Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transcriptional induction of the alpha or immediate-early gene class of herpes simplex virus type 1 effected by the alpha trans-induction factor (alpha TIF, ICP25, VP16, Vmw65) requires an alpha-specific cis-acting site. Increased transcription does not result from the direct, independent binding of alpha TIF, but rather from an alpha TIF-dependent formation of a protein-DNA complex containing, in addition to alpha TIF, at least one host cell factor. One of the host factors is a POU domain protein which recognizes an octamer element in the alpha-specific consensus. There is evidence that alpha TIF may drive the formation of multiple protein-DNA complexes containing a POU protein and additional host factors. Previously, the gene products of UL46 and UL47 have been implicated in modulating the alpha TIF-dependent transcriptional induction of alpha genes. Our current studies have extended these analyses from a transient-expression system to a series of viral deletion mutants. In these studies we demonstrate that neither UL46- nor UL47-encoded gene product, either separately or in combination, is required for viral growth in cell culture. The absence of UL47 reduces by up to 80% the ability of the virus to induce an alpha-regulated thymidine kinase reporter gene resident in 143TK- cells. Autoradiograms of [35S]methionine pulse-labeled infected cell proteins, separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, show that deleting UL46 and/or UL47 has no discernable effect on the synthesis of alpha TIF or alpha TIF-containing proteins. Subsequent Western immunoblot analysis, with rabbit anti-alpha TIF antibodies made to an alpha TIF-Staphylococcus aureus protein A fusion, demonstrated that the accumulation and steady-state levels of alpha TIF or alpha TIF-containing proteins was indistinguishable from that of the thymidine kinase-negative isogenic parental virus, R delta 305.
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PMID:Role of herpes simplex virus type 1 UL46 and UL47 in alpha TIF-mediated transcriptional induction: characterization of three viral deletion mutants. 184 1

A feature of the cascade regulation of herpes simplex virus 1 gene expression in productive infection is that the first genes to be expressed, the alpha genes, are transactivated by a structural component of the virion designated as the alpha transinducing factor (alpha TIF). In this study, we have tested the hypothesis that latent infection of sensory neurons results from the failure of alpha TIF, a tegument protein, to be transported from the nerve endings to the nucleus of the sensory neuron. Two viruses were constructed. The first recombinant virus (R6003) contained a second copy of the alpha TIF gene placed under the control of a metallothionein promoter. The second recombinant virus (R6004) is identical to R6003 except for the presence of a stop codon inserted at amino acid 70 of the second alpha TIF gene. The metallothionein promoter inserted into the viral genome was shown to be expressed, and alpha TIF mRNA was detected by in situ hybridization of sections of trigeminal ganglia of mice infected with R6003, both untreated and those given cadmium injections. In all experiments, there were no significant differences in the recovery of latent virus from mice infected with R6003 or R6004, whether injected with cadmium or not. Cadmium administration at the time of infection and at intervals thereafter did not preclude establishment of latency. In another series of experiments, transgenic mice expressing the metallothionein-driven alpha TIF did not differ from nontransgenic siblings with respect to the incidence of latent virus in trigeminal ganglia. We conclude that the absence of alpha TIF cannot alone account for the establishment of latency.
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PMID:Expression of the herpes simplex virus 1 alpha transinducing factor (VP16) does not induce reactivation of latent virus or prevent the establishment of latency in mice. 185 65

To evaluate the air pollution in operating rooms when anesthesia is carried out with an open-circuit anesthesia delivery system, two analyzers were tested both in the laboratory and in an operating room. The TIF 5500, a laptop instrument, allows the detection of gas with low ionisation potential such as chloro-fluorocarbons (lower detection threshold: 3 ppm). The Bruel & Kjaer 1302 allows the simultaneous determination of the concentrations of the different inhalation anesthetics in the room by photoacoustic spectrometry. For this type of study, the latter proved an excellent instrument.
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PMID:[Techniques for evaluating the level of pollution in operating rooms due to gaseous or volatile anesthetics]. 188 67

Cells of the human erythroleukemia cell line K562 constitutively secrete a factor that inhibits human T lymphocyte proliferation induced via CD3/Ti. The factor, termed K-TIF (K562-derived T cell inhibitory factor) is produced in either the presence or absence of fetal calf serum in cultures of K562 cells and can be precipitated by 70% NH4SO4. Gel filtration chromatography on Superose 12 resin by FPLC showed that the inhibitory factor has a molecular weight of approximately 30-35 kDa. A protein of this size, metabolically labeled with [35S]methionine, specifically bound human peripheral blood mononuclear cells. Chromatofocusing with Mono P by FPLC (pH gradient 7.2-5) indicates that the inhibitory factor has an isoelectric point of 6.0-6.4.
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PMID:Identification and characterization of a T cell growth inhibitory factor produced by K562 erythromyeloid cells. 191 42

