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Literature summary for 1.6.2.4 extracted from

  • Polusani, S.R.; Kar, R.; Riquelme, M.A.; Masters, B.S.; Panda, S.P.
    Regulation of gap junction function and Connexin 43 expression by cytochrome P450 oxidoreductase (CYPOR) (2011), Biochem. Biophys. Res. Commun., 411, 490-495.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 1.6.2.4

Protein Variants

Protein Variants Comment Organism
additional information knock-down CYPOR in multiple osteoblast cell lines using RNAi technology decreasing the expression of Connexin 43, known to play a critical role in bone formation, modeling, and remodeling. Knock-down of CYPOR also decreases Gap Junction Intercellular Communication (GJIC) and hemichannel activity Mus musculus
additional information knock-down CYPOR in multiple osteoblast cell lines using RNAi technology decreasing the expression of Connexin 43, known to play a critical role in bone formation, modeling, and remodeling. Knock-down of CYPOR also decreases Gap Junction Intercellular Communication (GJIC) and hemichannel activity Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
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Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
MG-63 cell
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 Homo sapiens
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osteoblast primary from mouse calvariae Mus musculus
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osteosarcoma cell
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 Homo sapiens
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Synonyms

Synonyms Comment Organism
CYPOR
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 Mus musculus
CYPOR
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 Homo sapiens
cytochrome P450 oxidoreductase
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 Mus musculus
cytochrome P450 oxidoreductase
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 Homo sapiens

General Information

General Information Comment Organism
malfunction human patients with severe forms of CYPOR mutation show bone defects such as cranio- and humeroradial synostoses and long bone fractures, known as Antley-Bixler-like syndrome, ABS Homo sapiens
physiological function regulation of gap junction function by CYPOR, Cx43 may play an important role(s) in CYPOR-mediated bone defects Mus musculus
physiological function regulation of gap junction function by CYPOR, Cx43 may play an important role(s) in CYPOR-mediated bone defects seen in patients Homo sapiens