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At least 595 records · Page 33Linked to original sources
PubMed2001

A MEK inhibitor, PD98059 enhances IL-1-induced NF-kappaB activation by the enhanced and sustained degradation of IkappaBalpha.

Interleukin-1 (IL-1) mediates numerous host responses through rapid activation of nuclear factor-kappaB (NF-kappaB), but signal pathways leading to the NF-kappaB activation appear to be complicated and multiplex. We propose a novel regulatory system for NF-kappaB activation by the extracellular signal-related kinase (ERK) pathway. In a human glioblastoma cell line, T98G, IL-1-induced NF-kappaB activation was significantly augmented by the pretreatment of a specific MEK inhibitor, PD98059. In contrast, ectopic expression of a constitutive activated form of Raf (v-Raf) reduced IL-1-induced NF-kappaB activation, and this inhibition was completely reversed by PD98059. Interestingly, PD98059 sustained IL-1-induced NF-kappaB DNA binding activity by an electrophoretic mobility shift assay and also IkappaBalpha degradation, presumably by augmenting and sustaining the proteasome activation. Concomitantly, two NF-kappaB dependent genes, A20 and IkappaBalpha expression were prolonged with PD98059. These data suggested that MEK-ERK pathway exerts a regulatory effect on NF-kappaB activation, providing a novel insight on the role of MEK-ERK pathway.

Binding, Competitive↗
PubMed1997

Enhanced levels of biochemical markers for cobalamin deficiency in totally gastrectomized rats: uncoupling of the enhancement from the severity of spongy vacuolation in spinal cord.

The totally gastrectomized (TGX) rat is a new experimental model for studying the pathogenesis of cobalamin (Cbl)-deficient myelopathy, i.e., subacute combined degeneration, total gastrectomy (TG) serving as a surgical paradigm of human pernicious anemia. We determined the serum levels of some biochemical indicators of Cbl deficiency in TGX rats at 2 to 10 months after TG. Methylmalonic acid (MMA) rose within 2 months and progressively increased thereafter until the end of the investigation period. 2-Methylcitric acid (MCA) rose significantly by 6 months and showed a further increment 4 months later. Homocysteine was only clearly elevated much later than the serum MMA, i.e., 10 months after the operation. The concentrations of MMA, MCA, and cystathionine were increased in kidney, liver, and spinal cord (SC) of TGX rats at 10 months. Chronic treatment of TGX rats with Cbl greatly decreased the serum levels of all the metabolic indicators of Cbl deficiency. Chronic peroral administration of the antibiotic lincomycin to TGX rats in an attempt to suppress the enteric flora markedly decreased serum MMA levels. Only Cbl, however, given either for the first 2 months after TG or for the third and fourth postoperative months (i.e., after SC abnormalities had already appeared) significantly decreased the severity of spongy vacuolation in SC white matter, although not completely preventing or repairing the neuropathological damage. Therefore, neither the early impairment in TGX rats of the Cbl-dependent methylmalonyl-coenzyme A mutase reaction nor the more delayed impairment of the Cbl-dependent methionine synthase step, as reflected by changes in serum metabolite levels, seems to be causally related to the TG-induced spongy vacuolation in SC white matter.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1984

Enhanced recombination between lambda plac5 and mini-F-lac: the tra regulon is required for recombination enhancement.

F42lac recombination with lambda plac is normally 20-fold to 50-fold higher than recombination between lambda plac and a chromosomal lac gene. Transductional crosses with lambda plac and a recombinant plasmid containing the lac operon and F replication functions show only two to four-fold higher recombination than similar crosses with a chromosomal lac gene. Insertion of a BamHI fragment containing the entire tra regulon of F into the mini-F-lac plasmid restores the high level of recombination seen with F42lac.

Bacteriophage lambda↗
PubMed1995

Inhibition of proteolysis enhances aluminum-induced perikaryal neurofilament accumulation but does not enhance tau accumulation.

As observed for neurons in situ, phosphorylated neurofilament (NF) epitopes are normally segregated within the axonal cytoskeleton of NB2a/d1 cells. However, accumulations of phosphorylated NFs develop in NB2a/d1 perikarya following exposure to aluminum salts and following inhibition of proteolysis. In the present study, we observed that perikarya of cells exposed to both aluminum and the protease inhibitor C1 (also known as "AllNal") were more intensely labeled by monoclonal antibodies directed against both nonphosphorylated and phosphorylated epitopes than were cells treated with either aluminum or protease inhibitor alone. Since these monoclonal antibodies crossreact with tau, we also immunostained cells treated under these conditions with monoclonal antibodies directed against phosphate-insensitive (5E2) and phosphorylated (PHF-1) epitopes of tau. Aluminum treatment, but not C1 treatment, induced accumulation of total tau isoforms as judged by an increase in 5E2 immunoreactivity. Neither treatment, either separately or in combination, induced an increase in PHF-1 immunoreactivity. These findings suggest that alterations in immunoreactivity with SMI antibodies reflected increases in NF epitopes. This was confirmed by immunoblot analyses. Since proteolysis is apparently instrumental in maintaining the normal distribution patterns of phosphorylated NF epitopes, these findings implicate deficiencies in proteolytic mechanisms in the development of neurofibrillary pathology, and underscore the possibility of a multiple etiology in human neuropathological conditions.

Aluminum↗
PubMed2005

Enhancement of dorsal random-pattern skin flap survival in rats with topical lidocaine and prilocaine (EMLA): enhancement of flap survival by EMLA.

BACKGROUND: Various topical pharmacologic agents have been investigated for their efficacy in preventing or reversing skin flap ischemia. Most of these studies have focused on agents that act on the vascular smooth muscles to cause vasodilatation and improve circulation in the flap. Most of local anesthetics relax vascular smooth muscle and produce peripheral vasodilatation. Topical lidocaine administration was shown that it was an effective and prompt resolution of mechanically induced vasospasm. The topical analgesia cream, EMLA is a mixture of the substances lidocaine and prilocaine. EMLA causes a biphasic vascular response comprising initial blanching and vasoconstriction (maximal after 1.5 h of application) and late erythema and vasodilatation at application times longer than 3 h. MATERIALS AND METHODS: To investigate the effect of EMLA on random flap survival, 40 rats were divided in 2 groups of 20 animals. Caudally based random pattern skin flaps were elevated on dorsa of the rats in 10 x 3 cm dimensions. In group 1 which was the treatment group, topical EMLA was applied and covered with Opsite for 1 week whereas in group 2 which was the control group, carrier for EMLA was applied to the flaps. At the end of treatment period, the areas of flap necrosis were measured and percentages of flap survivals were calculated. RESULTS: The mean percentages of flap survivals in group 1 and 2 were 81.2 +/- 1.2 percent and 58.7 +/- 2.3 percent, respectively. CONCLUSION: Topically administered EMLA might lead to a significant improvement in flap survival. In addition, it is safe, cost-effective, easily applied, and clinically available.

Administration, Topical↗