Trkc
Mostrando 1-12 de 30 artigos, teses e dissertações.
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1. A expressão imuno-histoquímica de Ki67, EGFR E TRKC e sua correlação com fatores prognósticos em meduloblastomas
Introdução: O meduloblastoma é o tumor maligno do cerebelo com prognóstico reservado. Seu tratamento baseia-se somente em critérios clínicos, como os grupos de risco que levam em consideração apenas idade, extensão de ressecção, recidiva e metástase. Objetivo: Avaliar uma possível relação entre a imunoexpressão de biomarcadores (Ki67, rece
J. Bras. Patol. Med. Lab.. Publicado em: 2014-08
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2. Neurotrofinas na epilepsia do lobo temporal
INTRODUÇÃO: A neurotrofinas NGF, BDNF, NT-3 e NT-4 são os principais representantes da família das neurotrofinas no sistema nervoso central de mamíferos. Estão presentes em estágios específicos do crescimento e sobrevivência neuronal como a divisão celular, diferenciação e axogênese e também nos processos naturais de morte celular neuronal. A a
Journal of Epilepsy and Clinical Neurophysiology. Publicado em: 2010
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3. trkC encodes multiple neurotrophin-3 receptors with distinct biological properties and substrate specificities.
The trkC gene product gp145trkC is a high affinity signaling receptor for neurotrophin-3 (NT-3), a member of the NGF family of neurotrophic factors. We now report that trkC encodes at least two additional tyrosine protein kinase receptors. These receptors, designated TrkC K2 and TrkC K3, have the same amino acid sequences as gp145trkC (now designated TrkC K1
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4. Targeted deletion of all isoforms of the trkC gene suggests the use of alternate receptors by its ligand neurotrophin-3 in neuronal development and implicates trkC in normal cardiogenesis
We have generated null mutant mice that lack expression of all isoforms encoded by the trkC locus. These mice display a behavioral phenotype characterized by a loss of proprioceptive neurons. Neuronal counts of sensory ganglia in the trkC mutant mice reveal less severe losses than those in NT-3 null mutant mice, strongly suggesting that NT-3, in vivo, may si
The National Academy of Sciences of the USA.
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5. The neurotrophin-3 receptor TrkC directly phosphorylates and activates the nucleotide exchange factor Dbs to enhance Schwann cell migration
During the development of the peripheral nervous system, Schwann cells, the myelin-forming glia, migrate along axons before initiating myelination. We previously demonstrated that endogenous neurotrophin-3 (NT3) acting through the TrkC tyrosine kinase receptor enhances migration of premyelinating Schwann cells. This signaling pathway is mediated by the c-Jun
National Academy of Sciences.
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6. Distinct requirements for TrkB and TrkC signaling in target innervation by sensory neurons
Signaling by brain-derived neurotrophic factor (BDNF) via the TrkB receptor, or by neurotrophin-3 (NT3) through the TrkC receptor support distinct populations of sensory neurons. The intracellular signaling pathways activated by Trk (tyrosine kinase) receptors, which in vivo promote neuronal survival and target innervation, are not well understood. Using mic
Cold Spring Harbor Laboratory Press.
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7. Expression of the neurotrophin receptor TrkC is linked to a favorable outcome in medulloblastoma.
Medulloblastoma, the most common malignant brain tumor of childhood, has a variable prognosis. Although half of the children and young adults with the disease survive longer than 10 years after diagnosis, the others relapse and die despite identical therapy. We have examined the expression of neurotrophins and their receptors in medulloblastoma samples snap
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8. The Runx3 transcription factor regulates development and survival of TrkC dorsal root ganglia neurons
The RUNX transcription factors are important regulators of linage-specific gene expression in major developmental pathways. Recently, we demonstrated that Runx3 is highly expressed in developing cranial and dorsal root ganglia (DRGs). Here we report that within the DRGs, Runx3 is specifically expressed in a subset of neurons, the tyrosine kinase receptor C (
Oxford University Press.
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9. Ras activation of a Rac1 exchange factor, Tiam1, mediates neurotrophin-3-induced Schwann cell migration
Endogenous neurotrophins positively and negatively regulate migration of premyelinating Schwann cells before the initiation of myelination. Neurotrophin-3 (NT3) acting through the TrkC receptor tyrosine kinase stimulates Schwann cell migration via the Rho GTPases Rac1 and Cdc42. We previously demonstrated that TrkC directly phosphorylates and activates Dbs,
National Academy of Sciences.
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10. Neurotrophin 3 activation of TrkC induces Schwann cell migration through the c-Jun N-terminal kinase pathway
During development and nerve injury, complex interactions between glial cells and neurons are essential for establishing proper nerve function. Neurotrophins play multiple roles in the developing nervous system, including cell survival, growth, and differentiation. Here we show that migration of Schwann cells, isolated from sciatic nerves, is significantly e
National Academy of Sciences.
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11. Directing oncogenic fusion genes into stem cells via an SCL enhancer
TEL-TRKC is a fusion gene generated by chromosomal translocation and encodes an activated tyrosine kinase. Uniquely, it is found in both solid tumors and leukemia. However, a single exon difference (in TEL) in TEL-TRKC fusions is associated with the two sets of cancer phenotypes. We expressed the two TEL-TRKC variants in vivo by using the 3′ regulatory ele
National Academy of Sciences.
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12. An immunoglobulin-like domain determines the specificity of neurotrophin receptors.
The neurotrophins influence survival and maintenance of vertebrate neurons in the embryonic, early post-natal and post-developmental stages of the nervous system. Binding of neurotrophins to receptors encoded by the gene family trk initiates signal transduction into the cell. trkA interacts preferably with nerve growth factor (NGF), trkB with brain-derived n