Disease relevance of gntT

• Analysis of the Escherichia coli gntT and gntU genes and comparison of the products with their homologues [1].

High impact information on gntT

• Positive and negative transcriptional regulation of the Escherichia coli gluconate regulon gene gntT by GntR and the cyclic AMP (cAMP)-cAMP receptor protein complex [2].
• Transcription of gntT is activated by binding of the cyclic AMP (cAMP)-cAMP receptor protein (CRP) complex to a CRP binding site positioned at -71 upstream of the gntT transcription start site [2].
• A gntT::lacZ operon fusion was constructed and used to examine gntT expression [3].
• Molecular genetic characterization of the Escherichia coli gntT gene of GntI, the main system for gluconate metabolism [3].
• In addition, two putative gnt operator sites were identified in the gntT regulatory region [3].

Chemical compound and disease context of gntT

• The gntT gene of Escherichia coli is specifically induced by gluconate and repressed via catabolite repression [2].

Associations of gntT with chemical compounds

• The results indicated that gntT is maximally induced by 500 microM gluconate, modestly induced by very low levels of gluconate (4 microM), and partially catabolite repressed by glucose [3].

Regulatory relationships of gntT

• Our observations suggest that these loci might conform an operon distinct of gntT under the control of the gntR gene product [4].

Analytical, diagnostic and therapeutic context of gntT

• Primer extension analysis indicated two transcriptional start sites for gntT, which are separated by 66 bp and which give rise to what appears on a Northern blot to be a single, gluconate-inducible, 1.42-kb gntT transcript [3].

References