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At least 1,027 records · Page 57Linked to original sources
PubMed1985

Improved hybridization assays employing tailed oligonucleotide probes: a direct comparison with 5'-end-labeled oligonucleotide probes and nick-translated plasmid probes.

Terminal deoxynucleotidyl transferase was used to add labeled dAMP residues to the 3' end of oligonucleotide probes that hybridize to the 5' end of the neomycin phosphotransferase II gene. Southern hybridization conditions were described in which the sensitivity per unit of exposure time was about 30-fold greater for the tailed probe as compared to the 5'-end-labeled probe. The tailed oligonucleotide probe had the sensitivity per unit of exposure time comparable to that of a nick-translated probe of high specific activity: in 3 h of autoradiographic exposure both easily detected an amount of target equivalent to a single-copy gene in 10 micrograms of human DNA. The thermal dissociation profiles of 5'-end-labeled and tailed oligonucleotide probes were virtually identical and the tailed oligonucleotide probe was as allele specific as the 5'-end-labeled oligonucleotide probe. The useful lifetime of a 32P-tailed probe was about 1-2 weeks. Finally, by adding 50 35S-labeled nucleotides to the 3' end, we prepared a stable oligonucleotide probe with a sensitivity per unit of exposure time comparable to that of the unstable 5'-32P-labeled oligonucleotide probe.

Adenosine Triphosphate↗
PubMed1987

Tail-pinch stress increases extracellular DOPAC levels (as measured by in vivo voltammetry) in the rat nucleus accumbens but not frontal cortex: antagonism by diazepam and zolpidem.

The effect of a tail-pinch stress on dopamine metabolism in the nucleus accumbens and frontal cortex was investigated in the awake unrestrained rat by measuring extracellular 3,4-dihydroxyphenylacetic acid (DOPAC) levels through the use of in vivo differential pulse voltammetry. Mild tail pressure for 8 min caused a large (maximal effect + 70%) and sustained (more than 2 h) increase in the amplitude of the DOPAC oxidation peak in the nucleus accumbens but not in the prefrontal cortex. A similar increase in DOPAC levels was observed in the nucleus accumbens postmortem 1 h after tail-pinch stress. The tail-pinch induced increase in extracellular DOPAC levels in the nucleus accumbens was antagonized by pretreatment with diazepam (5 mg/kg i.p.) or zolpidem (5 mg/kg i.p.), a novel non-benzodiazepine hypnotic possessing anxiolytic properties. These results suggest that in contrast to other stressors, tail-pinch selectively activates dopaminergic systems projecting to the nucleus accumbens.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Delta opiate receptors mediate tail-shock induced antinociception at supraspinal levels.

Previous work has demonstrated that 3 pharmacologically and neuroanatomically distinct analgesia systems can be sequentially activated by increasing numbers of transcutaneous tail-shock. To date, the categorization of the early (after 2 tail-shocks) and late (after 80-100 tail-shocks) analgesias as opiate-mediated has been based on the ability of systemic naltrexone and morphine tolerance to block these effects. In contrast, the analgesia observed after 5-40 tail-shocks is unaffected by these manipulations, leading to its categorization as non-opiate. The preceding companion paper and the present work were aimed at identifying the neuroanatomical loci at which opiates exert their analgesic effects in this tail-shock paradigm and, further, to identify which opiate receptor subtypes are involved. The 8 experiments included in the present paper examined the effect of microinjecting either naltrexone (a relatively non-selective opiate receptor antagonist), binaltorphimine (kappa receptor antagonist), Cys2-Tyr3-Orn5-Pen7-amide (CTOP) (mu receptor antagonist), or naltrindole (delta receptor antagonist) either into the third ventricle or over the frontal cortex. Taken together, these experiments demonstrate that the late (80-100 shock) opiate analgesia is mediated by delta opiate receptors located within subcortical structures rostral to the 4th ventricle. No evidence for supraspinal opiate involvement in the early (2 shock) opiate analgesia was found.

