FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2013914418> ?p ?o ?g. }

• W2013914418 endingPage "2859" @default.
• W2013914418 startingPage "2855" @default.
• W2013914418 abstract "Elucidation of signaling networks and their specialized functions in different cell types represents a challenging scientific question. Establishment of signaling crosstalk between different pathways relies on biochemical evidence coupled to genetic analysis of key components of the pathways at stake, and definition of the epistatic relationships between such components. A new key contribution to the building of ever increasingly complex signal transduction networks appears in this issue of Genes & Development by Xiao et al. (2003). Using a combination of genetic analysis in the mouse and in vitro biochemical experiments in mammalian cells, those authors established that the adaptor protein Ecsit represents a signaling node intersecting the pathways downstream of Toll-like receptors (TLRs) and receptors for transforming growth factor(TGF) superfamily members. Toll-like signal transduction initiates at the cell surface by extracellular ligands, such as the Drosophila Spatzle protein, which upon physiological activation by extracellular proteases leads to proper dorsoventral patterning during early embryogenesis (Morisato and Anderson 1995). Alternatively, pathophysiological activation of Spatzle by fungal pathogens in adult Drosophila leads to innate immune responses (Takeda et al. 2003). Similar responses are induced by mammalian TLRs, which recognize a large variety of collectively known pathogen-associated molecular patterns (PAMPs), abundant in viruses, bacteria, fungi, and drugs. Both embryonic and adult Toll-like pathways lead to activation of the NFB family of transcription factors, critical regulators of dorsoventral patterning, but also of inflammatory cytokines and mediators of the innate immune response (Ghosh and Karin 2002). In addition, TLR signaling can activate the Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways leading to additional gene regulatory inputs, whereas specialized TLR members can activate interferon regulatory factors (IRFs) that induce interferon gene expression, another critical factor of the immune response (Akira 2003). The TGFsuperfamily of cytokines, which includes TGFs as well as bone morphogenetic proteins (BMPs), is involved in the specification of embryonic patterning and in adult tissue homeostasis (Piek et al. 1999). TGFmembers regulate proliferation, differentiation, migration, and programmed death of diverse cell types, including mediators of innate and adaptive immunity (Letterio and Roberts 1998; McCartney-Francis et al. 1998; ten Dijke et al. 2002). These cellular responses are mediated by binding of the extracellular ligands to cell surface receptor serine/threonine kinases, whereby the Smad family of signal transducers are activated and translocated to the nucleus to control expression of target genes (Shi and Massague 2003). Additional signaling cascades, including Erk, JNK, and p38 MAPK pathways may also be activated by TGFmembers, and modulate the output of the Smad pathway (Derynck and Zhang 2003). The findings of Xiao et al. (2003) provide a new molecular link between TLR and BMP signaling pathways, involving the adaptor protein Ecsit. Ecsit seems to participate in a specific branch of the TLR signaling cascade that activates JNK or p38 MAPK (Kopp et al. 1999). The new work places Ecsit into the BMP pathway and enhances the accumulating evidence for common signaling mediators of the two evolutionarily conserved pathways. Such points of physical and functional contact between TLR and TGF/BMP signal transduction include, in addition to Ecsit, the TGF-activated kinase 1 (TAK1) protein complex, JNK and p38 MAPK, the IRFs, NFB, and Smads." @default.
• W2013914418 created "2016-06-24" @default.
• W2013914418 creator A5072088923 @default.
• W2013914418 creator A5084535456 @default.
• W2013914418 date "2003-12-01" @default.
• W2013914418 modified "2023-10-17" @default.
• W2013914418 title "Ecsit-ement on the crossroads of Toll and BMP signal transduction: Figure 1." @default.
• W2013914418 cites W1531792564 @default.
• W2013914418 cites W1840163537 @default.
• W2013914418 cites W1901605442 @default.
• W2013914418 cites W1965583863 @default.
• W2013914418 cites W1976382352 @default.
• W2013914418 cites W1978691428 @default.
• W2013914418 cites W1984760520 @default.
• W2013914418 cites W1989343086 @default.
• W2013914418 cites W2035031081 @default.
• W2013914418 cites W2035653659 @default.
• W2013914418 cites W2037368492 @default.
• W2013914418 cites W2037961284 @default.
• W2013914418 cites W2052599076 @default.
