rat central nervous system. 8032912

    Neurotropin-3 (NT3) is a nerve growth factor (NGF) homologue whose function is presently unknown. The factor promotes the survival of a subpopulation of sensory and sympathetic neurons in vitro. NT3 mRNA is widely distributed in both the peripheral and central nervous system but the distribution of NT3 has not yet been examined. In the present study we have determined the regional distribution and cellular localization of NT3-like immunoreactivity (-IR) in the central nervous system by immunohistochemistry. Both glia and neurons were stained. NT3-IR glia were distributed in corpus callosum, substantia nigra, fimbria of hippocampus, subependymal areas of the ventricles and cerebellum. In the forebrain, NT3-IR was detected in a number of neuronal cells, including pyramidal cells in the fifth layer of the cerebral cortices, subpopulations of neurons in the septal nuclei, diagonal bands of Broca, olfactory primary cortex, amygdala and islands of Calleja. In the hippocampus, pyramidal cells in the CA1, CA2 and lateral regions of CA3 and granular cells in dorsal dentate gyrus were labelled with different intensities. Neurons in the bed nuclei of the striatum terminalis, mesencephalic trigeminal nuclei and motoneurons in the brain stem and spinal cord were intensively labelled. A subpopulation of neurons in the reticular thalamic nuclei and midbrain were moderately labelled. Finally, in the cerebellum, NT3-IR was also found in Purkinje cells and neurons in the deep cerebellar nuclei. In some brain regions such as hippocampus, the distribution of NT3-IR correlates with that of mRNANT3 as described by others. In contrast in other regions such as spinal cord and brain stem, little correlation was found between protein and mRNA. The results suggest that some NT3 immunoreactive neurons in the central nervous system accumulate NT3 in accord with a neurotrophic role for their maintenance or survival, while others may synthesize and secrete the factor to provide support for innervating neurons.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB1532P
    Nombre del producto:
    Anti-Neurotrophin 3 Antibody

  • NGF 2.5S, mouse - NG1929388

    Tipo de documento:
    Certificado de análisis
    Número de lote:
    NG1929388
    Referencia del producto:
    01-125
    Nombre del producto:
    NGF 2.5S Protein, mouse

  • NGF 7S, mouse - 24056

    Tipo de documento:
    Certificado de análisis
    Número de lote:
    24056
    Referencia del producto:
    01-170

  • NGF 7S, mouse - 2159635

    Tipo de documento:
    Certificado de análisis
    Número de lote:
    2159635
    Referencia del producto:
    01-170