Faithful and efficient transcription initiation at the mouse ribosomal gene promoter requires besides RNA polymerase I (pol I) four polypeptide trans-acting factors, termed TIF-IA, TIF-IB, TIF-IC, and mUBF. We have partially purified these proteins from cultured Ehrlich ascites cells and show that in the presence of TIF-IA and TIF-IB, pol I directs very low amounts of specific transcripts. Neither TIF-IC nor mUBF on their own significantly stimulate the efficiency of template utilization. However, both factors together strongly activate transcription. Interestingly, factor TIF-IB - the murine homologue of human SL1 - fails to program a human extract to transcribe the murine template, but requires its homologous RNA polymerase I. This finding implicates that not only some rDNA transcription factors but also pol I exhibits species-specific differences. The growth-related factor TIF-IA, on the other hand, stimulates both mouse and human rDNA transcription. This regulatory factor whose amount or activity fluctuates according to the proliferation rate of the cells, is functionally inactivated by antibodies against cdc2 protein kinase. This result together with the observation that transcription is stimulated by ATP-gamma S, an ATP analogue which is a substrate for protein kinases but not for protein phosphatases, strongly suggests that post-translational protein modification is involved in rDNA transcription regulation.
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PMID:Trans-acting factors involved in species-specificity and control of mouse ribosomal gene transcription. 192 92

Trans-activation by the herpes simplex virus (HSV) protein, alpha TIF (VP16), is dependent on an inducible enhancer sequence that contains a homolog of the octamer element. An ordered series of multiprotein complexes can be assembled on this enhancer, requiring the interactions of Oct-1, alpha TIF, and two additional cellular factors (C1 and C2). Oct-1 binds to the octamer homolog, whereas alpha TIF, also a sequence-specific DNA-binding protein, recognizes sequences within the HSV enhancer core. The partially purified C1 factor interacts directly with alpha TIF in the absence of DNA and is required to form a stabile Oct-1/alpha TIF/C1 factor complex. The POU domain of Oct-1 is a bipartite sequence recognition structure, as both the POU-specific box and the POU homeo box contribute directly to the recognition of the octamer element. Surprisingly, the POU homeo box alone is sufficient to direct the cooperative binding of alpha TIF and to assemble the Oct-1/alpha TIF/C1 factor complex.
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PMID:Interactions of the Oct-1 POU subdomains with specific DNA sequences and with the HSV alpha-trans-activator protein. 198 Jun 58

The new SKY epidural catheter was evaluated, based upon information collected about implant and use of 53 catheters by 51 patients. Catheters were used to treat chronic pain of a malignant (n = 25) and nonmalignant (n = 28) origin. Of 3450 treatment days, 89% occurred at home. Mean catheter use for malignant and nonmalignant conditions were 58.6 and 76.3 days/patient, respectively. Visual analogue pain scores in the first wk after implant indicated 79% of patients achieved good to excellent pain relief. Clinical impressions indicated this group achieved substantial long-term pain relief. No serious complications were observed. Two types of leakage required removing 5 catheters, prompting changes that eliminated subsequent leakages of both types. Accidental patient retraction and subcutaneous infection each required a catheter removal. No subarachnoid or epidural infections occurred. The SKY catheter proved to be safe and reliable. Therapy was cost-effective, since patients achieved substantial pain relief while treated at home.
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PMID:Initial clinical experience with the SKY epidural catheter. 201 55

