Disease relevance of POLYGLUTAMIC ACID

• These data show that in Escherichia coli potassium glutamate stimulates transcription by disengaging inhibitory polymerase interactions at a sigma(38) promoter [1].
• Enteric bacteria and osmotic stress: intracellular potassium glutamate as a secondary signal of osmotic stress [2]?
• Studies performed with crude membrane preparations showed that cyclic 1,2-beta-glucan synthetase of BRUCELLA: spp. was not inhibited by 0.5 M KCl or potassium glutamate; concentrations that completely inhibit the osmosensitive enzymes of A. tumefaciens A348 or R. meliloti 102F34, respectively encoded by the chvB or ndvB genes [3].
• In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA: cyclic 1, 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM: or RHIZOBIUM: backgrounds [3].
• The bidisperse, so-called dual sedimentation was shown to occur mainly with nascent high-concentration phage stocks in potassium glutamate containing media [4].

High impact information on POLYGLUTAMIC ACID

• The adaptation strategy involves production of the salt potassium glutamate, which induces a specific gene expression program that produces electro-neutral osmolytes while inhibiting general sigma(70) transcription [1].
• Potassium glutamate as a transcriptional inhibitor during bacterial osmoregulation [5].
• Thus, potassium glutamate mediates a global transcription switch by acting differentially on RNA polymerase at sets of genomic promoters that differ in their built-in direct response to this salt [5].
• The ionic compound potassium glutamate specifically stimulated proU-lacZ expression in a concentration-dependent manner [6].
• In the presence of 120 mmol/L potassium glutamate, the slope conductance of single rat Cx40 gap junction channels measured 158 +/- 2 pS (n = 4) [7].

Chemical compound and disease context of POLYGLUTAMIC ACID

• Transient accumulation of potassium glutamate and its replacement by trehalose during adaptation of growing cells of Escherichia coli K-12 to elevated sodium chloride concentrations [8].
• We used our human head injury data base to determine relationships between potassium, glutamate, lactate and cerebral blood flow (CBF) [9].
• In filtered natural seawater supplemented with potassium glutamate, the ability of Escherichia coli MC4100 cells to grow on a complex medium was enhanced as a logarithmic function of the external glutamate concentration [10].
• Analysis of the hematoma contents showed that hemolysis-related parameters, such as potassium, glutamate oxaloacetate transaminase, bilirubin, lactate dehydrogenase, and protein concentration, were markedly higher than in the peripheral blood, and there were significant correlations between these parameters [11].

Biological context of POLYGLUTAMIC ACID

• Further analysis revealed that the activation of ATP hydrolysis is an outcome of a shift in the optimum magnesium salt concentration from 0.5 mM with 0.05 M KCl to 4 mM with 0.15 M potassium glutamate [12].
• The motion of optically detected organelles in myelinated axons of Xenopus laevis was studied in axons bathed in a potassium glutamate based medium and in axons in a similar medium to which various inhibitors of axonal transport were added [13].

Anatomical context of POLYGLUTAMIC ACID

• Effective nucleosome assembly in HeLa cell extracts occurred at 125 to 200 mM KCl or potassium glutamate [14].
• High concentrations of KCl, but not of potassium glutamate, were found to inhibit glycogen synthesis in permeabilized hepatocytes [15].
• The swelling of enterocyte mitochondria in potassium glutamate was slow [16].
• This short review surveys the mechanisms of the intracellular pH changes induced in astrocytes by extracellular potassium, glutamate, and ammonium [17].
• Furthermore, at optimal salt concentration, KCl and potassium glutamate activated AIIt-dependent aggregation of chromaffin granules to maximum values of about 210% and 195% of control, respectively, whereas potassium phosphate supported AIIt-dependent aggregation of chromaffin granules to only 120% of control [18].

Associations of POLYGLUTAMIC ACID with other chemical compounds

• Osmotic shock caused the release of potassium glutamate, trehalose, and glycine betaine from wild type cells and cells lacking MscL [19].
• Pol epsilon (as well as pols alpha and delta) is optimally active in 100-150 mM potassium glutamate and 15 mM MgCl2 [20].
• In the presence of natural osmolytes trimethylamine N-oxide (TMAO) or potassium glutamate, refolding GS monomers readily aggregate into very large inactive complexes and fail to reactivate even at low protein concentration [21].
• When IMP was added, synergistic responses were shown only for MPG and L-AP4, but not for NMDA, KA and AMPA [22].
• We demonstrate here that replacing potassium chloride (KCl) with potassium acetate (KAc) or potassium glutamate (KGlu) routinely enhances the yield of RNA intermediates and products obtained from in vitro splicing reactions performed in HeLa cell nuclear extract [23].

Gene context of POLYGLUTAMIC ACID

• MAP4 enhanced the responses to MPG and L-AP4 [22].
• The termination efficiencies with lambda-tR1 and the promoter proximal lacZ intragenic terminators were significantly higher with 0.1-0.2 M potassium glutamate as the major electrolyte than with the optimal concentrations of KCl (approximately 0.05 M) or potassium acetate (approximately 0.15 M) [12].
• Equimolar ion substitution of 120 mmol/L KCl for potassium glutamate was used to determine the unitary conductance ratios for rat connexin40 and connexin43, chicken connexin43 and connexin45, and human connexin37 channels functionally expressed in communication-deficient mouse neuroblastoma (N2A) cells [24].
• The concentrations of potassium acetate and of the physiologically relevant osmolyte potassium glutamate for maximal expression of the proU promoter are approximately 2-fold higher than the concentrations of these salts providing maximal expression of the lacUV5 promoter [25].
• Enhancement of transcription termination factor rho activity with potassium glutamate [12].

Analytical, diagnostic and therapeutic context of POLYGLUTAMIC ACID

• Using gel retardation assays, an affinity constant for IHF binding to the three main sites was estimated in the presence and absence of 0.1 M potassium glutamate, which increased the avidity of IHF binding to the weaker sites by two orders of magnitude [26].
• Stimulatory effect of potassium glutamate in PCR [27].

References