Matches in SemOpenAlex for { <https://semopenalex.org/work/W2143702582> ?p ?o ?g. }
- W2143702582 endingPage "282" @default.
- W2143702582 startingPage "274" @default.
- W2143702582 abstract "We have demonstrated that insulin-like growth factor binding protein-5 (IGFBP-5) production by mammary epithelial cells increases dramatically during forced involution of the mammary gland in rats, mice and pigs. We proposed that growth hormone (GH) increases the survival factor IGF-I, whilst prolactin (PRL) enhances the effects of GH by decreasing the concentration of IGFBP-5, which would otherwise inhibit the actions of IGFs. To demonstrate a causal relationship between IGFBP-5 and cell death, we created transgenic mice expressing IGFBP-5, specifically, in the mammary gland. DNA content in the mammary glands of transgenic mice was decreased as early as day 10 of pregnancy. Mammary cell number and milk synthesis were both decreased by approximately 50% during the first 10 days of lactation. The concentrations of the pro-apoptotic molecule caspase-3 was increased in transgenic animals whilst the concentrations of two pro-survival molecules Bcl-2 and Bcl-x were both decreased. In order to examine whether IGFBP-5 acts by inhibiting the survival effect of IGF-I, we examined IGF receptor- and Akt-phoshorylation and showed that both were inhibited. These studies also indicated that the effects of IGFBP-5 could be mediated in part by IGF-independent effects involving potential interactions with components of the extracellular matrix involved in tissue remodeling, such as components of the plasminogen system, and the matrix metallo-proteinases (MMPs). Mammary development was normalised in transgenic mice by R3-IGF-I, an analogue of IGF-I which binds weakly to IGFBPs, although milk production was only partially restored. In contrast, treatment with prolactin was able to inhibit early involutionary processes in normal mice but was unable to prevent this in mice over-expressing IGFBP-5, although it was able to inhibit activation of MMPs. Thus, IGFBP-5 can simultaneously inhibit IGF action and activate the plasminogen system thereby coordinating cell death and tissue remodeling processes. The ability to separate these properties, using mutant IGFBPs, is currently under investigation." @default.
- W2143702582 created "2016-06-24" @default.
- W2143702582 creator A5005974685 @default.
- W2143702582 creator A5007064567 @default.
- W2143702582 creator A5009466330 @default.
- W2143702582 creator A5049130253 @default.
- W2143702582 creator A5050764885 @default.
- W2143702582 creator A5057557990 @default.
- W2143702582 creator A5058309022 @default.
- W2143702582 creator A5066082558 @default.
- W2143702582 creator A5067996327 @default.
- W2143702582 creator A5073359098 @default.
- W2143702582 date "2005-08-01" @default.
- W2143702582 modified "2023-10-06" @default.
- W2143702582 title "Insulin-like growth factor binding proteins initiate cell death and extracellular matrix remodeling in the mammary gland" @default.
- W2143702582 cites W105659622 @default.
- W2143702582 cites W127801142 @default.
- W2143702582 cites W1892136299 @default.
- W2143702582 cites W1974065088 @default.
- W2143702582 cites W1974668166 @default.
- W2143702582 cites W1981986845 @default.
- W2143702582 cites W1991650445 @default.
- W2143702582 cites W1992221874 @default.
- W2143702582 cites W1992934249 @default.
- W2143702582 cites W1996045917 @default.
- W2143702582 cites W2012791690 @default.
- W2143702582 cites W2020636054 @default.
- W2143702582 cites W2024028788 @default.
- W2143702582 cites W2028086623 @default.
- W2143702582 cites W2031310019 @default.
- W2143702582 cites W2039537001 @default.
- W2143702582 cites W2041228471 @default.
- W2143702582 cites W2042619286 @default.
- W2143702582 cites W2045516074 @default.
- W2143702582 cites W2052768254 @default.
- W2143702582 cites W2060561390 @default.
- W2143702582 cites W2063564135 @default.
- W2143702582 cites W2063981235 @default.
- W2143702582 cites W2065452930 @default.
- W2143702582 cites W2065816786 @default.
- W2143702582 cites W2073640832 @default.
- W2143702582 cites W2074611304 @default.
- W2143702582 cites W2075449661 @default.
- W2143702582 cites W2077566574 @default.
- W2143702582 cites W2078939389 @default.
- W2143702582 cites W2094605760 @default.
- W2143702582 cites W2095086608 @default.
- W2143702582 cites W2095814042 @default.
- W2143702582 cites W2117460322 @default.
- W2143702582 cites W2120622189 @default.
- W2143702582 cites W2122935853 @default.
- W2143702582 cites W2132066292 @default.
- W2143702582 cites W2150081825 @default.
- W2143702582 cites W2157639904 @default.
- W2143702582 cites W2159110682 @default.
- W2143702582 cites W2159318197 @default.
- W2143702582 cites W2165067126 @default.
- W2143702582 cites W2250407743 @default.
- W2143702582 cites W2321337829 @default.
- W2143702582 cites W2414934949 @default.
- W2143702582 cites W311989460 @default.
- W2143702582 cites W4230531563 @default.
- W2143702582 cites W4233597105 @default.
- W2143702582 cites W4241758207 @default.
- W2143702582 cites W4242762277 @default.
- W2143702582 cites W4245353998 @default.
- W2143702582 cites W4249523397 @default.
- W2143702582 cites W4255695860 @default.
- W2143702582 cites W85516301 @default.
- W2143702582 cites W978376681 @default.
- W2143702582 doi "https://doi.org/10.1016/j.domaniend.2005.02.021" @default.
- W2143702582 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15998501" @default.
- W2143702582 hasPublicationYear "2005" @default.
- W2143702582 type Work @default.
- W2143702582 sameAs 2143702582 @default.
- W2143702582 citedByCount "43" @default.
- W2143702582 countsByYear W21437025822012 @default.
- W2143702582 countsByYear W21437025822013 @default.
- W2143702582 countsByYear W21437025822015 @default.
- W2143702582 countsByYear W21437025822016 @default.
- W2143702582 countsByYear W21437025822017 @default.
- W2143702582 countsByYear W21437025822018 @default.
- W2143702582 countsByYear W21437025822019 @default.
- W2143702582 countsByYear W21437025822020 @default.
- W2143702582 countsByYear W21437025822022 @default.
- W2143702582 crossrefType "journal-article" @default.
- W2143702582 hasAuthorship W2143702582A5005974685 @default.
- W2143702582 hasAuthorship W2143702582A5007064567 @default.
- W2143702582 hasAuthorship W2143702582A5009466330 @default.
- W2143702582 hasAuthorship W2143702582A5049130253 @default.
- W2143702582 hasAuthorship W2143702582A5050764885 @default.
- W2143702582 hasAuthorship W2143702582A5057557990 @default.
- W2143702582 hasAuthorship W2143702582A5058309022 @default.
- W2143702582 hasAuthorship W2143702582A5066082558 @default.
- W2143702582 hasAuthorship W2143702582A5067996327 @default.
- W2143702582 hasAuthorship W2143702582A5073359098 @default.
- W2143702582 hasBestOaLocation W21437025823 @default.
- W2143702582 hasConcept C102230213 @default.