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AASS encodes a bifunctional enzyme that catalyzes the first two steps in the mammalian lysine degradation pathway. Additionally we are shipping Aminoadipate Semialdehyde Synthase Proteins (4) and many more products for this protein.
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Human Polyclonal AASS Primary Antibody for ICC, IF - ABIN4277111
Houten, Te Brinke, Denis, Ruiter, Knegt, de Klerk, Augoustides-Savvopoulou, Häberle, Baumgartner, Coşkun, Zschocke, Sass, Poll-The, Wanders, Duran: Genetic basis of hyperlysinemia. in Orphanet journal of rare diseases 2013
GR and KLF15 physically interact via low affinity GR binding sites within glucocorticoid response elements (GREs) for PRODH and AASS that contribute to combinatorial regulation with KLF15.
Mitochondrial NADPH (show NQO1 Antibodies) is crucial for AASS function
Hyperlysinemia is caused by mutations in AASS
These results indicate AASS knockdown decreases the lysine requirement of the cell via a reduction of lysine catabolism through the saccharopine pathway.
Mice receiving the high-protein diet had greater AASS mRNA compared to mice fed the adequate protein diet.
This gene encodes a bifunctional enzyme that catalyzes the first two steps in the mammalian lysine degradation pathway. The N-terminal and the C-terminal portions of this enzyme contain lysine-ketoglutarate reductase and saccharopine dehydrogenase activity, respectively, resulting in the conversion of lysine to alpha-aminoadipic semialdehyde. Mutations in this gene are associated with familial hyperlysinemia.
alpha-aminoadipate semialdehyde synthase
, alpha-aminoadipic semialdehyde synthase, mitochondrial
, aminoadipic semialdehyde synthase
, lysine-2-oxoglutarate reductase
, lysine-ketoglutarate reductase /saccharopine dehydrogenase
, lysine oxoglutarate reductase
, saccharopine dehydrogenase