FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W48703749> ?p ?o ?g. }

• W48703749 endingPage "289" @default.
• W48703749 startingPage "278" @default.
• W48703749 abstract "Parathyroid hormone-related protein (PTHrP) occurs in a high proportion of breast cancer and is strongly implicated in their metastatic spread to bone. Epidermal growth factor receptor (EGFR) activated by autocrine growth factors in many types of tumors, including breast tumor. EGFR (ErbB1) has been linked to a poor prognosis in breast cancer and promote extracellular-regulated kinase/mitogen-activated protein kinase (Erk/MAPK) which is a critical signal transduction event-mediated cell proliferation, cell migration and tumor progression. We investigated the role of PTHrP-1-34, PTHrP-7-34 and PTHrP-1-86 peptides in the Erk pathway in MCF7 breast carcinoma cell line with and without Heregulins β1 (HRG β1). MCF7 were transfected with EGFR and treated overnight with 10nM of PTHrP-1-34, PTHrP-7-34, or PTHrP-1-86 and for 30min with 10ng of HRG β1 in serum free medium. PTHrP-1-34 significantly overexpressed ErbB1 receptor compared with PTHrP-7-34 and PTHrP-1-86 treatment. Erk activity was significantly enhanced with HRG β1 and PTHrP-1-34. However, with PTHrP-7-34 and PTHrP-1-86, Erk activity was less significantly enhanced. The level of protein kinase C found to be higher with PTHrP-1-34 than PTHrP-7-34 and PTHrP-1-86 treated cells. PKC was demolished in HRG β1 treated cells and PKC activation had no effect on erbB1 induced Erk activation. Our results indicate that ErbB1 receptor induced Erk activation through the presence of HRG β1 and PTHrP and the mitogenic effects are mainly dependent on MAPK activities which might be modulated by both Erk and PKC. This evaluation of downstream signaling could potentially explain PTHrP dependent growth-promoting effects in tumor progression." @default.
• W48703749 created "2016-06-24" @default.
• W48703749 creator A5056667039 @default.
• W48703749 date "2009-12-28" @default.
• W48703749 modified "2023-09-24" @default.
• W48703749 title "The Role of PTHrP in Mitogenic Signaling via EGFR-Dependent Pathways in Breast Cancer Cells" @default.
• W48703749 cites W1565334506 @default.
• W48703749 cites W1576004006 @default.
• W48703749 cites W1965963242 @default.
• W48703749 cites W1967096085 @default.
• W48703749 cites W1967432915 @default.
• W48703749 cites W1968905163 @default.
• W48703749 cites W1974024530 @default.
• W48703749 cites W1975898119 @default.
• W48703749 cites W1988229096 @default.
• W48703749 cites W1988773935 @default.
• W48703749 cites W1989167460 @default.
• W48703749 cites W1991535761 @default.
• W48703749 cites W1994824150 @default.
• W48703749 cites W2000170857 @default.
• W48703749 cites W2007410879 @default.
• W48703749 cites W2017211434 @default.
• W48703749 cites W2020814497 @default.
• W48703749 cites W2032614844 @default.
• W48703749 cites W2039262401 @default.
• W48703749 cites W2043345702 @default.
• W48703749 cites W2048440069 @default.
• W48703749 cites W2051120695 @default.
• W48703749 cites W2053174155 @default.
• W48703749 cites W2054351138 @default.
• W48703749 cites W2057675721 @default.
• W48703749 cites W2062731377 @default.
• W48703749 cites W2076392488 @default.
• W48703749 cites W2083763149 @default.
• W48703749 cites W2090855460 @default.
• W48703749 cites W2110228428 @default.
• W48703749 cites W2110358014 @default.
• W48703749 cites W2111848398 @default.
• W48703749 cites W2116012629 @default.
• W48703749 cites W2117553531 @default.
• W48703749 cites W2128635872 @default.
• W48703749 cites W2136607961 @default.
• W48703749 cites W2142217243 @default.
• W48703749 cites W2152554878 @default.
• W48703749 cites W2160217360 @default.
• W48703749 cites W2160753380 @default.
• W48703749 cites W2169673209 @default.
• W48703749 cites W2169816639 @default.
• W48703749 cites W2184549179 @default.
• W48703749 hasPublicationYear "2009" @default.
• W48703749 type Work @default.
• W48703749 sameAs 48703749 @default.
• W48703749 citedByCount "0" @default.
• W48703749 crossrefType "journal-article" @default.
• W48703749 hasAuthorship W48703749A5056667039 @default.
• W48703749 hasConcept C126322002 @default.
• W48703749 hasConcept C128240485 @default.
• W48703749 hasConcept C134018914 @default.
• W48703749 hasConcept C170493617 @default.
• W48703749 hasConcept C184235292 @default.
• W48703749 hasConcept C185592680 @default.
• W48703749 hasConcept C195794163 @default.
• W48703749 hasConcept C2776362946 @default.
• W48703749 hasConcept C2778828131 @default.
• W48703749 hasConcept C2779438470 @default.
• W48703749 hasConcept C2781208988 @default.
• W48703749 hasConcept C502942594 @default.
• W48703749 hasConcept C519063684 @default.
• W48703749 hasConcept C57074206 @default.
• W48703749 hasConcept C62478195 @default.
• W48703749 hasConcept C71924100 @default.
• W48703749 hasConcept C86803240 @default.
• W48703749 hasConcept C95444343 @default.
• W48703749 hasConcept C97029542 @default.
• W48703749 hasConceptScore W48703749C126322002 @default.
• W48703749 hasConceptScore W48703749C128240485 @default.
• W48703749 hasConceptScore W48703749C134018914 @default.
• W48703749 hasConceptScore W48703749C170493617 @default.
• W48703749 hasConceptScore W48703749C184235292 @default.
• W48703749 hasConceptScore W48703749C185592680 @default.
• W48703749 hasConceptScore W48703749C195794163 @default.
• W48703749 hasConceptScore W48703749C2776362946 @default.
• W48703749 hasConceptScore W48703749C2778828131 @default.
• W48703749 hasConceptScore W48703749C2779438470 @default.
• W48703749 hasConceptScore W48703749C2781208988 @default.
• W48703749 hasConceptScore W48703749C502942594 @default.
• W48703749 hasConceptScore W48703749C519063684 @default.
• W48703749 hasConceptScore W48703749C57074206 @default.
• W48703749 hasConceptScore W48703749C62478195 @default.
• W48703749 hasConceptScore W48703749C71924100 @default.
• W48703749 hasConceptScore W48703749C86803240 @default.
• W48703749 hasConceptScore W48703749C95444343 @default.
• W48703749 hasConceptScore W48703749C97029542 @default.
• W48703749 hasIssue "5" @default.
• W48703749 hasLocation W487037491 @default.
• W48703749 hasOpenAccess W48703749 @default.
• W48703749 hasPrimaryLocation W487037491 @default.
• W48703749 hasRelatedWork W1975898119 @default.

• next