Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.3 (diaphorase)
5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To understand the mechanisms leading to the progressive loss of intrinsic neuronal growth properties during central nervous system development, we have investigated the evolution of the response to injury and regenerative potential of immature Purkinje cells, axotomized at different postnatal ages from postnatal day (P)3 to P12. In adult rodents, these neurons are characterised by a weak cell body response to axotomy, which is associated with a remarkable resistance to injury and a poor regenerative capability. During the first postnatal week, Purkinje cells are strongly sensitive to injury and massively degenerate within a few days. Immature Purkinje cells react to neurite transection by a strong upregulation of c-Jun, accompanied by a moderate, but consistent, expression of the growth-associated protein (GAP)-43. In contrast, nicotinamide adenine dinucleotide monophosphate (NADPH)-diaphorase reactivity, which can be activated by adult Purkinje neurons, is not modified in their juvenile counterparts. The severed Purkinje axons show a vigorous regenerative sprouting both into the lesioned cerebellar environment and into embryonic neocortical tissue transplanted into the injury site. The typical adult features of the response to injury progressively develop during the second postnatal week, when the injured neurons acquire resistance, cell body changes become milder, the regenerative potential declines, and the severed axons undergo characteristic morphological modifications, including torpedoes and the hypertrophy of recurrent collateral branches. This complete reversal of the features and the outcome of the Purkinje cell reaction to axotomy likely results from the profound changes that occur in the maturing Purkinje cells and/or in their microenvironment during this phase of cerebellar development.
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PMID:Evolution of the Purkinje cell response to injury and regenerative potential during postnatal development of the rat cerebellum. 1113 48

White Spot Syndrome Virus (WSSV) is the major viral pathogen of culture shrimp. Although remarkable progress has been made in characterizing the WSSV genome, information concerning the antiviral process of host is still limited. To identify the genes differentially expressed along with their expression profile in the hemocytes of the virus-resistant shrimp, suppression subtractive hybridization (SSH) and differential hybridization (DH) were employed. Relying on the sequences identified in the subtractive cDNA library, 30 genes were characterized to be involved in the antiviral process as defense-relevant, among them, 22 are found for the first time in penaeid shrimp. The most interesting finding is that the interferon-like protein (IntlP) and (2'-5') oligo(A) synthetase-like protein (data not shown) known as the antiviral factors showed increased expression in virus-resistant shrimp and the non-specific antiviral activity of IntlP protein was verified by cytotoxicity experiment. A number of proteins with certain similarities to the components of the complement and cytokines system in vertebrates were also found in the subtracted library. The high expression of redox-related factors (NADH dehydrogenase, glutathione peroxidase and transcription factor AP-1 precursor), plasma defensive protein (C-type lectin and laminin-like protein) and translationally controlled tumor protein (TCTP) in the virus-resistant shrimp suggested that they are essential components participating in the antiviral process. Our work provides a wide array of genes differentially expressed in the virus-resistant shrimp, and a framework for further studies aimed at antiviral mechanism in shrimp.
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PMID:Differential profile of genes expressed in hemocytes of White Spot Syndrome Virus-resistant shrimp (Penaeus japonicus) by combining suppression subtractive hybridization and differential hybridization. 1578 Nov 31