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Expression, localisation and hormone regulation of the human copper transporter hCTR1 in placenta and choriocarcinoma Jeg-3 cells

Hardman, Belinda, Manuelpillai, U., Wallace, E. M., Monty, J.-F., Kramer, David, Kuo, Y. M., Mercer, Julian and Ackland, Leigh 2006, Expression, localisation and hormone regulation of the human copper transporter hCTR1 in placenta and choriocarcinoma Jeg-3 cells, Placenta, vol. 27, no. 9-10, pp. 968-977, doi: 10.1016/j.placenta.2005.10.011.

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Title Expression, localisation and hormone regulation of the human copper transporter hCTR1 in placenta and choriocarcinoma Jeg-3 cells
Author(s) Hardman, Belinda
Manuelpillai, U.
Wallace, E. M.
Monty, J.-F.
Kramer, David
Kuo, Y. M.
Mercer, Julian
Ackland, LeighORCID iD for Ackland, Leigh orcid.org/0000-0002-7474-6556
Journal name Placenta
Volume number 27
Issue number 9-10
Start page 968
End page 977
Publisher Elsevier
Place of publication London, England
Publication date 2006-09
ISSN 0143-4004
1532-3102
Keyword(s) hCTR1
copper
placenta
hormone regulation
Jeg-3 cells
Summary Copper is an essential trace element necessary for normal growth and development. During pregnancy, copper is transported from the maternal circulation to the fetus by mechanisms which have not been clearly elucidated. The copper uptake protein, hCTR1 is predicted to play a role in copper transport in human placental cells. This study has examined the expression and localisation of hCTR1 in human placental tissue and Jeg-3 cells. In term placental tissue the hCTR1 protein was detected as a 105 kDa protein, consistent with the size of a trimer which may represent the functional protein. A 95 kDa band, possibly representing the glycosylated protein, was also detected. hCTR1 was localised within the syncytiotrophoblast layer and the fetal vascular endothelial cells in the placental villi and interestingly was found to be localised toward the basal plasma membrane. It did not co-localise with either the Menkes or the Wilson copper transporting ATPases. Using the placental cell line Jeg-3, it was shown that the 35 kDa monomer was absent in the extracts of cells exposed to insulin, estrogen or progesterone and in cells treated with estrogen an additional 65 kDa band was detected which may correspond to a dimeric form of the protein. The 95 kDa band was not detected in the cultured cells. These results provide novel insights indicating that hormones have a role in the formation of the active hCTR1 protein. Furthermore, insulin altered the intracellular localisation of hCTR1, suggesting a previously undescribed role of this hormone in regulating copper uptake through the endocytic pathway.
Language eng
DOI 10.1016/j.placenta.2005.10.011
Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2005, Elsevier
Persistent URL http://hdl.handle.net/10536/DRO/DU:30003770

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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