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Literature summary for 1.14.11.7 extracted from

  • Fujita, N.; Gogate, S.S.; Chiba, K.; Toyama, Y.; Shapiro, I.M.; Risbud, M.V.
    Prolyl hydroxylase 3 (PHD3) modulates catabolic effects of tumor necrosis factor-alpha (TNF-alpha) on cells of the nucleus pulposus through co-activation of nuclear factor kappaB (NF-kappaB)/p65 signaling (2012), J. Biol. Chem., 287, 39942-39953.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
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Rattus norvegicus
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-
-

Source Tissue

Source Tissue Comment Organism Textmining
nucleus pulposus
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Homo sapiens
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nucleus pulposus
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Rattus norvegicus
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Synonyms

Synonyms Comment Organism
PHD3
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Homo sapiens
PHD3
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Rattus norvegicus

Expression

Organism Comment Expression
Homo sapiens TNF-alpha and IL-1beta robustly increase PHD3 expression in an NF-kappaB dependent fashion up
Rattus norvegicus TNF-alpha and IL-1beta robustly increase PHD3 expression in an NF-kappaB dependent fashion up

General Information

General Information Comment Organism
malfunction loss-of function studies show that PHD3 serves as a co-activator of NF-kappaB signaling activity in NP cells. PHD3 interacts with, and co-localizes with, p65 Homo sapiens
malfunction silencing PHD3 leads to a significant decrease in TNF-alpha-induced expression of catabolic markers that include ADAMTS5, syndecan4, MMP13, and COX2, and at the same time, there is restoration of aggrecan and collagen type II expression Homo sapiens
physiological function by positively controlling NF-kappaB signaling activity, PHD3 promotes the catabolic effects of the inflammatory cytokines on nucleus pulposus cells Rattus norvegicus