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:2.7.7.6 (RNA polymerase)
34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although recent results suggest roles for NMDA and AMPA receptors in odor encoding, little is known about kainate receptors (KARs) in the olfactory bulb (OB). Molecular, immunological, and electrophysiological techniques were used to provide a functional analysis of KARs in the OB. Reverse transcriptase-polymerase chain reaction revealed that the relative level of expression of KAR subunits was GluR5 approximately GluR6 approximately KA2 > KA1 >> GluR7. In situ hybridization data imply that mitral/tufted cells express mostly GluR5 and KA2, whereas interneurons express mostly GluR6 and KA2. Immunohistochemical double-labeling experiments (GluR5/6/7 or GluR5 + synapsin) suggest that KARs are expressed at both synaptic and extrasynaptic loci. This heterogeneous expression of KAR subunits suggests that KARs may play a multitude of roles in odor processing, each tailored to the function of specific OB circuits. A functional analysis, using whole-cell electrophysiology, suggests that one such role is to increase the frequency of glutamate transmission while attenuating the amplitude of individual events, likely via a presynaptic depolarizing mechanism. Such effects would be important to odor processing particularly by OB glomeruli. In these highly compartmentalized structures, an increase in the frequency of glutamate release and the high density of extrasynaptic KARs, activated by spillover, could enhance glomerular synchronization and thus the transfer of more specific sensory information to cortical structures.
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PMID:Expression and function of kainate receptors in the rat olfactory bulb. 1731 80

In the light of the various neurobiological effects of glutamate in brain development, although some embryonic cells are a probable source of glutamate involved in the development of precursor cells and/or immature neurons, little is known about when and where glutamate plays its crucial roles during corticogenesis. To investigate these roles, we focused on the developmental expression of vesicular glutamate transporter (VGLUT)1 and VGLUT2, which are regarded as the best markers for verifying glutamatergic neuron identity, especially the spatiotemporal distributions of their transcripts and proteins in the developing mouse cortex and hippocampus. In situ hybridization studies revealed that VGLUT1 mRNA is expressed in preplate and marginal zone cells at embryonic day (E)10 and in subplate cells by E13, whereas VGLUT2 mRNA is expressed in preplate and marginal zone cells at E10 and in cells of the subventricular zone by E13. Reverse transcriptase-polymerase chain reaction analysis detected full-length VGLUT1 and VGLUT2 gene transcripts in the embryonic brain. By dual labeling combined with immunostaining for microtubule-associated protein 2 (MAP2) or reelin, we showed that MAP2-positive preplate and marginal zone neurons and subplate neurons express VGLUT1, while reelin-positive preplate and marginal zone cells and MAP2-negative subventricular zone cells express VGLUT2. The present study is the first to provide morphologically reliable evidence showing that Cajal-Retzius cells and subplate neurons are glutamatergic, and that the two cells differentially express VGLUT1 and VGLUT2, respectively, as the specific transport system of glutamate in some events orchestrated by these cells during the cortical development of mice.
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PMID:Cajal-Retzius cells and subplate neurons differentially express vesicular glutamate transporters 1 and 2 during development of mouse cortex. 1765 22

To trigger transcription termination, the ring-shaped RNA-DNA helicase Rho from Escherichia coli chases the RNA polymerase along the nascent transcript, starting from a single-stranded C-rich Rut (Rho utilization) loading site. In some instances, a small hairpin structure divides harmlessly the C-rich loading region into two smaller Rut subsites, best exemplified by the tR1 terminator from phage lambda. Here, we show that the Rho helicase can also elude a RNA structural block located far downstream from the single-stranded C-rich region but upstream from a reporter RNA-DNA hybrid. In this process, Rho hexamers do not melt the intervening RNA motif but require single-stranded RNA segments on both of its sides. The reaction is also favored by physiological glutamate ions and can implicate Rho primary recognition of 5'-YC dimers (as for Rut binding) significantly upstream (>70 nucleotides) from the intervening motif. Surprisingly, we also found that primary interactions of Rho with 2'-hydroxyl groups located upstream from the intervening RNA structure serve to elude the motif. This demonstrates that the preference of Rho for RNA residues is not limited to the secondary interaction site that mediates ATPase-fuelled mechanochemistry within the hexamer central channel. These features could be part of an energy-effective mechanism in which Brownian exploration of the conformation of the Rho-substrate complex and accommodation of downstream secondary structures within a composite primary interaction site replace ATP-dependent translocation of the Rho enzyme along corresponding structured portions of the RNA chain.
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PMID:Noncanonical interactions in the management of RNA structural blocks by the transcription termination rho helicase. 1765 25

