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Results 1 - 10 of 21 > >>
EC Number Protein Variants Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11395A396A an enzymatically inactive proPME mutant 679828
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11D178A site-directed mutagenesis, inactive mutant 679502
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11D199A site-directed mutagenesis, inactive mutant 679502
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11food industry fruit juice industry 730283
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11M306A site-directed mutagenesis, the mutant shows reduced activity compared to the wild-type enzyme 679502
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11more analysis of allelic T-DNA insertional KO mutants of the enzyme, pme31-1 (SALK_074820) and pme31-2 (CS25163). The pme31 mutants are more sensitive to Na+ toxicity than the wild-type, the mutations in PME31 lead to salt hypersensitive phenotypes, overview. The cotyledon greening rate of pme31 mutants are significantly lower in the presence of NaCl and NaNO3, but not in the presence of KCl, KNO3, and osmotic stress, pme31 mutants are only sensitive to Na+ toxicity -, 749822
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11more construction of a enzyme-deficient pmt- mutant strain by gene disruption. A complementing strain (pmt-/pHM1+ pmt) expressing the Pmt protein from the overexpression vector pHM1 restored the pectin deesterifying activity and thus formed a red zone like wild-type strain -, 751955
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11more construction of a hms-1 mutant from gene PME6 by a transposon insertion. The hms-1 embryo defect phenotype is caused by a mutation in HMS, molecular complementation is performed, phenotype overview. Analysis of a second hms allele, allele gabi-kat-278G11, i.e. hms-2. The T-DNA in hms-2 is inserted at 229 from the +1 site in the 5' UTR. The hms-2 mutant has no mucilage phenotype, and HMS transcript in hms-2 is comparable with the wild-type. No other alleles are available in the coding region of HMS 751875
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11more construction of Atpme3-1 loss-of-function mutants, phenotypes with earlier germination and reduction of root hair production compared to wild-type, overview. A PME isoform with a pI 9.6 is lacking in all organs of the Atpme3-1 mutant, and loss of AtPME3 activity in the mutant cotyledon triggers the expression of the other PME isoform migrating at gpI 9.2. Altered Genome regulation in the mutant, overview. Genes encoding proteins putatively involved in cell wall organization and remodeling are mainly downregulated in hypocotyls of the Atpme3-1 mutant. Atpme3-1 seedlings display no specific phenotype except an increased adventitious rooting -, 751100
Display the word mapDisplay the reaction diagram Show all sequences 3.1.1.11more expression of proPME enhances the GFP transgene-induced gene silencing accompanied by relocation of the DCL1 protein from nucleus to the cytoplasm and activation of siRNAs and miRNAs production, inhibition of proPME gene expression stimulates the TMV vector reproduction, overview 679828
Results 1 - 10 of 21 > >>