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Mutation in the non-oxidative phase of RPI2 leads to premature cell death and altered morphology in Arabidopsis plants.
A mutation of the ribose-5-phosphate isomerase is characterized and its effects on plant root phenotype is discussed.
The results are consistent with a model in which RPIA suppresses autophagy and LC3 (show MAP1LC3A Proteins) processing by modulation of redox signaling.
CRC (show CALR Proteins) cells that overexpressed miR124 or with knockdown of RPIA or PRPS1 (show PRPS1 Proteins) had reduced DNA synthesis and proliferation, whereas cells incubated with an inhibitor of miR124 had significantly increased DNA synthesis and proliferation and formed more colonies.
In this work, through an in silico comparative analysis between the genomes of Leishmania major and Homo sapiens, the enzyme ribose 5-phosphate isomerase (R5PI) was indicated as a promising molecular target.
Study provides new insight into the molecular mechanisms by which RPIA overexpression can induce oncogenesis in hepatocellular carcinoma.
RPI is the second known inborn error in the reversible phase of the pentose-phosphate-pathway, confirming that defects in pentose and polyol metabolism constitute a new area of inborn metabolic disorders
The protein encoded by this gene is an enzyme, which catalyzes the reversible conversion between ribose-5-phosphate and ribulose-5-phosphate in the pentose-phosphate pathway. This gene is highly conserved in most organisms. The enzyme plays an essential role in the carbohydrate metabolism. Mutations in this gene cause ribose 5-phosphate isomerase deficiency. A pseudogene is found on chromosome 18.
ribose 5-phosphate isomerase A
, ribose 5-phosphate isomerase A (ribose 5-phosphate epimerase)
, ribose-5-phosphate isomerase
, ribose-5-phosphate isomerase A
, ribose 5-phosphate isomerase-like protein
, ribose 5-phosphate epimerase