In herpes simplex virus 1-infected cells, the first set of genes to be expressed (alpha genes) is induced by the alpha gene trans-inducing factor (alpha TIF), a virion structural protein. The cis-acting site in the 5' untranscribed domain of alpha genes was previously reported to be the sequence 5'-GYATGNTAATGARATTCYTTGNGGG noncoding (where Y is a pyrimidine, R is a purine, N is any base), which binds a host protein designated alpha H1 (also termed the octamer binding protein, OTF-1, Oct-1, etc.) and which, together with this and possibly other proteins, forms complexes with alpha TIF. To determine the role of the various components of this cis-acting site and of other sequences shared by the alpha genes, we constructed 17 mutants spanning 110 nucleotides of the promoter domain of the alpha 27 gene and made a series of chimeric genes. Each chimeric gene embodying one set of these mutations was inserted into the viral genome and measurements were made of (i) accumulated mRNA under conditions in which only alpha genes were expressed and (ii) the capacity of the mutated sequence to form complexes containing alpha TIF and alpha H1 proteins. We report that (i) transversions in the "TAAT" sequence abolished both complex formation and induction of the chimeric alpha gene, (ii) mutations in the octamer binding site sequence upstream from TAAT or of the downstream GARAT abolished alpha TIF complex formation and also reduced alpha mRNA accumulation, (iii) mutations in a "CAAT" box also reduced expression of mRNA without affecting the formation of DNA-protein complexes containing alpha TIF, and (iv) mutations in sequences immediately downstream from TAATGARAT and in a pair of GA-rich elements reduced alpha mRNA expression whereas mutations between these elements had no effect on the accumulation of the mRNA. The results are consistent with the conclusion that both the alpha H1 octamer binding site ATGNTAAT and the GARAT sequence play a significant role in the induction of alpha genes. For optimal gene expression, however, additional elements downstream from the GARAT sequence and in other regions of the alpha promoter must be present.
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PMID:Mutational analysis of the promoter region of the alpha 27 gene of herpes simplex virus 1 within the context of the viral genome. 216 72

The murine ribosomal gene promoter contains two cis-acting control elements which operate in concert to promote efficient and accurate transcription initiation by RNA polymerase I. The start site proximal core element which is indispensable for promoter recognition by RNA polymerase I (pol I) encompasses sequences from position -39 to -1. An upstream control element (UCE) which is located between nucleotides -142 and -112 stimulates the efficiency of transcription initiation both in vivo and in vitro. Here we report the isolation and functional characterization of a specific rDNA binding protein, the transcription initiation factor TIF-IB, which specifically interacts with the core region of the mouse ribosomal RNA gene promoter. Highly purified TIF-IB complements transcriptional activity in the presence of two other essential initiation factors TIF-IA and TIF-IC. We demonstrate that the binding efficiency of purified TIF-IB to the core promoter is strongly enhanced by the presence in cis of the UCE. This positive effect of upstream sequences on TIF-IB binding is observed throughout the purification procedure suggesting that the synergistic action of the two distant promoter elements is not mediated by a protein different from TIF-IB. Increasing the distance between both control elements still facilitates stable factor binding but eliminates transcriptional activation. The results demonstrate that TIF-IB binding to the rDNA promoter is an essential early step in the assembly of a functional transcription initiation complex. The subsequent interaction of TIF-IB with other auxiliary transcription initiation factors, however, requires the correct spacing between the UCE and the core promoter element.
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PMID:Isolation and functional characterization of TIF-IB, a factor that confers promoter specificity to mouse RNA polymerase I. 232 84

The blood-brain barrier (BBB) transport of choline was compared between stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar KY rats (WKY). The permeability surface area product (PS) of [3H]choline through the BBB in SHRSP (3.03 X 10(-3) +/- 1.09 X 10(-3) ml/min/g brain) was significantly lower than that in WKY (7.23 X 10(-3) +/- 0.97 X 10(-3) ml/min/g brain) in the presence of respective rat sera. No significant difference in the brain vascular space was indicated from the apparent uptake of [3H]sucrose between SHRSP and SKY. There was no significant difference for the Michaelis constant of choline transport between SHRSP (262 +/- 97 microM) and WKY (180 +/- 32 microM). However, the maximum velocity in SHRSP (3.41 +/- 1.19 nmol/min/g brain) was 37% lower than in WKY (5.40 +/- 0.38 nmol/min/g brain). Brain microdialysis technique was employed to collect the brain interstitial fluid in the rat hippocampus. The concentration of free choline in the brain dialysate in SHRSP was about half of that in WKY, while no significant difference was observed for the plasma concentration of free choline between SHRSP and WKY. In contrast, no significant difference was observed for the transport of D-[3H]glucose, 3-methyl-[3H]D-glucose and [3H]-phenylalanine through the BBB between SHRSP and WKY. Accordingly, the decreased choline concentration in the brain interstitial fluid ascribed to the specific dysfunction of the BBB choline transport has been demonstrated in SHRSP.
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PMID:Dysfunction of choline transport system through blood-brain barrier in stroke-prone spontaneously hypertensive rats. 234 66


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