FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2082119653> ?p ?o ?g. }

• W2082119653 endingPage "36187" @default.
• W2082119653 startingPage "36179" @default.
• W2082119653 abstract "Nucleotides are new players in the intercellular communication network. P2X7 is a member of the P2X family of receptors, which are ATP-gated plasma membrane ion channels with diverse biological functions. Abnormal expression and dysfunction of P2X7 have been reported in leukemias. Here, we report a new P2X7 mutant (an A559-to-G substitution causing N187D P2X7) cloned from J6-1 leukemia cells. The characteristics of N187D P2X7 were studied by establishing stably transfected K562 cell lines. Our results show that N187D P2X7 required a higher concentration of agonist for its activation, leading to Ca2+ influx (EC50 = 293.3 ± 6.6 μm for the mutant and 93.6 ± 2.2 μm for wild-type P2X7) and ERK phosphorylation, which were not caused by differential cell-surface expression or related to high ATPase activity on the cell surface and in the extracellular space. K562 cells expressing this N187D mutant showed a proliferative advantage and reduced pro-apoptosis effects in vitro and in vivo. Furthermore, elevated angiogenesis and CD206-positive macrophage infiltration were found in tumor tissues formed by K562-M cells. In addition, higher expression of VEGF and MCP1 could be detected in tumor tissues formed by K562-M cells. Our results suggest that N187D P2X7, representing mutants hyposensitive to agonist, might be a positive regulator in the progression of hematopoietic malignancies. Nucleotides are new players in the intercellular communication network. P2X7 is a member of the P2X family of receptors, which are ATP-gated plasma membrane ion channels with diverse biological functions. Abnormal expression and dysfunction of P2X7 have been reported in leukemias. Here, we report a new P2X7 mutant (an A559-to-G substitution causing N187D P2X7) cloned from J6-1 leukemia cells. The characteristics of N187D P2X7 were studied by establishing stably transfected K562 cell lines. Our results show that N187D P2X7 required a higher concentration of agonist for its activation, leading to Ca2+ influx (EC50 = 293.3 ± 6.6 μm for the mutant and 93.6 ± 2.2 μm for wild-type P2X7) and ERK phosphorylation, which were not caused by differential cell-surface expression or related to high ATPase activity on the cell surface and in the extracellular space. K562 cells expressing this N187D mutant showed a proliferative advantage and reduced pro-apoptosis effects in vitro and in vivo. Furthermore, elevated angiogenesis and CD206-positive macrophage infiltration were found in tumor tissues formed by K562-M cells. In addition, higher expression of VEGF and MCP1 could be detected in tumor tissues formed by K562-M cells. Our results suggest that N187D P2X7, representing mutants hyposensitive to agonist, might be a positive regulator in the progression of hematopoietic malignancies." @default.
• W2082119653 created "2016-06-24" @default.
• W2082119653 creator A5006095124 @default.
• W2082119653 creator A5015965233 @default.
• W2082119653 creator A5048689751 @default.
• W2082119653 creator A5052076760 @default.
• W2082119653 creator A5070160539 @default.
• W2082119653 creator A5081950834 @default.
• W2082119653 creator A5086969890 @default.
• W2082119653 date "2010-11-01" @default.
• W2082119653 modified "2023-10-18" @default.
• W2082119653 title "The Hyposensitive N187D P2X7 Mutant Promotes Malignant Progression in Nude Mice" @default.
• W2082119653 cites W1480357432 @default.
• W2082119653 cites W1481135965 @default.
• W2082119653 cites W1564075285 @default.
• W2082119653 cites W1964755615 @default.
• W2082119653 cites W1975496939 @default.
• W2082119653 cites W1983449340 @default.
• W2082119653 cites W1989598674 @default.
• W2082119653 cites W1993059138 @default.
• W2082119653 cites W1996799865 @default.
• W2082119653 cites W2001142764 @default.
• W2082119653 cites W2018612932 @default.
• W2082119653 cites W2020013385 @default.
• W2082119653 cites W2028684902 @default.
• W2082119653 cites W2038602542 @default.
