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retinal degeneration/l tyrosin
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Seite 1 von 78 Ergebnisse
Altered regulation of L-type channels by protein kinase C and protein tyrosine kinases as a pathophysiologic effect in retinal degeneration.
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The effect of protein tyrosine kinases (PTK) on L-type calcium channels in cultured retinal pigmented epithelium (RPE) from rats with retinal dystrophy was investigated. Barium currents through Bay K 8644 (10(-6) M) sensitive L-type channels were measured using the patch-clamp technique. The current
Genistein, a protein tyrosine kinase inhibitor, ameliorates retinal degeneration after ischemia-reperfusion injury in rat.
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OBJECTIVE
The authors sought to determine the effect of genistein, a naturally occurring protein tyrosine kinase inhibitor, in a model of ischemia-reperfusion injury in the rat retina.
METHODS
Ischemia-reperfusion injury was induced by temporary optic nerve ligation. A dose of 0.034 mg, 0.34 mg, and
Deficiency of SHP-1 protein-tyrosine phosphatase in "viable motheaten" mice results in retinal degeneration.
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OBJECTIVE
Viable motheaten mutant mice (abbreviated allele symbol me(v)) are deficient in Src-homology 2-domain phosphatase (SHP)-1, a critical negative regulator of signal transduction in hematopoietic cells. These mice exhibit immune dysfunction, hyperproliferation of myeloid cells, and
PACAP-mediated neuroprotection of neurochemically identified cell types in MSG-induced retinal degeneration.
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Pituitary adenylate cyclase-activating polypeptide (PACAP) is neuroprotective in animal models of different brain pathologies and injuries, including cerebral ischemia, Parkinson's disease, and different types of retinal degenerations. We have previously shown that PACAP is protective against
Activation of oncogenic tyrosine kinase signaling promotes insulin receptor-mediated cone photoreceptor survival.
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In humans, daylight vision is primarily mediated by cone photoreceptors. These cells die in age-related retinal degenerations. Prolonging the life of cones for even one decade would have an enormous beneficial effect on usable vision in an aging population. Photoreceptors are postmitotic, but shed
Inactivation of the Akt survival pathway during photoreceptor apoptosis in the retinal degeneration mouse.
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OBJECTIVE
Previous work has indicated that the serine-threonine protein kinase Akt is a general mediator of cellular survival signals and that loss of Akt-mediated signaling can lead to the activation of apoptosis. This study was conducted to establish whether regulation of the Akt survival pathway
Microglia Inhibition Delays Retinal Degeneration Due to MerTK Phagocytosis Receptor Deficiency
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Retinitis Pigmentosa (RP) is a group of inherited retinal diseases characterized by progressive loss of rod followed by cone photoreceptors. An especially early onset form of RP with blindness in teenage years is caused by mutations in mertk, the gene encoding the clearance phagocytosis
Blue Autofluorescence Fundus Imaging for Monitoring Retinal Degeneration in Royal College of Surgeons Rats.
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Purpose
Development of a method for noninvasive longitudinal follow-up of retinal degeneration in the whole retina for Royal College of Surgeons (RCS) rats, a commonly used model of retinitis pigmentosa associated with mutations in the MER-proto-oncogene tyrosine kinaseAn ENU-induced mutation in the Mertk gene (Mertknmf12) leads to a slow form of retinal degeneration.
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OBJECTIVE
To determine the basis and to characterize the phenotype of a chemically induced mutation in a mouse model of retinal degeneration.
METHODS
Screening by indirect ophthalmoscopy identified a line of N-ethyl-N-nitrosourea (ENU) mutagenized mice demonstrating retinal patches. Longitudinal
Ectopic synaptogenesis during retinal degeneration in the royal college of surgeons rat.
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Rod photoreceptor-specific mutations cause ectopic synapses to form between cone photoreceptor terminals and rod bipolar cell dendrites in degenerating retinas of rhodopsin transgenic (P347L) pigs and retinal degeneration mice. Since the mutations occur in rod photoreceptor-specific genes in these
Expression pattern of Ccr2 and Cx3cr1 in inherited retinal degeneration.
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BACKGROUND
Though accumulating evidence suggests that microglia, resident macrophages in the retina, and bone marrow-derived macrophages can cause retinal inflammation which accelerates photoreceptor cell death, the details of how these cells are activated during retinal degeneration (RD) remain
The radioprotector ortho-phospho-L-tyrosine (pTyr) attenuates the side effects of fractionated irradiation in retinoblastoma mouse models but also decreases the local tumour control.
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Radiotherapy (RT) is used to treat retinoblastoma (Rb), the most frequent ocular tumour in children. Besides eradicating the tumour, RT can cause severe side effects including secondary malignancies. This study aimed to define whether the radioprotector ortho-phospho-L-tyrosine (pTyr) prevents
Development and survival of tyrosine hydroxylase containing neurons in RCS rat retinae.
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OBJECTIVE
Dopamine serves a variety of functions in the retina. Abnormalities of the retinal dopaminergic system have been described in the Royal College of Surgeons (RCS) rat as well as other models of retinal degeneration. Dopamine has been implicated in several retinal dysfunctions of retinitis
Light-induced retinal damage involves tyrosine 33 phosphorylation, mitochondrial and nuclear translocation of WW domain-containing oxidoreductase in vivo.
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WW domain-containing oxidoreductase WOX1, also named WWOX or FOR, is a known proapoptotic protein and a candidate tumor suppressor. Stress stimuli activate WOX1 via tyrosine 33 (Tyr33) phosphorylation and translocation to the mitochondria and nuclei in vitro. Here, the potential role of WOX1 in
Expression of neurturin, glial cell line-derived neurotrophic factor, and their receptor components in light-induced retinal degeneration.
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OBJECTIVE
Dysregulation of neurturin (NTN) expression has been linked to photoreceptor apoptosis in a mouse model of inherited retinal degeneration. To investigate the extent to which any such dysregulation depends on the nature of the apoptotic trigger, the expression of NTN, glial cell
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