Disease relevance of kefC

• Analysis of this phenomenon has shown that suppression is specific to the KefC system, but that cloned kefC from Klebsiella and Erwinia can also mediate suppression of the mutant phenotype [1].
• Using the cloned Escherichia coli kefC gene as a probe for Southern hybridization it was shown that only limited DNA sequence homology exists with other bacteria, even when closely related members of the enteric group were examined [2].

High impact information on kefC

• These results suggest that the products of trkB and trkC genes are essential for the formation of the potassium channel and glutathione plays an important role in the gating process [3].
• Cloned kefC was found to suppress the phenotype of two such mutants kefC121 and kefC103 [1].
• A number of kefC mutants that affect K+ retention by the KefC system have been isolated and all retain activation by NEM [1].
• Targeted disruption of the neurotrophin-3 gene with lacZ induces loss of trkC-positive neurons in sensory ganglia but not in spinal cords [4].
• Furthermore, trimethoprim resistance and elevated enzyme levels were associated with ColE1 plasmids that carried DNA from the trkC ksgA pdxA region of the E. coli chromosome [5].

Anatomical context of kefC

• In contrast, we did not find any morphological abnormalities, significant cell loss or decreased levels of trkC expression in the motor neurons present in the ventral horn of the spinal cord [4].

Associations of kefC with chemical compounds

• The critical factor is the formation of specific glutathione metabolites that activate transport systems encoded by the kefB and kefC gene products [6].

References