• W2013914418 cites W2062903004 @default.
• W2013914418 cites W2064434771 @default.
• W2013914418 cites W2069392982 @default.
• W2013914418 cites W2071448910 @default.
• W2013914418 cites W2076439289 @default.
• W2013914418 cites W2077243848 @default.
• W2013914418 cites W2089919211 @default.
• W2013914418 cites W2091203739 @default.
• W2013914418 cites W2101363646 @default.
• W2013914418 cites W2111167213 @default.
• W2013914418 cites W2117410908 @default.
• W2013914418 cites W2117671996 @default.
• W2013914418 cites W2129379081 @default.
• W2013914418 cites W2132805386 @default.
• W2013914418 cites W2134569957 @default.
• W2013914418 cites W2135757180 @default.
• W2013914418 cites W2154568166 @default.
• W2013914418 cites W2329649547 @default.
• W2013914418 cites W2441700042 @default.
• W2013914418 cites W4296927411 @default.
• W2013914418 cites W4297022993 @default.
• W2013914418 cites W4365787052 @default.
• W2013914418 doi "https://doi.org/10.1101/gad.1161403" @default.
• W2013914418 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14665666" @default.
• W2013914418 hasPublicationYear "2003" @default.
• W2013914418 type Work @default.
• W2013914418 sameAs 2013914418 @default.
• W2013914418 citedByCount "36" @default.
• W2013914418 countsByYear W20139144182012 @default.
• W2013914418 countsByYear W20139144182014 @default.
• W2013914418 countsByYear W20139144182015 @default.
• W2013914418 countsByYear W20139144182016 @default.
• W2013914418 countsByYear W20139144182018 @default.
• W2013914418 countsByYear W20139144182020 @default.
• W2013914418 countsByYear W20139144182021 @default.
• W2013914418 countsByYear W20139144182022 @default.
• W2013914418 countsByYear W20139144182023 @default.
• W2013914418 crossrefType "journal-article" @default.
• W2013914418 hasAuthorship W2013914418A5072088923 @default.
• W2013914418 hasAuthorship W2013914418A5084535456 @default.
• W2013914418 hasBestOaLocation W20139144181 @default.
• W2013914418 hasConcept C199360897 @default.
• W2013914418 hasConcept C2778025104 @default.
• W2013914418 hasConcept C2779843651 @default.
• W2013914418 hasConcept C41008148 @default.
• W2013914418 hasConcept C54355233 @default.
• W2013914418 hasConcept C62478195 @default.
• W2013914418 hasConcept C86803240 @default.
• W2013914418 hasConcept C95444343 @default.
• W2013914418 hasConceptScore W2013914418C199360897 @default.
• W2013914418 hasConceptScore W2013914418C2778025104 @default.
• W2013914418 hasConceptScore W2013914418C2779843651 @default.
• W2013914418 hasConceptScore W2013914418C41008148 @default.
• W2013914418 hasConceptScore W2013914418C54355233 @default.
• W2013914418 hasConceptScore W2013914418C62478195 @default.
• W2013914418 hasConceptScore W2013914418C86803240 @default.
• W2013914418 hasConceptScore W2013914418C95444343 @default.
• W2013914418 hasIssue "23" @default.
• W2013914418 hasLocation W20139144181 @default.
• W2013914418 hasLocation W20139144182 @default.
• W2013914418 hasOpenAccess W2013914418 @default.
• W2013914418 hasPrimaryLocation W20139144181 @default.
• W2013914418 hasRelatedWork W2074776620 @default.
• W2013914418 hasRelatedWork W207823365 @default.
• W2013914418 hasRelatedWork W2085624021 @default.
• W2013914418 hasRelatedWork W2157937554 @default.
• W2013914418 hasRelatedWork W2165562009 @default.
• W2013914418 hasRelatedWork W2202933656 @default.
• W2013914418 hasRelatedWork W2365541820 @default.
• W2013914418 hasRelatedWork W2393953455 @default.
• W2013914418 hasRelatedWork W4212844121 @default.
• W2013914418 hasRelatedWork W2181308405 @default.
• W2013914418 hasVolume "17" @default.
• W2013914418 isParatext "false" @default.
• W2013914418 isRetracted "false" @default.
• W2013914418 magId "2013914418" @default.
• W2013914418 workType "article" @default.