Literature summary for 2.2.1.2 extracted from

Qian, Y.; Banerjee, S.; Grossman, C.E.; Amidon, W.; Nagy, G.; Barcza, M.; Niland, B.; Karp, D.R.; Middleton, F.A.; Banki, K.; Perl, A.
Transaldolase deficiency influences the pentose phosphate pathway, mitochondrial homoeostasis and apoptosis signal processing (2008), Biochem. J., 415, 123-134.

Search for more literature for 2.2.1.2

Application

Application	Comment	Organism
molecular biology	TAL deficiency is shown as a modulator of mitochondrial homoeostasis, Ca2+ fluxing and apoptosis	Homo sapiens

Protein Variants

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 [Da]	Molecular Weight Maximum [Da]	Comment	Organism
38000	-	SDS-PAGE	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
B-lymphocyte cell line	human EBV-transformed human B-cells	Homo sapiens	-
fibroblast cell line	-	Homo sapiens	-

Synonyms

Synonyms	Comment	Organism
TAL	-	Homo sapiens
transaldolase	-	Homo sapiens

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Release 2023.1 (January 2023)