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ApalaDH expression is upregulated by NaCl. PvRA and GxRA activities are detected in vivo and increase about 1.2- and 2.7fold upon salt stress, respectively
both mRNA levels and enzymatic activity increase during entry into nonreplicating persistence. Expression is also induced in vitro by persistence-inducing stresses such as nitric oxide, and the gene is expressed at high levels in vivo during the initial lung infection in mice
expression of the ald gene is strongly upregulated in Mycolicibacterium smegmatis grown in the presence of alanine. Alanine-dependent regulation of ald is mediated by the AldR transcriptional regulator that belongs to the Lrp/AsnC (leucine-responsive regulatory protein/asparagine synthase C) family. A decrease in functionality of the ETC shifts the redox state of the NADH/NAD+x02 pool toward a more reduced state, which in turn leads to an increase in cellular levels of alanine by Ald catalyzing the conversion of pyruvate to alanine with the concomitant oxidation of NADH to NAD+. The induction of ald expression under respiration-inhibitory conditions in Mycolicibacterium smegmatis is mediated by the alanine-responsive AldR transcriptional regulator. Respiration inhibition by KCN induces ald expression in the wild-type strain, but not DELTAaldR mutant strain of Mycolicibacterium smegmatis grown under aerobic conditions
expression of the ald gene is upregulated in Mycobacterium marinum during longterm granulomatous infection in its host
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria. Expression of the ald gene is upregulated in Mycobacterium tuberculosis under nutrient starvation and energy-limiting conditions. The enzyme is strongly induced by the nitric oxide (NO) donor diethylenetriamine/NO, and in vivo during initial lung infection in mice
regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview
regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview. AldR exerts its regulatory effect on ald expression by binding AldR binding sites bearing a consensus sequence of GA/T-N2-NWW/WWN-N2-T/AC (W = A or T, /= or) in Mycobacterium tuberculosis. Three-dimensional structure of AldR and phylogenetic analysis of AldRs from mycobacteria
regulatory gene AldR serves as both activator and repressor for the regulation of ald gene expression, depending on the presence or absence of L-alanine. The purified AldR protein exists as a homodimer in the absence of L-alanine, while it adopts the quaternary structure of a homohexamer in the presence of L-alanine. The binding affinity of AldR for the ald control region is significantly increased by L-alanine
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transcription of ald is induced when alanine is the sole nitrogen source
ApalaDH expression is upregulated by NaCl. PvRA and GxRA activities are detected in vivo and increase about 1.2- and 2.7fold upon salt stress, respectively
ApalaDH expression is upregulated by NaCl. PvRA and GxRA activities are detected in vivo and increase about 1.2- and 2.7fold upon salt stress, respectively
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both mRNA levels and enzymatic activity increase during entry into nonreplicating persistence. Expression is also induced in vitro by persistence-inducing stresses such as nitric oxide, and the gene is expressed at high levels in vivo during the initial lung infection in mice
both mRNA levels and enzymatic activity increase during entry into nonreplicating persistence. Expression is also induced in vitro by persistence-inducing stresses such as nitric oxide, and the gene is expressed at high levels in vivo during the initial lung infection in mice
-
-
expression of the ald gene is strongly upregulated in Mycolicibacterium smegmatis grown in the presence of alanine. Alanine-dependent regulation of ald is mediated by the AldR transcriptional regulator that belongs to the Lrp/AsnC (leucine-responsive regulatory protein/asparagine synthase C) family. A decrease in functionality of the ETC shifts the redox state of the NADH/NAD+x02 pool toward a more reduced state, which in turn leads to an increase in cellular levels of alanine by Ald catalyzing the conversion of pyruvate to alanine with the concomitant oxidation of NADH to NAD+. The induction of ald expression under respiration-inhibitory conditions in Mycolicibacterium smegmatis is mediated by the alanine-responsive AldR transcriptional regulator. Respiration inhibition by KCN induces ald expression in the wild-type strain, but not DELTAaldR mutant strain of Mycolicibacterium smegmatis grown under aerobic conditions
