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2.3.1.35: glutamate N-acetyltransferase

This is an abbreviated version!
For detailed information about glutamate N-acetyltransferase, go to the full flat file.

Word Map on EC 2.3.1.35

Reaction

N2-Acetyl-L-ornithine
+
L-glutamate
=
L-ornithine
 +
N-acetyl-L-glutamate

Synonyms

acetylglutamate synthetase, acetylglutamate-acetylornithine transacetylase, acetylglutamic synthetase, acetylglutamic-acetylornithine transacetylase, acetylornithinase, acetylornithine glutamate acetyltransferase, acetyltransferase, glutamate, alpha-N-acetyl-L-ornithine:L-glutamate N-acetyltransferase, argJ, CcOATase, CLGAT, glutamate acetyltransferase, glutamate N-acetyltransferase, L-ornithine acetyltransferase, Mtb OAT, N-acetyl-L-glutamate synthetase, OAT, OAT2, OATase, ornithine acetyl transferase, ornithine acetyltransferase, ornithine transacetylase

ECTree

     2 Transferases
         2.3 Acyltransferases
             2.3.1 Transferring groups other than aminoacyl groups
                2.3.1.35 glutamate N-acetyltransferase

Inhibitors

Inhibitors on EC 2.3.1.35 - glutamate N-acetyltransferase

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INHIBITOR
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
IMAGE
2-Methylornithine
-
-
L-ornithine
N-Bromoacetylornithine
-
-
p-chloromercuribenzoate
-
-
pranlukast
i.e. PRK, is an allosteric inhibitor of the arginine biosynthetic enzyme ornithine acetyltransferase (MtArgJ) in Mycobacterium tuberculosis. PRK treatment remarkably abates the survival of free as well as macrophage-internalized Mtb, and shows enhanced efficacy in combination with standard-of-care drugs. Notably, PRK also reduces the 5-lipoxygenase (5-LO) signaling in the infected macrophages, thereby surmounting an enhanced response against intracellular pathogen. Further, treatment with PRK alone or with rifampicin leads to significant decrease in Mtb burden and tubercular granulomas in Mycobacterium tuberculosis-infected mice lungs. The allosteric inhibitor of MtArgJ acts as a dual-edged sword, by targeting the intracellular bacteria as well as the bacterial pro-survival signaling in the host. PRK treatment reduces the infection-associated apoptosis in the host. PRK is highly effective against in vitro and in vivo survival of Mtb and being an FDA-approved drug, it shows a potential for development of advanced combinatorial therapy against tuberculosis. The selectivity and specificity of this inhibitor lies in its ability to allosterically modulate the substrate-binding interface, binding structure, overview. PRK also targets the host macrophage leukotriene signaling to limit the intracellular Mtb growth
sorafenib
i.e. SRB, shows marked reduction in Mycobacterium tuberculosis survival in combination with standard-of-care anti-TB drugs
additional information
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