Analysis of Variance↗
PubMed1983

Root growth of two grass species on iron ore tailings at elevated levels of manganese, iron, and copper.

The iron ore tailings located on the coastal area of Tolo Harbour impose severe pollution problems to the environment. Two grass species, Paspalum distichum and Sporobolus virginicus, were found extensively on the excavated tailings, with the former found in waterlogged areas and the latter in dry areas. These plants may have a potential use in reclaiming the tailings. The present experiment is aimed at studying the reclamation ability of the two local species. Samples of the grass species collected from the tailings were cultured in a series of concentrations of manganese, iron, and copper, separately. Heavy metal tolerance was found to be species specific. S. virginicus collected from the tailings had the higher index of tolerance (0.9) and ED50 (0.85 ppm) to copper whereas P. distichum had the higher index of tolerance and ED50 to manganese (0.98 and 9.2 ppm, respectively) and iron (0.66 and 41 ppm, respectively). Plants of the two species collected from uncontaminated sites showed low index of tolerance and ED50 values for all three metals.

Copper↗
PubMed1991

Antagonists at the NMDA recognition site and blockers of the associated ion channel induce spontaneous tail-flicks in the rat.

The non-competitive N-methyl-D-aspartate (NMDA) antagonists (channel blockers), MK 801, phencyclidine (PCP) and ketamine induced spontaneous tail-flicks in rats. Their order of relative potency (MK 801 greater than PCP greater than ketamine) corresponds to their relative affinities for the ion channel coupled to NMDA receptors. Drugs interacting with their other potential targets (sigma receptors as well as dopamine, serotonin and noradrenaline uptake sites) failed to induce spontaneous tail-flicks. In addition, the catecholamine stimulants, methylphenidate and cocaine were inactive. CPP and CGS 19755, antagonists at the NMDA recognition site, also dose dependently elicited spontaneous tail-flicks: their maximal effect was equal to that of the channel blockers. In contrast, HA-966 and ifenprodil, putative antagonists at the glycine and polyamine recognition sites, respectively, failed to elicit spontaneous tail-flicks. These data demonstrate that both antagonists of the NMDA recognition site and non-competitive blockers of the associated channel induce spontaneous tail-flicks in rats.

Animals↗
PubMed1992

Different radiant heat intensities differentiate intracerebroventricular morphine- from beta-endorphin-induced inhibition of the tail-flick response in the mouse.

The antinociceptive effects of morphine and beta-endorphin given intracerebroventricularly (i.c.v.) or intrathecally (i.t.) were evaluated by inhibition of the tail-flick and hot-plate paw-licking responses evoked by three different intensities of heat stimulation (low, intermediate and high) in male ICR mice. Morphine given i.c.v. was more potent in inhibiting the tail-flick response evoked by low than high intensity of heat stimulus. beta-Endorphin given i.c.v., on the other hand, was equally potent in inhibiting the tail-flick response evoked by different intensities of heat. This differential effect of morphine and beta-endorphin was not shown when morphine and beta-endorphin were given i.t. Morphine and beta-endorphin given i.c.v. or i.t. were equally potent in inhibiting the paw-licking response at different intensities of hot-plate temperature. Our results suggest that morphine given i.c.v. may inhibit high intensity heat-evoked tail-flick response spinally and inhibits low intensity heat-evoked tail-flick response supraspinally. Our results also provide additional evidence for different neural mechanisms of antinociceptive action of morphine and beta-endorphin.

Analgesia↗
PubMed1988

cDNA cloning and primary structure of yellow tail (Seriola quinqueradiata) pregrowth hormone.