• W2082119653 cites W2045270601 @default.
• W2082119653 cites W2050434108 @default.
• W2082119653 cites W2065319956 @default.
• W2082119653 cites W2068284025 @default.
• W2082119653 cites W2070663123 @default.
• W2082119653 cites W2072023433 @default.
• W2082119653 cites W2085850146 @default.
• W2082119653 cites W2109509015 @default.
• W2082119653 cites W2118652772 @default.
• W2082119653 cites W2119517477 @default.
• W2082119653 cites W2121594719 @default.
• W2082119653 cites W2122246903 @default.
• W2082119653 cites W2126695278 @default.
• W2082119653 cites W2131464730 @default.
• W2082119653 cites W2132958789 @default.
• W2082119653 cites W2151516998 @default.
• W2082119653 cites W2161619210 @default.
• W2082119653 cites W2163175900 @default.
• W2082119653 cites W2333209163 @default.
• W2082119653 doi "https://doi.org/10.1074/jbc.m110.128488" @default.
• W2082119653 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2975240" @default.
• W2082119653 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20837475" @default.
• W2082119653 hasPublicationYear "2010" @default.
• W2082119653 type Work @default.
• W2082119653 sameAs 2082119653 @default.
• W2082119653 citedByCount "23" @default.
• W2082119653 countsByYear W20821196532012 @default.
• W2082119653 countsByYear W20821196532013 @default.
• W2082119653 countsByYear W20821196532014 @default.
• W2082119653 countsByYear W20821196532015 @default.
• W2082119653 countsByYear W20821196532016 @default.
• W2082119653 countsByYear W20821196532017 @default.
• W2082119653 countsByYear W20821196532019 @default.
• W2082119653 countsByYear W20821196532020 @default.
• W2082119653 countsByYear W20821196532021 @default.
• W2082119653 countsByYear W20821196532023 @default.
• W2082119653 crossrefType "journal-article" @default.
• W2082119653 hasAuthorship W2082119653A5006095124 @default.
• W2082119653 hasAuthorship W2082119653A5015965233 @default.
• W2082119653 hasAuthorship W2082119653A5048689751 @default.
• W2082119653 hasAuthorship W2082119653A5052076760 @default.
• W2082119653 hasAuthorship W2082119653A5070160539 @default.
• W2082119653 hasAuthorship W2082119653A5081950834 @default.
• W2082119653 hasAuthorship W2082119653A5086969890 @default.
• W2082119653 hasBestOaLocation W20821196531 @default.
• W2082119653 hasConcept C104317684 @default.
• W2082119653 hasConcept C109159458 @default.
• W2082119653 hasConcept C11960822 @default.
• W2082119653 hasConcept C143065580 @default.
• W2082119653 hasConcept C153911025 @default.
• W2082119653 hasConcept C170493617 @default.
• W2082119653 hasConcept C171122931 @default.
• W2082119653 hasConcept C190283241 @default.
• W2082119653 hasConcept C2778938600 @default.
• W2082119653 hasConcept C2780394083 @default.
• W2082119653 hasConcept C28328180 @default.
• W2082119653 hasConcept C28406088 @default.
• W2082119653 hasConcept C502942594 @default.
• W2082119653 hasConcept C54009773 @default.
• W2082119653 hasConcept C54355233 @default.
• W2082119653 hasConcept C55493867 @default.
• W2082119653 hasConcept C57074206 @default.
• W2082119653 hasConcept C79879829 @default.
• W2082119653 hasConcept C81885089 @default.
• W2082119653 hasConcept C86803240 @default.
• W2082119653 hasConcept C95444343 @default.
• W2082119653 hasConceptScore W2082119653C104317684 @default.
• W2082119653 hasConceptScore W2082119653C109159458 @default.
• W2082119653 hasConceptScore W2082119653C11960822 @default.
• W2082119653 hasConceptScore W2082119653C143065580 @default.
• W2082119653 hasConceptScore W2082119653C153911025 @default.
• W2082119653 hasConceptScore W2082119653C170493617 @default.

• next