Application | Comment | Organism |
---|---|---|
molecular biology | TAL deficiency is shown as a modulator of mitochondrial homoeostasis, Ca2+ fluxing and apoptosis | Homo sapiens |
Protein Variants | Comment | Organism |
---|---|---|
TALDELTAS171 | TAL-deficient lymphoblasts (caused by deletion of Ser 171) reveal co-ordinated changes in expression of genes involved in the pentose phosphate pathway, mitochondrial biogenesis, oxidative stress, and Ca2+ fluxing. Sedoheptulose 7-phosphate and ADP-ribose are accumulated, glucose 6-phosphate, NADPH and NAD+ are depleted. TAL-deficient cells have diminished mitochondrial transmembrane potential and increased mitochondrial mass associated with increased production of nitric oxide and ATP. TAL deficiency results in enhanced spontaneous and H2O2-induced apoptosis. Normalization of TAL activity by adeno-associated-virus-mediated gene transfer reverses the TAL-deficient phenotype | Homo sapiens |
Molecular Weight [Da] | Molecular Weight Maximum [Da] | Comment | Organism |
---|---|---|---|
38000 | - |
SDS-PAGE | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
B-lymphocyte cell line | human EBV-transformed human B-cells | Homo sapiens | - |
fibroblast cell line | - |
Homo sapiens | - |
Synonyms | Comment | Organism |
---|---|---|
TAL | - |
Homo sapiens |
transaldolase | - |
Homo sapiens |