Full-length cDNA of yellow tail (Seriola quinqueradiata) growth hormone (GH) was cloned from the pituitary gland and nucleotide sequence was analyzed. The cDNA clone contained one open reading frame to encode a preprotein consisting of 204 amino acids. The deduced amino acid sequence shows two possible sites for signal peptide cleavage, suggesting that the mature forms of yellow tail growth hormone consist of 185 or 187 amino acids. Yellow tail growth hormone exhibits a typical structural feature as growth hormone, including four cysteine residues to form two disulfide bonds and other identical amino acids with other vertebrate GHs. Amino acid sequence of yellow tail growth hormone shows homology of approximately 66, 42, 37, and 34% with those of salmon, eel, bovine, and human GHs, respectively. Nucleotide sequence of the coding region of yellow tail growth hormone cDNA shows approximately 58 and 40% homology with those of salmon and human growth hormone cDNAs, respectively.

Amino Acid Sequence↗
PubMed1993

Why, when and how does the poly(A) tail shorten during mRNA translation?

1. The length of the poly(A) tail at the 3'-end of mRNA may control protein synthesis by bringing the 3'-end in close proximity to the 5'-end of the noncoding region as well as increasing the duration of mRNA translation by its binding to the poly(A) binding protein. 2. The rate-limiting step in the decay of the body of the message is the shortening of a long poly(A) tail during mRNA translation. The shortening of the poly(A) tail occurs during pre-elongation in the protein synthesis cycle. 3. The shortening of the poly(A) tail during mRNA translation may not involve RNase activity, however poly(A) binding protein seems to play a role, at least in part, in shortening of the poly(A) tail.

Animals↗
PubMed1992

Arginine-tail method, an affinity tag procedure utilizing anhydrotrypsin agarose.

The arginine-tail method is a recently developed affinity tag procedure utilizing immobilized anhydrotrypsin for specific enrichment of a recombinant protein. Three model proteins (originally human beta-galactoside-binding lectin with a relative sub-unit molecular mass of 14,000) were prepared by mutagenesis, each of which has a tail of either Arg, Gly-Arg, or Gly-Gly-Arg at the C-terminus. All of them retained their original sugar-binding activity and antigenicity, and became recognizable by anhydrotrypsin. They were adsorbed on an anhydrotrypsin-agarose column at pH 5 after treatment with 4 M urea or 10 mM HCl to expose the C-terminal tails. The adsorbed arginine-tailed lectins were eluted either specifically with benzoylglycylarginine (Bz-Gly-Arg) or with 5 mM HCl. Added arginine was removed by carboxypeptidase B, but very slowly. When urea-denatured Escherichia coli lysate containing one of the arginine-tailed lectins was applied to the column, the lectin was adsorbed together with some host proteins, which are expected to have arginine or lysine at their C-termini. However, more than a ten-fold enrichment was attained by this procedure. The described method would be useful for purifying various recombinant proteins, even those which are inactive as a result of mutagenesis. The smallest tag arginine at the C-terminus should have a minimum effect on both the structure and function of a target protein.

Adsorption↗
PubMed1989

Bacteriophage P1 tail-fibre and dar operons are expressed from homologous phage-specific late promoter sequences.

Two plasmid systems, containing the easily assayable galK and lacZ functions, were employed to study the regulation of the bacteriophage P1 tail-fibre and dar operons. Various P1 DNA fragments carrying either the 5' end of lydA (the 1st gene in the dar operon) or the tail-fibre gene 19 precede the promoterless coding region of galK or were fused, in-frame, to the lacZ gene. In the presence of an induced P1 prophage, GalK and LacZ activities were both detected after a 20 to 30 minute lag period, indicating that the dar and tail-fibre operons are expressed from positively regulated, late promoters. The corresponding DNA operons are expressed from positively regulated, late promoters. The corresponding DNA region of the closely related p15B plasmid exhibits comparable promoter properties. Deletion analysis mapped the promoter of a gene 19-lacZ fusion to a DNA region upstream from gene R, an open reading frame that precedes the coding frame of gene 19. The tail-fibre gene thus forms the second gene in a three gene operon (genes R, 19 (S) and U). Sequence comparison between this promoter region, upstream sequences of the lydA gene and the corresponding portions of the p15B genome allowed the identification of a highly conserved 38 base-pair sequence, which most likely represents a P1-specific late promoter. This was confirmed by 5' mapping of P1 mRNA. Transcription of both the tail-fibre and dar operons is initiated at sites five and six base-pairs, respectively, downstream from the first conserved nucleotide of this sequence. The conserved motif consists of a standard Escherichia coli -10 region followed by a nine base-pair palindromic sequence located centrally about position -22.

