Please use this identifier to cite or link to this item:
|Title:||Pim-1 kinase expression during murine mammary development||Authors:||Gapter, L.A.
Growth and development
Mammary cell line
|Issue Date:||7-Jul-2006||Citation:||Gapter, L.A., Magnuson, N.S., Ng, K.-y., Hosick, H.L. (2006-07-07). Pim-1 kinase expression during murine mammary development. Biochemical and Biophysical Research Communications 345 (3) : 989-997. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2006.04.110||Abstract:||Pim-1 kinase phosphorylates substrates whose activities are linked to proliferation, survival, differentiation, and apoptosis. Although pim-1 is induced by hormones and cytokines, the hormonal control and contribution of Pim-1 to mammary gland development have not been evaluated. We examined Pim-1 expression in mammary cell lines, investigated whether Pim-1 levels could be altered in breast epithelia by mammogenic hormones, and evaluated Pim-1 expression during mammary development. We found that Pim-1 was elevated in most mammary carcinoma cell lines and progesterone increased Pim-1 protein to some extent in non-tumorigenic mammary epithelia. Pim-1 expression in situ was consistent with the documented profile of progesterone activity in mouse mammary glands. Pim-1 nuclear localization correlated with cytoplasmic distribution for its substrate, p21CIP/Waf1, and we found that Pim-1 and p21 associate in vitro. Our results suggest that Pim-1 expression may be regulated by progesterone during mammary development and Pim-1 associates with p21 in mammary epithelial cells. © 2006 Elsevier Inc. All rights reserved.||Source Title:||Biochemical and Biophysical Research Communications||URI:||http://scholarbank.nus.edu.sg/handle/10635/106222||ISSN:||0006291X||DOI:||10.1016/j.bbrc.2006.04.110|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on May 27, 2022
WEB OF SCIENCETM
checked on May 19, 2022
checked on May 26, 2022
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.