expression of the ald gene is strongly upregulated in Mycolicibacterium smegmatis grown in the presence of alanine. Alanine-dependent regulation of ald is mediated by the AldR transcriptional regulator that belongs to the Lrp/AsnC (leucine-responsive regulatory protein/asparagine synthase C) family. A decrease in functionality of the ETC shifts the redox state of the NADH/NAD+x02 pool toward a more reduced state, which in turn leads to an increase in cellular levels of alanine by Ald catalyzing the conversion of pyruvate to alanine with the concomitant oxidation of NADH to NAD+. The induction of ald expression under respiration-inhibitory conditions in Mycolicibacterium smegmatis is mediated by the alanine-responsive AldR transcriptional regulator. Respiration inhibition by KCN induces ald expression in the wild-type strain, but not DELTAaldR mutant strain of Mycolicibacterium smegmatis grown under aerobic conditions
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-
expression of the ald gene is strongly upregulated in Mycolicibacterium smegmatis grown in the presence of alanine. Alanine-dependent regulation of ald is mediated by the AldR transcriptional regulator that belongs to the Lrp/AsnC (leucine-responsive regulatory protein/asparagine synthase C) family. A decrease in functionality of the ETC shifts the redox state of the NADH/NAD+x02 pool toward a more reduced state, which in turn leads to an increase in cellular levels of alanine by Ald catalyzing the conversion of pyruvate to alanine with the concomitant oxidation of NADH to NAD+. The induction of ald expression under respiration-inhibitory conditions in Mycolicibacterium smegmatis is mediated by the alanine-responsive AldR transcriptional regulator. Respiration inhibition by KCN induces ald expression in the wild-type strain, but not DELTAaldR mutant strain of Mycolicibacterium smegmatis grown under aerobic conditions
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-
expression of the ald gene is upregulated in Mycobacterium marinum during longterm granulomatous infection in its host
expression of the ald gene is upregulated in Mycobacterium marinum during longterm granulomatous infection in its host
-
-
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria
-
-
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria
-
-
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria. Expression of the ald gene is upregulated in Mycobacterium tuberculosis under nutrient starvation and energy-limiting conditions. The enzyme is strongly induced by the nitric oxide (NO) donor diethylenetriamine/NO, and in vivo during initial lung infection in mice
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria. Expression of the ald gene is upregulated in Mycobacterium tuberculosis under nutrient starvation and energy-limiting conditions. The enzyme is strongly induced by the nitric oxide (NO) donor diethylenetriamine/NO, and in vivo during initial lung infection in mice
-
-
hypoxic induction of ald, which is independent of the DevSR (DosSR) two-component system, a major regulatory system involved in oxygen and NO sensing in mycobacteria. Expression of the ald gene is upregulated in Mycobacterium tuberculosis under nutrient starvation and energy-limiting conditions. The enzyme is strongly induced by the nitric oxide (NO) donor diethylenetriamine/NO, and in vivo during initial lung infection in mice
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regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview
regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview
regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview
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regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview
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regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview
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regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview. AldR exerts its regulatory effect on ald expression by binding AldR binding sites bearing a consensus sequence of GA/T-N2-NWW/WWN-N2-T/AC (W = A or T, /= or) in Mycobacterium tuberculosis. Three-dimensional structure of AldR and phylogenetic analysis of AldRs from mycobacteria
regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview. AldR exerts its regulatory effect on ald expression by binding AldR binding sites bearing a consensus sequence of GA/T-N2-NWW/WWN-N2-T/AC (W = A or T, /= or) in Mycobacterium tuberculosis. Three-dimensional structure of AldR and phylogenetic analysis of AldRs from mycobacteria
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regulation mechanism of ald expression by the AldR transcription factor in response to alanine availability, model for the regulation of ald expression by AldR, overview. AldR exerts its regulatory effect on ald expression by binding AldR binding sites bearing a consensus sequence of GA/T-N2-NWW/WWN-N2-T/AC (W = A or T, /= or) in Mycobacterium tuberculosis. Three-dimensional structure of AldR and phylogenetic analysis of AldRs from mycobacteria
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transcription of ald is induced when alanine is the sole nitrogen source
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transcription of ald is induced when alanine is the sole nitrogen source
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