4.1.1.22: histidine decarboxylase
This is an abbreviated version!
For detailed information about histidine decarboxylase, go to the full flat file.
Word Map on EC 4.1.1.22
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4.1.1.22
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high-dose
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mast
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autologous
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histaminergic
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mucosa
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stomach
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gastrin
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marrow
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alpha-fluoromethylhistidine
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hypothalamus
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hematopoietic
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enterochromaffin-like
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cyclophosphamide
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oxyntic
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allergic
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etoposide
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biogenic
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relapsed
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chromogranin
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thiotepa
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basophil
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decarboxylases
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melphalan
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cimetidine
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tuberomammillary
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carboplatin
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pyrilamine
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stem-cell
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omeprazole
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event-free
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hypergastrinemia
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h1-receptors
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morganii
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morganella
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thioperamide
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mucositis
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carmustine
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standard-dose
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busulfan
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pentagastrin
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tourette
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mepyramine
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sleep-wake
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fundic
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mastocytoma
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reinfusion
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cell-deficient
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drug development
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medicine
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aminergic
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diagnostics
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nutrition
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chlorpheniramine
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snell
- 4.1.1.22
-
high-dose
-
mast
-
autologous
-
histaminergic
- mucosa
- stomach
- gastrin
- marrow
- alpha-fluoromethylhistidine
- hypothalamus
-
hematopoietic
-
enterochromaffin-like
- cyclophosphamide
-
oxyntic
-
allergic
- etoposide
-
biogenic
-
relapsed
-
chromogranin
-
thiotepa
-
basophil
- decarboxylases
- melphalan
- cimetidine
-
tuberomammillary
- carboplatin
-
pyrilamine
-
stem-cell
- omeprazole
-
event-free
-
hypergastrinemia
-
h1-receptors
- morganii
- morganella
- thioperamide
- mucositis
- carmustine
-
standard-dose
-
busulfan
- pentagastrin
- tourette
-
mepyramine
-
sleep-wake
- fundic
- mastocytoma
-
reinfusion
-
cell-deficient
- drug development
- medicine
-
aminergic
- diagnostics
- nutrition
-
chlorpheniramine
-
snell
Reaction
Synonyms
DCHS, Decarboxylase, histidine, HDC, HdcA, HisDCase, histamine-forming enzyme, L-Histidine decarboxylase, pyruvoyl-dependent decarboxylase, pyruvoyl-dependent histidine decarboxylase, TOM92
ECTree
4.1.1.22 histidine decarboxylaseAdvanced search results
results (
results (Inhibitors
Inhibitors on EC 4.1.1.22 - histidine decarboxylase
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INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
epigallocatechin gallate
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time-dependent inhibition, only under aerobic conditions
methyl L-histidinate
the compound is able to block the reaction at the Michaelis complex step in HDC
pyridoxal 5'-phosphate
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non-competitive inhibition with respect to His, at high concentrations
pyridoxyl-histidine methyl ester conjugate
structure-based inhibitor, binding structure
rugosin A methyl ester
compound isolated from Filipendula ulmaria, non-competitive
tellimagrandin II
compound isolated from Filipendula ulmaria, non-competitive
alpha-Fluoromethylhistidine
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the (S)-isomer is a suicide substrate inhibitor, the (R)-isomer is an at least 10times less potent inhibitor
epigallocatechin-3-gallate
EGCG, the inhibitory effect is mediated by blocking the entrance to the catalytic site, therefore, preventing substrate binding
epigallocatechin-3-gallate
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antiproliferative and antangiogenic component of green tea, 0.1 mM, 67% and 57% inhibition of recombinant and native HDC, respectively
epigallocatechin-3-gallate
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direct inhibitory effect on both histidine decarboxylase and DOPA decarboxylase. Modeling of binding to the enzymes. The presence of epigallocatechin-3-gallate contiguous to the active site entrance leads to the movement of several residues in the active site. Epigallocatechin-3-gallate occludes the entrance channel to the enzyme active site and establishes new interactions with residues in the active site. These residues turn outward when the active site collapses. After docking of epigallocatechin-3-gallate, neither histidine nor the inhibitors histidine methyl ester and alpha-fluoromethyl histidine are able to bind to the enzyme
NaCl
2 M, 50% residual activity, 4.3 M, residual activity is 80%, 69%, and 38% of that of the enzyme in NaCl-free conditions at pH 5.0, 5.5, 6.0, respectively
additional information
design, synthesis, and test of potentially membrane-permeable pyridoxyl-substrate conjugates as inhibitors for human HDC and modeling of an active site for hHDC, which is compatible with the experimental data, structure-activity relationship, overview
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additional information
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design, synthesis, and test of potentially membrane-permeable pyridoxyl-substrate conjugates as inhibitors for human HDC and modeling of an active site for hHDC, which is compatible with the experimental data, structure-activity relationship, overview
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additional information
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treatment of mast cells in systemic mastocytosis with pharmacologic inhibitors prednisone, IFNalpha, and 2CdA only slightly inhibit expression of HDC, overview
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additional information
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poor inhibition by procatechiuc acid, ferulic acid, chlorogenic acid, and ellagic acid, no inhibition by luteorin, apigenin and rutin
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additional information
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1-metylhistidine, L-phenylalanine, L-tryptophan, tert-butyloxycarbonyl-modified ornithine, and tert-butyloxycarbonyl-modified alpha,gamma-diaminobutyric acid do not inhibit human HDC in mast cells and cell extracts significantly
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additional information
successful strategies to inhibit the decarboxylase have included the synthesis of fluoro-derivatives, which act as competitive and/or suicide inhibitors, as it is the case of alpha-fluoromethylhistidine
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additional information
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successful strategies to inhibit the decarboxylase have included the synthesis of fluoro-derivatives, which act as competitive and/or suicide inhibitors, as it is the case of alpha-fluoromethylhistidine
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additional information
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histamine causes a decrease in the expression of gene hdc
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additional information
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knockdown of the transcription factor C/EBPbeta by dehydroxymethylepoxyquinomicin reduces the HDC expression in lipopolysaccharide-treated cells
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additional information
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histamine causes a decrease in the expression of gene hdc
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additional information
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histamine causes a decrease in the expression of gene hdc
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additional information
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Lac-B (a mixture of freeze-dried Bifidobacterium infantis and Bifidobacterium longum) shows significant anti-allergic effect through suppression of both H1R and HDC gene expression followed by decrease in H1R, HDC protein level, and histamine content, oral administration of the Lac-B suspension significantly suppresses the toluene 2,4-diisocyanate-induced HDC mRNA up-regulation
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