FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2314993208> ?p ?o ?g. }

• W2314993208 endingPage "537" @default.
• W2314993208 startingPage "524" @default.
• W2314993208 abstract "Angiogenic remodeling during embryonic development and in adult tissue homeostasis is orchestrated by cooperative signaling between several distinct molecular pathways, which are often exploited by tumors. Indeed, tumors upregulate proangiogenic molecules while simultaneously suppressing angiostatic pathways to recruit blood vessels for growth, survival, and metastatic spread. Understanding how cancers exploit proangiogenic and antiangiogenic signals is a key step in developing new, molecularly targeted antiangiogenic therapies. While EphA2, a receptor tyrosine kinase (RTK), is required for VEGF-induced angiogenesis, the mechanism through which these pathways intersect remains unclear. Slit2 expression is elevated in EphA2-deficient endothelium, and here it is reported that inhibiting Slit activity rescues VEGF-induced angiogenesis in cell culture and in vivo, as well as VEGF-dependent tumor angiogenesis, in EphA2-deficient endothelial cells and animals. Moreover, blocking Slit activity or Slit2 expression in EphA2-deficient endothelial cells restores VEGF-induced activation of Src and Rac, both of which are required for VEGF-mediated angiogenesis. These data suggest that EphA2 suppression of Slit2 expression and Slit angiostatic activity enables VEGF-induced angiogenesis in vitro and in vivo, providing a plausible mechanism for impaired endothelial responses to VEGF in the absence of EphA2 function.Modulation of angiostatic factor Slit2 by EphA2 receptor regulates endothelial responses to VEGF-mediated angiogenesis and tumor neovascularization." @default.
• W2314993208 created "2016-06-24" @default.
• W2314993208 creator A5004009810 @default.
• W2314993208 creator A5015690059 @default.
• W2314993208 creator A5020742692 @default.
• W2314993208 creator A5026328793 @default.
• W2314993208 creator A5044622075 @default.
• W2314993208 creator A5091666689 @default.
• W2314993208 creator A5091689383 @default.
• W2314993208 date "2014-12-12" @default.
• W2314993208 modified "2023-10-18" @default.
• W2314993208 title "Elevated Slit2 Activity Impairs VEGF-Induced Angiogenesis and Tumor Neovascularization in EphA2-Deficient Endothelium" @default.
• W2314993208 cites W1561902389 @default.
• W2314993208 cites W182557598 @default.
• W2314993208 cites W1965232435 @default.
• W2314993208 cites W1966339894 @default.
• W2314993208 cites W1966385034 @default.
• W2314993208 cites W1970131417 @default.
• W2314993208 cites W1980379135 @default.
• W2314993208 cites W1985972866 @default.
• W2314993208 cites W1990830502 @default.
• W2314993208 cites W1994137567 @default.
• W2314993208 cites W1994162941 @default.
• W2314993208 cites W1996806798 @default.
• W2314993208 cites W1998182442 @default.
• W2314993208 cites W2000000810 @default.
• W2314993208 cites W2006573558 @default.
• W2314993208 cites W2006734059 @default.
• W2314993208 cites W2009468127 @default.
• W2314993208 cites W2010486643 @default.
• W2314993208 cites W2017516431 @default.
• W2314993208 cites W2018981297 @default.
• W2314993208 cites W2019367530 @default.
• W2314993208 cites W2020493358 @default.
• W2314993208 cites W2021622839 @default.
• W2314993208 cites W2024906055 @default.
• W2314993208 cites W2025860624 @default.
• W2314993208 cites W2026308186 @default.
• W2314993208 cites W2030537346 @default.
• W2314993208 cites W2033222419 @default.
• W2314993208 cites W2034993026 @default.
• W2314993208 cites W2043955977 @default.
• W2314993208 cites W2045901576 @default.
• W2314993208 cites W2047338936 @default.
• W2314993208 cites W2049529144 @default.
• W2314993208 cites W2054601124 @default.
• W2314993208 cites W2056829254 @default.
• W2314993208 cites W2068555773 @default.
• W2314993208 cites W2073464835 @default.
• W2314993208 cites W2074196937 @default.
• W2314993208 cites W2082600036 @default.
• W2314993208 cites W2084964460 @default.
• W2314993208 cites W2103927033 @default.
• W2314993208 cites W2105396692 @default.
• W2314993208 cites W2109663830 @default.
• W2314993208 cites W2112967368 @default.
• W2314993208 cites W2115775016 @default.
• W2314993208 cites W2116393970 @default.
• W2314993208 cites W2117547652 @default.
• W2314993208 cites W2121291175 @default.
• W2314993208 cites W2122455451 @default.
• W2314993208 cites W2126389915 @default.
• W2314993208 cites W2131637001 @default.
• W2314993208 cites W2131874160 @default.
• W2314993208 cites W2137029911 @default.
• W2314993208 cites W2140120206 @default.
• W2314993208 cites W2149092068 @default.
• W2314993208 cites W2159351792 @default.
• W2314993208 cites W2159956893 @default.
• W2314993208 cites W2163357887 @default.
• W2314993208 cites W2163557331 @default.
• W2314993208 cites W2165365805 @default.
• W2314993208 cites W2167632684 @default.
• W2314993208 doi "https://doi.org/10.1158/1541-7786.mcr-14-0142" @default.
• W2314993208 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4416411" @default.
• W2314993208 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25504371" @default.
• W2314993208 hasPublicationYear "2014" @default.
• W2314993208 type Work @default.
• W2314993208 sameAs 2314993208 @default.
• W2314993208 citedByCount "16" @default.
• W2314993208 countsByYear W23149932082016 @default.
• W2314993208 countsByYear W23149932082017 @default.
• W2314993208 countsByYear W23149932082018 @default.
• W2314993208 countsByYear W23149932082019 @default.
• W2314993208 countsByYear W23149932082020 @default.
• W2314993208 countsByYear W23149932082021 @default.
• W2314993208 crossrefType "journal-article" @default.
• W2314993208 hasAuthorship W2314993208A5004009810 @default.
• W2314993208 hasAuthorship W2314993208A5015690059 @default.
• W2314993208 hasAuthorship W2314993208A5020742692 @default.
• W2314993208 hasAuthorship W2314993208A5026328793 @default.
• W2314993208 hasAuthorship W2314993208A5044622075 @default.
• W2314993208 hasAuthorship W2314993208A5091666689 @default.
• W2314993208 hasAuthorship W2314993208A5091689383 @default.
• W2314993208 hasBestOaLocation W23149932081 @default.
• W2314993208 hasConcept C101544691 @default.
• W2314993208 hasConcept C123012128 @default.
• W2314993208 hasConcept C146285616 @default.

• next