Base Sequence↗
PubMed1996

Assessment of the flexed-tail mouse as a possible model for Fanconi anemia: analysis of mitomycin C-induced micronuclei.

Fanconi anemia (FA) is a rare, autosomal recessive disorder characterized by elevated frequencies of chromosome aberrations, hypersensitivity to DNA cross-linking agents and predisposition to cancer. At least 5 complementation groups (FA-A to FA-E) underlie FA and the gene defective in FA-C (FAC) has been cloned. The mouse orthologue, Fac, maps in close proximity to the f locus, on chromosome 13, which codes for the flexed-tail mouse phenotype, raising the possibility that f and Fac are synonymous. If this were the case flexed-tail mice could be used as mouse models for FA-C to help determine the basic defect and to evaluate clinical intervention and gene therapy. To further characterize the flexed-tail mouse, the frequency of micronuclei (a measure of chromosomal aberrations) induced by mitomycin C (MMC), an alkylating and DNA cross-linking agent, was analyzed in peripheral blood and bone marrow erythrocytes. Although a higher spontaneous micronucleus frequency was seen in flexed tail mice in comparison to wild-type mice, the sensitivity to MMC was not elevated. This result suggests that f and Fac are different genes and that the flexed-tail mouse is not a model for FA-C.

Animals↗
PubMed1993

The Dictyostelium myosin IE heavy chain gene encodes a truncated isoform that lacks sequences corresponding to the actin binding site in the tail.

We have isolated cDNA and genomic clones which together span the entire coding sequence for the 114.8 kDa heavy chain of Dictyostelium myosin IE (DMIE). The deduced primary sequence reveals a pattern characteristic of all myosins I, i.e., a myosin-like globular head domain fused to a tail domain that shows no similarity to the coiled-coil rod-like tail of type II myosins. The approx. 35 kDa tail domain of DMIE shows some sequence similarity to the membrane interaction region of other myosins I (tail-homology-region 1; TH-1), but lacks completely the sequences that correspond to the second actin binding site (the glycine-, proline- and alanine-rich TH-2 region and the src-like TH-3 region). Therefore, DMIE more closely resembles DMIA (Titus et al. (1989) Cell Regul 1, 55-63), which is also truncated, than DMIB and DMID, both of which possess all three tail homology regions. The similarity between the DMIE and DMIA isoforms extends to their pattern of expression, in which the steady state level of transcript for both genes is highest in vegetative cells and falls gradually after five to ten hours of starvation-induced development. Together, these results have important implications for interpreting and prioritizing gene targeting experiments designed to identify the functions of myosins I in vivo.

Amino Acid Sequence↗
PubMed1987

Conformation similarities of the globular and tailed forms of acetylcholinesterase from Torpedo californica.

