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Literature summary for 5.3.4.1 extracted from

  • Fu, X.; Wang, P.; Zhu, B.T.
    Protein disulfide isomerase is a multifunctional regulator of estrogenic status in target cells (2008), J. Steroid Biochem. Mol. Biol., 112, 127-137.
    View publication on PubMed
Search for more literature for 5.3.4.1

Protein Variants

Protein Variants Comment Organism
additional information knockdown of PDI in MCF-7 human breast cancer cells with RNAi down-regulates estrogen receptor alpha protein but upregulates estrogen receptor beta protein, resulting in a drastic increase in estrogen receptor alpha/beta ratio, which is a crucial determinant of different cellular responses to estrogens. PDI can directly interact with estrogen receptor alpha, but it does not interact with estrogen receptor beta Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
additional information Homo sapiens PDI can function as a high-capacity intracellular 17beta-estradiol-binding protein that increases the concentration and accumulation of 17beta-estradiol in live cells. The intracellular PDI-bound 17beta-estradiol can be released from PDI upon a drop in 17beta-estradiol levels and the released 17beta-estradiol can augment estrogen receptor-mediated transcriptional activity and mitogenic actions in cultured cells. The binding of 17beta-estradiol by PDI also reduces the rate of metabolic disposition of this hormone ?
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Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
MCF-7 cell
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 Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information PDI can function as a high-capacity intracellular 17beta-estradiol-binding protein that increases the concentration and accumulation of 17beta-estradiol in live cells. The intracellular PDI-bound 17beta-estradiol can be released from PDI upon a drop in 17beta-estradiol levels and the released 17beta-estradiol can augment estrogen receptor-mediated transcriptional activity and mitogenic actions in cultured cells. The binding of 17beta-estradiol by PDI also reduces the rate of metabolic disposition of this hormone Homo sapiens ?
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 ?

Subunits

Subunits Comment Organism
More PDI can directly interact with estrogen receptor alpha, but it does not interact with estrogen receptor beta Homo sapiens