EC Number   |
General Information |
Reference |
|---|
    6.3.5.4 | evolution |
CaAS1 and its related plant proteins all contain an AsnB domain and an ASN synthetase domain |
716548 |
| 6.3.5.4 | evolution |
genes PpAS1 and PpAS2 encode both class II asparagine synthetases suggesting an ancient origin of the genes in plants. Amino acid residues essential for aspartate, AMP, and glutamine binding are conserved |
727578 |
| 6.3.5.4 | evolution |
genes PpAS1 and PpAS2 encode both class II asparagine synthetases suggesting an ancient origin of the genes in plants. Amino acid residues essential for aspartate, AMP, and glutamine binding are conserved, except valine268, included in the AMP binding site, which has been replaced by an isoleucine in the AS2 sequence |
727578 |
| 6.3.5.4 | evolution |
phylogenetic analysis has grouped ASN1 in dicot-subclass I while ASN2 and ASN3 are placed in dicot-subclass II |
-, 743980 |
| 6.3.5.4 | malfunction |
asparagine synthetase deficiency, ASD, is a neurological disorder having severe impacts on psychomotor development and mortality at an early age. Children with mutations in the ASNS gene exhibit developmental delays, intellectual disability, microcephaly, intractable seizures, and progressive brain atrophy. Mutations in the ASNS gene have been clinically associated with asparagine synthetase deficiency (ASD), phenotype. Neurologic disorder associated with asparagine synthetase deficiency (ASD). The transcription factor ATF4 binds to an enhancer element within the proximal promoter of the ASNS gene and activates transcription. Role of ATF4 in tumor cell survival and proliferation, ATF4 knockdown causes reduced survival in HT-1080 fibrosarcoma and DLD-1 colorectal adenocarcinoma cells in the absence of nonessential amino acids. Reduced proliferative capacity and increased apoptosis correlate with lower ASNS expression in the ATF4-deficient cells. Supplementation of the tumor cells with asparagine, but not other amino acids, leads to increased cell survival. Role of ASNS activity in modulating tumor growth |
745375 |
| 6.3.5.4 | malfunction |
enzyme AS-A ablation drives parasites auxotrophic to asparagine, but LiAS-A is not detrimental for parasite survival, growth or infectivity. The parasite burden in the spleen and liver of female BALB/c mice is not statistically different in LiASA mutants when compared to the wild-type |
-, 746172 |
| 6.3.5.4 | malfunction |
knockdown of asparagine synthetase (ASNS) leads to cell death even in the presence of glutamine, which can be reversed by addition of exogenous asparagine. Asparagine plays a critical role in regulating cellular adaptation to glutamine depletion. ASNS knockdown leads to profound apoptosis even in the presence of glutamine. Addition of extracellular asparagine completely restored cell survival and proliferation. Clinically, the expression of ASNS correlates with the progression of disease and poor prognosis of glioma and neuroblastoma patients. In neuroblastoma with unfavourable prognosis, ASNS expression is significantly higher. Asparagine-induced suppression of apoptosis: asparagine addition to glutamine-deprived cells alters the transcriptional response, suppressing the induction of the reported UPR effectors CHOP and XBP1 while maintaining the transcriptional induction of adaptive components of the UPR-response such as ASNS and HERPUD1. At the protein level, exogenous addition of asparagine suppresses CHOP induction without altering ATF4 accumulation or upstream eIF2alpha phosphorylation |
745756 |
| 6.3.5.4 | malfunction |
no visible phenotype is detected for the asn3-1 and asn3-2 mutant. Both asn3-1 and asn3-2 rosette leaves contain wild-type levels of chlorophyll and ammonium content, indicating that ASN3 disruption does not cause a defective nitrogen status during vegetative growth. During seed development, leaves and stems serve as source tissues to supply nitrogen resources to developing siliques which in turn deliver nitrogen to seeds. When compared to wild-type seeds, asn3-1 seeds display reduced glutamine (by 30%), asparagine (20%) and aspartate (20%) contents while exhibiting increased glutamate (10%) amounts |
-, 743980 |
| 6.3.5.4 | malfunction |
retrotransposon-mediated knockout mutants lacking AS1 show slight stimulation of shoot length and slight reduction in root length at the seedling stage. On the other hand, the mutation causes an approximately 80-90% reduction in free asparagine content in both roots and xylem sap |
746041 |
| 6.3.5.4 | malfunction |
salt tolerance of Arabidopsis knockout mutant with T-DNA insertion in ASN2 gene encoding asparagines synthetase is investigated. Results indicate that the knockout mutant is impaired in nitrogen assimilation and translocation under salt treatment |
716577 |
