2.3.1.97: glycylpeptide N-tetradecanoyltransferase
This is an abbreviated version!
For detailed information about glycylpeptide N-tetradecanoyltransferase, go to the full flat file.
Word Map on EC 2.3.1.97
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2.3.1.97
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myristate
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n-myristoylation
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albicans
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leishmania
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octapeptide
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co-translational
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pp60src
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14-carbon
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nonmyristoylated
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medicine
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benzofuran
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drug development
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molecular biology
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synthesis
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analysis
- 2.3.1.97
- myristate
-
n-myristoylation
- albicans
- leishmania
- octapeptide
-
co-translational
-
pp60src
-
14-carbon
-
nonmyristoylated
- medicine
- benzofuran
- drug development
- molecular biology
- synthesis
- analysis
Reaction
Synonyms
CaNMT, cell division control protein 72, dipeptide N-myristoyltransferase 2, glycylpeptide N-tetradecanoyltransferase, glycylpeptide N-tetradecanoyltransferase 1, glycylpeptide N-tetradecanoyltransferase 2, HsNMT1, HsNMT2, LmNMT, More, myristoyl-CoA-protein N-myristoyltransferase, myristoyl-CoA: protein N-myristoyltransferase, myristoyl-CoA:protein N-myristoyltransferase, myristoyl-CoA:protein N-myristoyltransferase 1, myristoyl-CoA:protein N-myristoyltransferase 2, myristoyl-CoA:protein N-myristoyltransferase type 2, myristoyl-coenzyme A:protein N-myristoyl transferase, myristoyl-coenzyme A:protein N-myristoyltransferase, myristoylating enzymes, myristoyltransferase, myristoyltransferase type 1, myristoyltransferase, protein N-, N-myristoyl transferase, N-myristoyltransferase, N-myristoyltransferase 1, N-myristoyltransferase 2, NMT, NMT 1, NMT 2, NMT-1, NMT-2, NMT1, Nmt1p, NMT2, peptide N-myristoyltransferase, peptide N-myristoyltransferase 1, peptide N-myristoyltransferase 2, protein N-myristoyltransferase, PVX_085815, TbNMT, type I N-myristoyltransferase, type II N-myristoyltransferase
ECTree
2.3.1.97 glycylpeptide N-tetradecanoyltransferaseAdvanced search results
results (
results (Engineering
Engineering on EC 2.3.1.97 - glycylpeptide N-tetradecanoyltransferase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
K107E/K252E
substitution does not alter catalytic efficiency with respect to the wild-type
Y180F/N246A
substitution does not alter catalytic efficiency with respect to the wild-type
A202T
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site-directed mutagenesis, alterations of both peptide and myristoyl binding sites, 3 to 6fold increased Ki for S-(2-oxo)-pentadecyl-CoA and 6 to 9fold increased Ki for SC-58272
C217R
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site-directed mutagenesis, 3 to 6fold increase in Ki for inhibitor SC-58272, selective alteration of the enzymes peptide binding site
D417V
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site-directed mutagenesis, reduced activity, temperature-sensitive
D451K
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site-directed mutagenesis, no functional complementation of enzyme deficient nmt1-181 mutant at 36°C
D451N
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site-directed mutagenesis, no functional complementation of enzyme deficient nmt1-181 mutant at 36°C
E167K
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site-directed mutagenesis, coexpression of wild-type with Asp451, functional complementation of enzyme deficient nmt1-181 mutant at 36°C
E293K
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site-directed mutagenesis, coexpression of wild-type with Asp451, functional complementation of enzyme deficient nmt1-181 mutant at 36°C
F170A/L171A
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site-directed mutagenesis, increased Ki for S-(2-oxo)-pentadecyl-CoA, increased Km for peptide substrate, altered enzyme conformation which modifies myristoyl-CoA polarization during catalytic reaction
F413S
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site-directed mutagenesis, reduced activity, temperature-sensitive
K389I
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site-directed mutagenesis, reduced activity, temperature-sensitive
L171S
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site-directed mutagenesis, reduced activity, temperature-sensitive
L408S
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site-directed mutagenesis, reduced activity, temperature-sensitive
L420S
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site-directed mutagenesis, reduced activity, temperature-sensitive
N102T
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site-directed mutagenesis, reduced activity, temperature-sensitive
N169L
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site-directed mutagenesis, slightly increased Km for peptide substrate, altered kinetics
N169L/T205A
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site-directed mutagenesis, increased Km for peptide substrate, altered kinetics
N426I