The conformation of the globular dimer (G2), the tailed asymmetric dodecamer (A12, also containing some tailed octamer A8) and the globular tetramer (G4, prepared by removing the collagen-like tail from A12) of acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7) was studied by circular dichroism (CD) in the ultraviolet region. The G2 and G4 forms had similar conformation with about 40% alpha-helix, 35% beta-sheets and 4% beta-turns; the tailed form had a lower helicity (about 34%) and beta-form (about 25%) content probably because of the presence of the tail whose CD spectrum resembles that of an unordered form, but it had about the same amount of beta-turns as the other two forms. All three forms also had similar CD spectra in the near-ultraviolet region due to their non-peptide chromophores. The pH, thermal and urea denaturation of the three acetylcholinesterase forms was also similar to each other. The pH-dependency of both the enzymatic activity and CD intensity of the three forms showed bell-shaped curves with a plateau at pH 7-8. The activity was completely lost at pH below 5 or above 10, but the corresponding CD spectra retained 70-80% of the original magnitudes. Thermal denaturation of the three forms at pH 7.5 showed a conformational transition and loss of activity between 30 and 40 degrees C, but the CD intensity of the helical band at 222 nm was reduced by only 20-30%. Urea denaturation of the three forms began at 1 M urea; it was protein concentration- and time-dependent. Again, the activity disappeared faster than the decreasing CD intensity. Thus, the overall conformation of the three acetylcholinesterase forms appears to be relatively stable, but their active site is easily perturbed by changing the environment. The loss of activity correlated well with the disappearance of the CD band of tryptophan(s) in the near-ultraviolet region, suggesting that the Trp residue(s) might be at or near the active center of the enzyme.

Acetylcholinesterase↗
PubMed1989

Apparent hyperalgesic action of the 5-HT1A agonist, 8-OH-DPAT, in the rat reflects induction of spontaneous tail-flicks.

The 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), induced a dose-dependent reduction in latency to withdraw the tail from noxious hot water (48 degrees C). However, a similar apparent 'hyperalgesia' was seen at a non-noxious temperature of 38 degrees C. Indeed, 8-OH-DPAT induced spontaneous 'tail-flicks' in the absence of external stimulation. This property was shared by lisuride and LSD, which also have high intrinsic activity at 5-HT1A sites. Agonists at other serotonin (5-HT) receptor types (5-HT1B, 5-HT1C, 5-HT2, 5-HT3) were inactive. Tail-flicks induced by 8-OH-DPAT could be antagonised by the 5-HT1 2 antagonist, methiothepin, but not by ritanserin or GR-38032F, which are antagonists at 5-HT2 and 5-HT3 sites, respectively. Ipsapirone and buspirone, partial 5-HT1A agonists, acted as antagonists. Further, BMY 7378, a proposed selective antagonist at 5-HT1A sites, also blocked the tail-flicks. Thus, the apparent 'hyperalgesia' induced by 8-OH-DPAT may reflect induction of spontaneous tail-flicks. These flicks appear to be mediated by 5-HT1A receptors and represent a novel model of 5-HT1A function in the rat.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

NMDA receptor antagonist blocks the facilitation of the tail flick reflex in the rat induced by intrathecal administration of substance P and by noxious cutaneous stimulation.

This study examined effects of the N-methyl-D-aspartate (NMDA) receptor antagonist, 2-amino-5-phosphonovaleric acid (APV), on facilitation of the tail flick reflex (1) by intrathecal administration of 6.5 nmol of substance P at the lumbar spinal level in awake rats and (2) by noxious cutaneous stimulation in anesthetized rats (by immersing the tip of the tail in hot water at 55 +/- 1 degrees C for 1.5 min). Reaction time was decreased by about 70% by intrathecal administration of substance P and by about 40% by tail immersion. Intrathecal administration of APV (2 nmol) or cerebrospinal fluid (CSF) failed to alter the baseline responses. However, APV but not CSF blocked the facilitation induced by intrathecal administration of substance P and by tail immersion. These results indicate that while NMDA receptors do not appear to be involved in mediating the tail flick reflex, they may be involved in expression of the facilitation of this reflex by substance P and/or by a related peptide.

2-Amino-5-phosphonovalerate↗
PubMed1989

Differential actions of the blockade of spinal opioid, adrenergic and serotonergic receptors on the tail-flick inhibition induced by morphine microinjected into dorsal raphe and central gray in rats.

