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Query: UMLS:C0016632 (Fox)
 1,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The leaky expression of the yeast mitochondrial gene oxi1, containing a framshift mutation (+1), is caused by natural frameshift suppression, as shown previously (Fox and Weiss-Brummer 1980). A drastic decrease in the natural level of frameshifting is found in the presence of the parr-454 mutation, localized at the 3' end of the 15 S rRNA gene. This mutation causes resistance to the antibiotic paromomycin in the yeast strains D273-10B and KL14-4A (Li et al. 1982; Tabak et al. 1982). The results of this study imply that in the yeast strain 777-3A this mutation alone is sufficient for restriction of the level of natural frameshifting but is insufficient to confer resistance to paromomycin. A second mutation, arising spontaneously with a frequency of 10(-4) leads, in combination with the parr-454 mutation, to full paromomycin resistance in strain 777-3A.
Mol Gen Genet 1989 Jun
PMID:The paromomycin resistance mutation (parr-454) in the 15 S rRNA gene of the yeast Saccharomyces cerevisiae is involved in ribosomal frameshifting. 267 60

The visual world appears unified, stable, and continuous despite rapid changes in eye position. How this is accomplished has puzzled psychologists for over a century. One possibility is that visual information from successive eye fixations is fused in memory according to environmental or spatiotopic coordinates. Evidence supporting this hypothesis was provided by Davidson, Fox, and Dick (1973). They presented a letter array in one fixation and a mask at one letter position in a subsequent fixation and found that the mask inhibited report of the letter that shared its retinal coordinates but appeared to occupy the same position as the letter that shared its spatial coordinates. This suggests the existence of a retinotopic visual persistence at which transsaccadic masking occurs and a spatiotopic visual persistence at which transsaccadic integration, or fusion, occurs. Using a similar procedure, we found retinotopic masking and retinotopic integration: The mask interfered with the letter that shared its retinal coordinates, but also appeared to cover that letter. In another experiment, instead of a mask we presented a bar marker over one letter position, and subjects reported the letter that appeared underneath the bar; subjects usually reported the letter with the same retinal coordinates as the bar, again suggesting retinotopic rather than spatiotopic integration across saccades. In Experiment 3 a bar marker was again presented over one letter position, but in addition a visual landmark was presented after the saccade so that subjects could localize the bar's spatial position; subjects still reported that the letter that shared the bar's retinal coordinates appeared to be under it, but they were also able to accurately specify the bar's spatial position. This ability could have been based on retinal information (the visual landmark) present in the second fixation only, however, rather than spatiotopic visual persistence. Because such a visual landmark was present in the Davidson et al. (1973) experiments, we conclude that their findings can be explained solely in retinotopic terms and provide no convincing evidence for spatiotopic visual persistence. But the exposure parameters that Davidson et al. (1973) and we used were biased in favor of retinotopic, rather than spatiotopic, coding: The stimuli were presented very briefly just before a saccadic eye movement, and subjects are poor at spatially localizing stimuli under these conditions. Thus, in Experiment 4 we presented the letter array about 200 ms before the saccade; then, subjects reported that the letter with the same spatial coordinates as the bar appeared under it.(ABSTRACT TRUNCATED AT 400 WORDS)
J Exp Psychol Gen 1988 Sep
PMID:Visual masking and visual integration across saccadic eye movements. 297 63

We have studied the inactivation of high-voltage-activated (HVA), omega-conotoxin-sensitive, N-type Ca2+ current in embryonic chick dorsal root ganglion (DRG) neurons. Voltage steps from -80 to 0 mV produced inward Ca2+ currents that inactivated in a biphasic manner and were fit well with the sum of two exponentials (with time constants of approximately 100 ms and > 1 s). As reported previously, upon depolarization of the holding potential to -40 mV, N current amplitude was significantly reduced and the rapid phase of inactivation all but eliminated (Nowycky, M. C., A. P. Fox, and R. W. Tsien. 1985. Nature. 316:440-443; Fox, A. P., M. C. Nowycky, and R. W. Tsien. 1987a. Journal of Physiology. 394:149-172; Swandulla, D., and C. M. Armstrong. 1988. Journal of General Physiology. 92:197-218; Plummer, M. R., D. E. Logothetis, and P. Hess. 1989. Neuron. 2:1453-1463; Regan, L. J., D. W. Sah, and B. P. Bean. 1991. Neuron. 6:269-280; Cox, D. H., and K. Dunlap. 1992. Journal of Neuroscience. 12:906-914). Such kinetic properties might be explained by a model in which N channels inactivate by both fast and slow voltage-dependent processes. Alternatively, kinetic models of Ca-dependent inactivation suggest that the biphasic kinetics and holding-potential-dependence of N current inactivation could be due to a combination of Ca-dependent and slow voltage-dependent inactivation mechanisms. To distinguish between these possibilities we have performed several experiments to test for the presence of Ca-dependent inactivation. Three lines of evidence suggest that N channels inactivate in a Ca-dependent manner. (a) The total extent of inactivation increased 50%, and the ratio of rapid to slow inactivation increased approximately twofold when the concentration of the Ca2+ buffer, EGTA, in the patch pipette was reduced from 10 to 0.1 mM. (b) With low intracellular EGTA concentrations (0.1 mM), the ratio of rapid to slow inactivation was additionally increased when the extracellular Ca2+ concentration was raised from 0.5 to 5 mM. (c) Substituting Na+ for Ca2+ as the permeant ion eliminated the rapid phase of inactivation. Other results do not support the notion of current-dependent inactivation, however. Although high intracellular EGTA (10 mM) or BAPTA (5 mM) concentrations suppressed the rapid phase inactivation, they did not eliminate it. Increasing the extracellular Ca2+ from 0.5 to 5 mM had little effect on this residual fast inactivation, indicating that it is not appreciably sensitive to Ca2+ influx under these conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
J Gen Physiol 1994 Aug
PMID:Inactivation of N-type calcium current in chick sensory neurons: calcium and voltage dependence. 780 51

