Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
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Gene/Protein
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Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: EC:1.4.1.2 (
glutamate dehydrogenase
)
4,380
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The nitrogen assimilation control protein (NAC) from Klebsiella aerogenes or Escherichia coli (NACK or NACE, respectively) is a transcriptional regulator that is both necessary and sufficient to activate transcription of the histidine utilization (hut) operon and to repress transcription of the
glutamate dehydrogenase
(gdh) operon in K. aerogenes. Truncated NAC polypeptides, generated by the introduction of stop codons within the nac open reading frame, were tested for the ability to activate hut and repress gdh in vivo. Most of the NACK and NACE fragments with 100 or more amino acids (wild-type NACK and NACE both have 305 amino acids) were functional in activating hut and repressing gdh expression in vivo. Full-length NACK and NACE were isolated as chimeric proteins with the maltose-binding protein (MBP). NACK and NACE released from such chimeras were able to activate hut transcription in a purified system in vitro, as were NACK129 and NACE100 (a NACK fragment of 129 amino acids and a NACE fragment of 100 amino acids) released from comparable chimeras. A set of NACE and NACK fragments carrying
nickel
-binding histidine tags (his6) at their C termini were also generated. All such constructs derived from NACE were insoluble, as was NACE itself. Of the his6-tagged constructs derived from NACK, NACK100 was inactive, but NACK120 was active. Several NAC fragments were tested for dimerization. NACK120-his6 and NACK100-his6 were dimers in solution. MBP-NACK and MBP-NACK129 were monomers in solution but dimerized when the MBP was released by cleavage with factor Xa. MBP-NACE was readily cleaved by factor Xa, but the resulting NACE was also degraded by the protease. However, MBP-NACE-his6 was completely resistant to cleavage by factor Xa, suggesting an interaction between the C and N termini of this protein.
...
PMID:The amino-terminal 100 residues of the nitrogen assimilation control protein (NAC) encode all known properties of NAC from Klebsiella aerogenes and Escherichia coli. 992 58
The effects of
nickel
ions on reductive amination and oxidative deamination activities of bovine liver
glutamate dehydrogenase
(
GDH
) were examined kinetically by UV spectroscopy, at 27 degrees C, using 50 mM Tris, pH 7.8, containing 0.1 M NaCl. Kinetic analysis of the data obtained by varying NADH concentration indicated strong inhibition, presumably due to binding of the coenzyme to the regulatory site. In contrast, almost no inhibition was observed in the forward reaction. The fact that
nickel
ions have the capacity to enhance binding of NADH to the enzyme was confirmed by an electrochemical method using a modified glassy carbon electrode. Use of NADPH instead of NADH showed only a weak substrate inhibition, presumably related to lower affinity of NADPH for binding to the regulatory site. Lineweaver-Burk plots with respect to alpha-ketoglutarate and ammonium ions indicated substrate and competitive inhibition patterns in the presence of
nickel
ions, respectively. ADP at 0.2 mM concentration protected inhibition caused by
nickel
. These observations are explained in terms of formation of a
nickel
-NADH complex with a higher affinity for binding to the regulatory site in
GDH
, as compared with the situation where
nickel
is not present. Such effects may be important for regulation of
GDH
and other NADH-utilizing enzymes.
...
PMID:Nickel-induced substrate inhibition of bovine liver glutamate dehydrogenase. 1103 89
A 44-year-old patient died from amyotrophic lateral sclerosis (ALS) after nine years of heavy exposure to cadmium (Cd) in a
nickel
cadmium (Ni-Cd) battery factory. Two years after starting work he and co-workers had experienced pruritus, loss of smell, nasal congestion, nosebleeds, cough, shortness of breath, severe headaches, bone pain, and proteinuria. Upper back pain and muscle weakness progressed to flaccid paralysis. EMG findings were consistent with motor neuron disease. Cd impairs the blood-brain barrier, reduces levels of brain copper-zinc (Cu-Zn) superoxide dismutase (SOD), and enhances excitoxicity of glutamate via up-regulation of
glutamate dehydrogenase
and down-regulation of glutamate uptake in glial cells. High levels of methallothionein, a sign of exposure to heavy metals, have been found in brain tissue of deceased ALS patients. The effects of Cd on enzyme systems that mediate neurotoxicity and motor neuron disease suggest a cause effect relationship between Cd and ALS in this worker.
...
PMID:Amyotrophic lateral sclerosis in a battery-factory worker exposed to cadmium. 1137 40
Hydrogen sulfide (H
2
S) modulates plant tolerance to abiotic stresses, but its regulatory effects on nitrogen metabolism and chloroplast protection under
nickel
(Ni) stress in crop plants remain elusive. Taking this into account, we investigated the potential roles of sodium hydrosulfide (NaHS), a H
2
S generator, in the improvement of growth performance of rice plants under Ni stress. Results showed that NaHS successfully reversed the adverse effects of Ni, as reflected in plant growth and biomass, and photosynthesis attributes including photosynthetic rates, stomatal conductance, transpiration rate, internal CO
2
concentration and photosynthetic pigment contents. NaHS generated H
2
S plays a crucial role in controlling the photosynthetic machinery of rice as evidenced by the ultrastructure of chloroplast viewed under transmission electron microscope (TEM). The reduced content of Ni in roots and leaves of NaHS-supplemented Ni-stressed plants has revealed the restricted uptake and accumulation of Ni. A rescue of NaHS to the Ni-induced decline in nitrate (NO
3
-
) content and the activities NO
3
-
biosynthesizing enzymes nitrate reductase, nitrite reductase, glutamate synthase, glutamate oxaloacetate transaminase, glutamine synthetase, and glutamate pyruvate transaminase in leaves indicated a positive role of H
2
S on NO
3
-
metabolism in rice under Ni stress. NaHS application also reverted Ni-mediated increases in ammonium (NH
4
+
) content and
glutamate dehydrogenase
activity, implying H
2
S-induced alleviation of NH
4
+
toxicity. The regulatory effects of H
2
S on nitrogen metabolism was further confirmed by increased and decreased transcript abundance of NO
3
-
and NH
4
+
metabolism associated genes, respectively. Our study suggests a decisive role of H
2
S in controlling Ni toxicity as elucidated by the novel findings such as enhanced gas exchanged parameters, Ni homeostasis and chloroplast protection. Moreover, this article highlights the significance of H
2
S in controlling chloroplast biogenesis and nitrogen metabolism in rice crop under Ni stress.
...
PMID:Hydrogen sulfide enhances rice tolerance to nickel through the prevention of chloroplast damage and the improvement of nitrogen metabolism under excessive nickel. 3085 14