The bacterial enhancer binding proteins (bEBP) are members of the AAA+ protein family and have a highly conserved 'DE' Walker B motif thought to be involved in the catalytic function of the protein with an active role in nucleotide hydrolysis. Based on detailed structural data, we analysed the functionality of the conserved 'DE' Walker B motif of a bEBP model, phage shock protein F (PspF), to investigate the role of these residues in the sigma(54)-dependent transcription activation process. We established their role in the regulation of PspF self-association and in the relay of the ATPase activity to the remodelling of an RNA polymerase.promoter complex (Esigma(54).DNA). Specific substitutions of the conserved glutamate (E) allowed the identification of new functional ATP.bEBP.Esigma(54) complexes which are stable and transcriptionally competent, providing a new tool to study the initial events of the sigma(54)-dependent transcription activation process. In addition, we show the importance of this glutamate residue in sigma(54).DNA conformation sensing, permitting the identification of new intermediate stages within the transcription activation pathway.
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PMID:Coupling nucleotide hydrolysis to transcription activation performance in a bacterial enhancer binding protein. 1788 90

In this study, the P2 receptor-mediated modulation of [3H]glutamate and [3H]noradrenaline release were examined in rat spinal cord slices. Adenosine 5'-triphosphate (ATP), adenosine 5'-diphosphate (ADP), and 2-methylthioadenosine 5'-diphosphate (2-MeSADP) decreased the electrical stimulation-evoked [3H]glutamate efflux with the following order of potency: ADP>2-MeSADP>ATP. The effect of ATP was antagonized by suramin (300microM), the P2Y12,13 receptor antagonist 2-methylthioadenosine 5'-monophosphate (2-MeSAMP, 10microM), and partly by 4-[[4-Formyl-5-hydroxy-6-methyl-3-[(phosphonooxy)methyl]-2-pyridinyl]azo]-1,3-benzenedisulfonic acid (PPADS, 30microM) and the P2Y1 receptor antagonist 2'-deoxy-N6-methyladenosine 3',5'-diphosphate (MRS 2179, 10muM). ATP, ADP and 2-MeSADP also decreased evoked [3H]noradrenaline outflow; the order of agonist potency was ADP> or =2-MeSADP>ATP. The effect of ATP was reversed by 2-MeSAMP (10microM), and partly by MRS 2179 (10microM). By contrast, 2-methylthioadenosine-5'-triphosphate (2-MeSATP, 10-300microM) increased resting and electrically evoked [3H]glutamate and [3H]noradrenaline efflux, and this effect was prevented by the P2X1 receptor selective antagonist 4,4',4'',4'''-[carbonylbis[imino-5,1,3-benzenetriyl bis (carbonyl-imino)]] tetrakis (benzene-1,3-disulfonic acid) octasodium salt (NF449, 100nM). Reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed that mRNAs encoding P2Y12 and P2Y13 receptors are expressed in the brainstem, whereas P2Y13 but not P2Y12 receptor mRNA is present in the dorsal root ganglion and spinal cord. P2Y1 receptor expression in the spinal cord is also demonstrated at the protein level. In conclusion, inhibitory P2Y and facilitatory P2X1-like receptors, involved in the regulation of glutamate (P2Y13 and/or P2Y1) and noradrenaline (P2Y13 and/or P2Y1, P2Y12) release have been identified, which provide novel target sites for analgesics acting at the spinal cord level.
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PMID:Modulation of neurotransmitter release by P2X and P2Y receptors in the rat spinal cord. 1806

Bacteria must adapt their transcription to overcome the osmotic stress associated with the gastrointestinal tract of their host. This requires the sigma 38 (rpoS) form of RNA polymerase. Here, chromatin immunoprecipitation experiments show that activation is associated with a poise-and-release mechanism in vivo. A C-terminal tail unique among sigma factors is shown to be required for in vivo recruitment of RNA polymerase to the promoter region prior to osmotic shock. C-terminal domain tail-dependent transcription in vivo can be mimicked by using the intracellular signaling molecule potassium glutamate in vitro. Following signaling, the barrier to elongation into the gene body is overcome and RNA polymerase is released to produce osmY mRNA.
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PMID:Poising of Escherichia coli RNA polymerase and its release from the sigma 38 C-terminal tail for osmY transcription. 1820 23