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site-directed mutagenesis, mutation of myristoyl-binding site
V395D
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site-directed mutagenesis, reduced activity, temperature-sensitive
additional information
additional information
transgenic plants expressing the enzyme under control of the cauliflower mosaic virus 35S promotor, down-regulation by anti-sense expression leads to a growth reduced or lethal phenotype
additional information
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transgenic plants expressing the enzyme under control of the cauliflower mosaic virus 35S promotor, down-regulation by anti-sense expression leads to a growth reduced or lethal phenotype
additional information
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NMT1 knockdown increases apoptosis in activated neutrophils
additional information
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diverse mutants, evaluation of inhibition mechanism of inhibitor SC-58272 and compounds 1-5
additional information
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NMT1 knockout in U-937 cells by siRNA leads to defective monocytic differentiation
additional information
selectively depletion by siRNA of NMT1 and/or NMT2 from HEK-293T cells expressing a recombinant NefsgGFP fusion protein, NMT1 depletion has minimal effect on the intracellular distribution of Nef-sgGFP, whereas depletion of NMT2 alters distribution to a diffuse, widespread pattern, mimicking that of a myristoylation-deficient mutant of Nef-sgGFP, overview
additional information
selectively depletion by siRNA of NMT1 and/or NMT2 from HEK-293T cells expressing a recombinant NefsgGFP fusion protein, NMT1 depletion has minimal effect on the intracellular distribution of Nef-sgGFP, whereas depletion of NMT2 alters distribution to a diffuse, widespread pattern, mimicking that of a myristoylation-deficient mutant of Nef-sgGFP, overview
additional information
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selectively depletion by siRNA of NMT1 and/or NMT2 from HEK-293T cells expressing a recombinant NefsgGFP fusion protein, NMT1 depletion has minimal effect on the intracellular distribution of Nef-sgGFP, whereas depletion of NMT2 alters distribution to a diffuse, widespread pattern, mimicking that of a myristoylation-deficient mutant of Nef-sgGFP, overview
additional information
characterziation of a truncation mutant devoid of 28 N-terminal amino acids from the catalytic module. The deletion of the N-terminal peptide has no effect on the enzyme stability. Mutant displays an 3fold increase in enzymatic. The N-terminal region in the catalytic module serves as a regulatory control element
additional information
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characterziation of a truncation mutant devoid of 28 N-terminal amino acids from the catalytic module. The deletion of the N-terminal peptide has no effect on the enzyme stability. Mutant displays an 3fold increase in enzymatic. The N-terminal region in the catalytic module serves as a regulatory control element
additional information
enzyme knockout leads to defective myelopoesis, NMT1 knockout in U-937 cells leads to defective monocytic differentiation. Suppressed macrophage colony forming units are observed in M-CSF-stimulated bone marrow cells from heterozygous Nmt1-deficient mice, while homozygous Nmt1-deficient mouse embryonic stem cells show a drastic reduction of macrophages when stimulated to differentiate by M-CSF
additional information
enzyme knockout leads to defective myelopoesis, NMT1 knockout in U-937 cells leads to defective monocytic differentiation. Suppressed macrophage colony forming units are observed in M-CSF-stimulated bone marrow cells from heterozygous Nmt1-deficient mice, while homozygous Nmt1-deficient mouse embryonic stem cells show a drastic reduction of macrophages when stimulated to differentiate by M-CSF
additional information
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enzyme knockout leads to defective myelopoesis, NMT1 knockout in U-937 cells leads to defective monocytic differentiation. Suppressed macrophage colony forming units are observed in M-CSF-stimulated bone marrow cells from heterozygous Nmt1-deficient mice, while homozygous Nmt1-deficient mouse embryonic stem cells show a drastic reduction of macrophages when stimulated to differentiate by M-CSF
additional information
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temperature sensitive mutant strain nmt1-181, exchange of Gly to Asp, 10fold increased Km for myristoyl-CoA at 36°C
additional information
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temperature sensitive mutant strain nmt1-181, exchange of Gly to Asp, 10fold increased Km for myristoyl-CoA at 36°C
additional information
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C-terminal deletion mutants M454 and L455 produce a 300-400fold reduction in the chemical transformation rate, shift of the rate-limite of the process steps
additional information
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disruption or deletion of nmt1-gene causes recessive lethality
additional information
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knockdown of NMT expression by tetracycline-inducible RNA interference leads to cell death with a block in endocytosis, but vesicle accumulation around the flagellar pocket indicates a defect in vesicular progression following endocytic fusion. Induced parasites have a wild-type or slightly enlarged Golgi apparatus, phenotype and pleiotropic effects, overview