In this study, we investigated the mechanism underlying the production of inwardly rectifying subconductance states induced in large conductance Ca(2+)-activated K+ channels (maxi K(Ca) channels) by the small, homologous proteins, bovine pancreatic trypsin inhibitor (BPTI) and dendrotoxin-I (DTX). Low-resolution bilayer recordings of BPTI-induced substates display excess noise that is well described by a beta-distribution characteristic of a filtered, two-state process. High-resolution patch recordings of maxi K(Ca) channels from vascular smooth muscle cells confirm that the BPTI-induced substate is actually comprised of rapid, voltage-dependent transitions between the open state and a nearly closed state. Patch recordings of DTX-induced substates also exhibit excess noise consistent with a similar two-state fluctuation process that occurs at rates faster than those measured for the BPTI-induced substate. The results indicate that these examples of ligand-induced substates originate by a fluctuating barrier mechanism that is similar to one class of models proposed by Dani, J.A., and J.A. Fox (1991. J. Theor. Biol. 153: 401-423) to explain subconductance behavior of ion channels. To assess the general impact of such rapid fluctuations on the practical measurement of unitary currents by amplitude histograms, we simulated single-channel records for a linear, three-state scheme of C (closed)-O(open)-S(substate). This simulation defines a range of transition rates relative to filter frequency where rapid fluctuations can lead to serious underestimation of actual unitary current levels. On the basis of these experiments and simulations, we conclude that fluctuating barrier processes and open channel noise may play an important physiological role in the modulation of ion permeation.
J Gen Physiol 1996 Jan
PMID:Rectifying conductance substates in a large conductance Ca(2+)-activated K+ channel: evidence for a fluctuating barrier mechanism. 874 30

The immunogenic properties of an E1-deleted, human adenovirus type 5 (Ad5) vaccine virus with activity against rabies were examined in mice, foxes and dogs using different routes of administration. NMRI mice received 10(5.8), 10(5.3), 10(4.3), 10(3.3) and 10(2.3) TCID(50) by peroral or intramuscular (i.m.) administration. Furthermore, six mice received 10(5.8) TCID(50) intracerebrally (i.c.). The construct elicited marked seroconversion in mice after oral administration. Immunoreactivity in mice was even more pronounced i.m. and i.c. After direct oral administration (10(8.0) TCID(50)) in foxes, six of eight animals developed rabies virus-neutralizing antibodies (VNA). All foxes immunized by direct injection (10(7.7) TCID(50)) in the membrane of the jejunum were shown to seroconvert. Pre-existing immunity against canine adenovirus did not hinder the development of rabies VNA after oral application of the construct (10(8.0) TCID(50)). Fox cubs (24-29 days old) born from rabies-immune vixens were shown to develop very high levels of rabies VNA after i.m. administration (10(8.0) TCID(50)), indicating that the immunogenicity of the construct could surpass maternally transferred immunity. In dogs, the construct (10(8.0) TCID(50)) induced a very strong immune response after i.m. administration. However, no immune response was detectable in dogs after direct oral administration (10(8.3) TCID(50)) or after endoscopic deposition in the smaller intestine (10(8.0) TCID(50)). Hence, it must be concluded that the construct is not suitable for oral vaccination of dogs against rabies.
J Gen Virol 2001 Sep
PMID:Immunogenicity of an E1-deleted recombinant human adenovirus against rabies by different routes of administration. 1151 29