Microinjection of morphine sulfate into dorsal raphe, ventrolateral central gray and dorsolateral central gray inhibits spinal nociceptive reflexes. The effects of the blockade of spinal opioid, adrenergic, and serotonergic receptors by intrathecal injection of naloxone, yohimbine and methysergide, respectively, on inhibition of the tail-flick response induced by morphine microinjected into dorsal raphe, ventrolateral central gray and dorsolateral central gray were studied. Naloxone (20 micrograms) given intrathecally effectively antagonized inhibition of the tail-flick response induced by morphine (4 micrograms) given into dorsal raphe and ventrolateral central gray, but not dorsolateral central gray. On the other hand, intrathecal injection of yohimbine (30 micrograms) antagonized inhibition of the tail-flick response induced by morphine given into ventrolateral central gray and dorsolateral central gray, but not dorsal raphe. Intrathecal injection of prazosin (30 micrograms) did not antagonize inhibition of the tail-flick response induced by morphine given into dorsal raphe or lateral central gray. Intrathecal injection of methysergide (30 micrograms) only partially antagonized inhibition of the tail-flick response induced by morphine given into dorsal raphe, but not ventrolateral central gray and dorsolateral central gray. It is concluded that the analgesia induced by morphine injected into dorsal raphe is mediated by spinal opioid receptors but not by spinal alpha 2-adrenergic receptors while the analgesia produced by morphine given into dorsolateral central gray is mediated by spinal alpha 2-adrenergic receptors. The analgesia induced by morphine given into ventrolateral central gray is mediated in part by both spinal alpha 2-adrenergic and opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Tail pinch-induced changes in the turnover and release of dopamine and 5-hydroxytryptamine in different brain regions of the rat.

Tail pinch was administered through a paper clip attached to the rat's tail. The ex vivo changes in the metabolite/transmitter ratio were used as a measure of changes in the turnover of dopamine and 5-hydroxytryptamine. After a 2-min tail pinch dopamine turnover was increased in the striatum but not in the frontal cortex, hypothalamus or olfactory tubercle; 5-hydroxytryptamine turnover was increased in frontal cortex and hippocampus and was unchanged in striatum, hypothalamus and olfactory tubercle. Microdialysis was used to monitor the changes in extracellular neurotransmitter and metabolite concentrations during and after tail pinch. A 5-min tail pinch caused a rapid rise of both dopamine in the striatum and 5-hydroxytryptamine in the hippocampus. There was a smaller increase in the 5-hydroxytryptamine metabolite 5-hydroxyindoleacetic acid and only a non-significant increase in the dopamine metabolite 3,4-dihydroxyphenylacetic acid.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

The tobacco etch viral 5' leader and poly(A) tail are functionally synergistic regulators of translation.

The 5' cap (m7GpppN) and the poly(A) tail of eukaryotic mRNAs work in concert to establish an efficient level of translation in vivo. Nevertheless, several mRNAs naturally lack a cap or a poly(A) tail. Determining how these messages effectively compete for the translational machinery not only reveals alternative mechanisms for translational competence, but can also underscore similarities between alternative mechanisms and the standard cap/poly(A) tail interaction. The genomic RNA of tobacco etch virus (TEV), a potyvirus, is a polyadenylated mRNA that naturally lacks a cap (m7GpppN) at the 5'-terminus and yet is a highly competitive mRNA during translation. The 144-nt 5'-leader is largely responsible for directing efficient translation and can greatly increase the translational competence of reporter mRNAs. We have examined the synergy between the TEV 5'-leader and the poly(A) tail in transfected plant and animal cells. The TEV 5'-leader functioned optimally as a regulator of reporter mRNA translation only when a poly(A) tail was present. The effect of the TEV 5'-leader on the translation of capped transcripts was significantly less than that for uncapped mRNAs, suggesting that the TEV 5'-leader and the cap may promote similar steps in translation.

Animals↗