Glutathione depletion is a key factor in the development of acute pancreatitis. Our aim was to study the regulation of glutamate cysteine ligase, the rate-limiting enzyme in glutathione synthesis, in edematous or necrotizing pancreatitis in rats. Glutathione levels were kept low in necrotizing pancreatitis for several hours, with no increase in protein or mRNA levels of glutamate cysteine ligase subunits, despite binding of RNA polymerase II to their promoters and coding regions. The survival signal pathway mediated by ERK and c-MYC was activated, and c-MYC was recruited to the promoters. The failure in gene up-regulation seems to be due to a marked increase in cytosolic ribonuclease activity. In contrast, in edematous pancreatitis glutathione levels were depleted and rapidly restored, and protein and mRNA expression of glutamate cysteine ligase increased markedly due to enhanced transcription mediated by recruitment of c-MYC, NF-kappaB, and SP-1 to the promoters. No increase in cytosolic ribonuclease activity was found in this case. We propose a novel pathophysiological mechanism to differentiate necrotizing from edematous pancreatitis, which is the inefficient up-regulation of glutamate cysteine ligase caused by increased cytosolic ribonuclease activity in the severe form of the disease. This mechanism would abrogate a rapid recovery of glutathione levels.
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PMID:Glutamate cysteine ligase up-regulation fails in necrotizing pancreatitis. 1827 77

Class III beta-tubulin isotype (betaIII-tubulin) is widely regarded as a neuronal marker in developmental neurobiology and stem cell research. To test the specificity of this marker protein, we determined its expression and distribution in primary cultures of glial fibrillary acidic protein (GFAP)-expressing astrocytes isolated from the cerebral hemispheres of 2 human fetuses at 18 to 20 weeks of gestation. Cells were maintained as monolayer cultures for 1 to 21 days without differentiation induction. By immunofluorescence microscopy, coexpression of betaIII-tubulin and GFAP was detected in cells at all time points but in spatially distinct patterns. The numbers of GFAP+ cells gradually decreased from Days 1 to 21 in vitro, whereas betaIII-tubulin immunoreactivity was present in 100% of cells at all time points. beta-III-tubulin mRNA and protein expression were demonstrated in cultured cells by reverse-transcriptase-polymerase chain reaction and immunoblotting, respectively. Glial fibrillary acidic protein+/beta-III-tubulin-positive cells coexpressed nestin and vimentin but lacked neurofilament proteins, CD133, and glutamate-aspartate transporter. Weak cytoplasmic staining was detected with antibodies against microtubule-associated protein 2 isoforms. Confocal microscopy, performed on autopsy brain samples of human fetuses at 16 to 20 gestational weeks, revealed widespread colocalization of GFAP and betaIII-tubulin in cells of the ventricular/subventricular zones and the cortical plate. Our results indicate that in the midgestational human brain, betaIII-tubulin is not neuron specific because it is constitutively expressed in GFAP+/nestin+ presumptive fetal astrocytes.
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PMID:Class III beta-tubulin is constitutively coexpressed with glial fibrillary acidic protein and nestin in midgestational human fetal astrocytes: implications for phenotypic identity. 1837 34

Mechanisms by which cupric glutamate, a novel algicide, extinguishes Alexandrium sp. LC3 are shown in this study. We show that cupric glutamate not only stimulated the production of malonaldehyde (MDA) and dramatically promoted cell plasma membrane permeability (p < 0.01) but also remarkably reduced sulfhydryl (SH) group content (p < 0.01). Analysis of protein expression profiles by two-dimensional electrophoresis (2-DE) indicated that only 47 protein spots were detected in both control and cupric glutamate treated cells. Three reliable spots were identified by matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS) as ribulose-bisphosphate carboxylase large subunit precursor, RNA polymerase beta chain, and hypothetical protein, which can be well correlated with cupric glutamate stress. Based on above results, we hypothesize that the extinguishing mechanisms include (1) the cell membrane being damaged by cupric glutamate; (2) cupric glutamate probably induced denaturation and disintegration of intracellular protein, which led to inhibition of cell growth.
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PMID:Characterization of cupric glutamate extinguishing mechanism of Alexandrium sp. LC3 with two-dimensional electrophoresis and MALDI-TOF MS. 1844 3

Escherichia coli responds to stress by a combination of specific and general transcription signalling pathways. The general pathways typically require the master stress regulator sigma38 (rpoS). Here we show that the signalling from multiple stresses that relax DNA is processed by a non-conserved eight-amino-acid tail of the sigma 38 C-terminal domain. By contrast, responses to two stresses that accumulate potassium glutamate do not rely on this short tail, but still require the overall C-terminal domain. In vitro transcription and footprinting studies suggest that multiple stresses can target a poised RNA polymerase and activate it by unwrapping DNA from a nucleosome-like state, allowing the RNA polymerase to escape into productive mode. This transition can be accomplished by either the DNA relaxation or potassium glutamate accumulation that characterizes many stresses.
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PMID:General stress response signalling: unwrapping transcription complexes by DNA relaxation via the sigma38 C-terminal domain. 1876 24


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