4.1.1.29: sulfinoalanine decarboxylase
This is an abbreviated version!
For detailed information about sulfinoalanine decarboxylase, go to the full flat file.
Word Map on EC 4.1.1.29
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4.1.1.29
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dioxygenase
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taut
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cystathionase
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transsulfuration
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taurine-deficient
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taurine-free
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nutrition
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medicine
- 4.1.1.29
- dioxygenase
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taut
- cystathionase
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transsulfuration
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taurine-deficient
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taurine-free
- nutrition
- medicine
Reaction
Synonyms
BsCSAD, CAD, CADCase, CgCSAD1, CgCSAD2, CSAD, CSAD/CAD, CSADCase, CSADI, CSADII, CSD, Cysteic acid decarboxylase, Cysteic decarboxylase, Cysteine sulfinate decarboxylase, Cysteine sulfinic acid decarboxylase, Cysteine-sulfinate decarboxylase, Cysteinesulfinate decarboxylase, Cysteinesulfinic acid decarboxylase, Decarboxylase, cysteinesulfinate, L-Cysteine sulfinate carboxy-lyase, L-cysteine sulfinate decarboxylase, L-Cysteinesulfinic acid decarboxylase, Sulfinoalanine decarboxylase, undec1A
ECTree
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Engineering
Engineering on EC 4.1.1.29 - sulfinoalanine decarboxylase
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Q377L
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mutation diminishes the decarboxylation activity to aspartate with no major effect on its activity to cysteine sulfinic acid. Mutation leads to increase in the zwitterion form of the internal aldimine tautomer
V81L/F240S/I250S/D266L
generation of mutant Undec1A-1180 by random mutagenxadesis through sequential error-prone PCR from a mutagenesis library. The mutant has 5.62fold highxader specific activity than wild-type Undec1A at 35°C and pH 7.0. The optimum pH of Undec1A-1180 does not change. Molecular docking results indicatxade that amino acid residues Ala235, Val237, Asp239, Ile267, Ala268, and Lys298 in mutant Unxaddec1A-1180 protein help recognize substrate molecules and catalyze the reaction with of L-cysteine sulfinic acid. Mutation efficiency analysis of different combinations of Mg2+ and Mn2+, overview
additional information
the dominant melanic mutation called chocolate implicates the gene encoding pyridoxal phosphate-dependant cysteine sulfinic acid decarboxylase. Mutation causes a dramatic darkening of larvae, without having any detectable effects during other developmental stages
additional information
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the dominant melanic mutation called chocolate implicates the gene encoding pyridoxal phosphate-dependant cysteine sulfinic acid decarboxylase. Mutation causes a dramatic darkening of larvae, without having any detectable effects during other developmental stages
additional information
CDO-CSD fusion protein, cysteine dioxygenase and cysteine sulfinate decarboxylase
additional information
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CDO-CSD fusion protein, cysteine dioxygenase and cysteine sulfinate decarboxylase
additional information
generation of CSAD knockout mice, chimeric CSAD KO mice are produced by injection of cells from a gene trap ES cell line (XP0392) into C57BL/6 (B6) blastocysts which are implanted into a pseudopregnant B6 mouse. Nine chimeric mice are mated with B6 in the animal colony. Agouti mice produced by this mating are back-crossed to B6 and offsprings are genotyped using PCR, overview. Although CSAD-/- generation (G)1 and G2 survive, offspring from G2 CSAD-/- have low brain and liver taurine concentrations and most die within 24 hrs of birth. Taurine concentrations in G3 CSAD-/- born from G2 CSAD-/- treated with taurine in the drinking water are restored and survival rates of G3 CSAD-/- increase from 15% to 92%. The mRNA expression of CDO, ADO, and TauT is not different in CSAD-/- compared to wild-type, and CSAD mRNA is not expressed in CSAD-/-. Expression of Gpx 1 and 3 is increased significantly in CSAD-/- and restored to normal levels with taurine supplementation. Lactoferrin and the prolactin receptor are significantly decreased in CSAD-/-. The prolactin receptor is restored with taurine supplementation
additional information
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generation of CSAD knockout mice, chimeric CSAD KO mice are produced by injection of cells from a gene trap ES cell line (XP0392) into C57BL/6 (B6) blastocysts which are implanted into a pseudopregnant B6 mouse. Nine chimeric mice are mated with B6 in the animal colony. Agouti mice produced by this mating are back-crossed to B6 and offsprings are genotyped using PCR, overview. Although CSAD-/- generation (G)1 and G2 survive, offspring from G2 CSAD-/- have low brain and liver taurine concentrations and most die within 24 hrs of birth. Taurine concentrations in G3 CSAD-/- born from G2 CSAD-/- treated with taurine in the drinking water are restored and survival rates of G3 CSAD-/- increase from 15% to 92%. The mRNA expression of CDO, ADO, and TauT is not different in CSAD-/- compared to wild-type, and CSAD mRNA is not expressed in CSAD-/-. Expression of Gpx 1 and 3 is increased significantly in CSAD-/- and restored to normal levels with taurine supplementation. Lactoferrin and the prolactin receptor are significantly decreased in CSAD-/-. The prolactin receptor is restored with taurine supplementation
additional information
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generation of CSAD knockout mice, chimeric CSAD KO mice are produced by injection of cells from a gene trap ES cell line (XP0392) into C57BL/6 (B6) blastocysts which are implanted into a pseudopregnant B6 mouse. Nine chimeric mice are mated with B6 in the animal colony. Agouti mice produced by this mating are back-crossed to B6 and offsprings are genotyped using PCR, overview. Although CSAD-/- generation (G)1 and G2 survive, offspring from G2 CSAD-/- have low brain and liver taurine concentrations and most die within 24 hrs of birth. Taurine concentrations in G3 CSAD-/- born from G2 CSAD-/- treated with taurine in the drinking water are restored and survival rates of G3 CSAD-/- increase from 15% to 92%. The mRNA expression of CDO, ADO, and TauT is not different in CSAD-/- compared to wild-type, and CSAD mRNA is not expressed in CSAD-/-. Expression of Gpx 1 and 3 is increased significantly in CSAD-/- and restored to normal levels with taurine supplementation. Lactoferrin and the prolactin receptor are significantly decreased in CSAD-/-. The prolactin receptor is restored with taurine supplementation
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