FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1781293224> ?p ?o ?g. }

• W1781293224 endingPage "159" @default.
• W1781293224 startingPage "151" @default.
• W1781293224 abstract "Sphingosine kinase (there are two isoforms, SK1 and SK2) catalyses the formation of sphingosine 1-phosphate (S1P), a bioactive lipid that can be released from cells to activate a family of G protein-coupled receptors, termed S1P1-5. In addition, S1P can bind to intracellular target proteins, such as HDAC1/2, to induce cell responses. There is increasing evidence of a role for S1P receptors (e.g. S1P4) and SK1 in cancer, where high expression of these proteins in ER negative breast cancer patient tumours is linked with poor prognosis. Indeed, evidence will be presented here to demonstrate that S1P4 is functionally linked with SK1 and the oncogene HER2 (ErbB2) to regulate mitogen-activated protein kinase pathways and growth of breast cancer cells. Although much emphasis is placed on SK1 in terms of involvement in oncogenesis, evidence will also be presented for a role of SK2 in both T-cell and B-cell acute lymphoblastic leukemia. In patient T-ALL lymphoblasts and T-ALL cell lines, we have demonstrated that SK2 inhibitors promote T-ALL cell death via autophagy and induce suppression of c-myc and PI3K/AKT pathways. We will also present evidence demonstrating that certain SK inhibitors promote oxidative stress and protein turnover via proteasomal degradative pathways linked with induction of p53-and p21-induced growth arrest. In addition, the SK1 inhibitor, PF-543 exacerbates disease progression in an experimental autoimmune encephalomyelitis mouse model indicating that SK1 functions in an anti-inflammatory manner. Indeed, sphingosine, which accumulates upon inhibition of SK1 activity, and sphingosine-like compounds promote activation of the inflammasome, which is linked with multiple sclerosis, to stimulate formation of the pro-inflammatory mediator, IL-1β. Such compounds could be exploited to produce antagonists that diminish exaggerated inflammation in disease. The therapeutic potential of modifying the SK-S1P receptor pathway in cancer and inflammation will therefore, be reviewed." @default.
• W1781293224 created "2016-06-24" @default.
• W1781293224 creator A5018753334 @default.
• W1781293224 creator A5023834954 @default.
• W1781293224 creator A5034750261 @default.
• W1781293224 creator A5037164805 @default.
• W1781293224 creator A5060561968 @default.
• W1781293224 creator A5068117615 @default.
• W1781293224 creator A5080970040 @default.
• W1781293224 creator A5081910376 @default.
• W1781293224 creator A5083844423 @default.
• W1781293224 date "2016-01-01" @default.
• W1781293224 modified "2023-10-01" @default.
• W1781293224 title "Role of sphingosine 1-phosphate receptors, sphingosine kinases and sphingosine in cancer and inflammation" @default.
• W1781293224 cites W146176651 @default.
• W1781293224 cites W1581414531 @default.
• W1781293224 cites W1974735495 @default.
• W1781293224 cites W1980524113 @default.
• W1781293224 cites W1983079076 @default.
• W1781293224 cites W1990405181 @default.
• W1781293224 cites W1991120891 @default.
• W1781293224 cites W1994625058 @default.
• W1781293224 cites W1995004385 @default.
• W1781293224 cites W1996386552 @default.
• W1781293224 cites W1996605319 @default.
• W1781293224 cites W1996784003 @default.
• W1781293224 cites W1997458456 @default.
• W1781293224 cites W2001160697 @default.
• W1781293224 cites W2005467120 @default.
• W1781293224 cites W2013230402 @default.
• W1781293224 cites W2019728679 @default.
• W1781293224 cites W2020730385 @default.
• W1781293224 cites W2021433993 @default.
• W1781293224 cites W2023293937 @default.
• W1781293224 cites W2023595695 @default.
• W1781293224 cites W2023962954 @default.
• W1781293224 cites W2037013426 @default.
• W1781293224 cites W2043847489 @default.
• W1781293224 cites W2046116275 @default.
• W1781293224 cites W2046605217 @default.
• W1781293224 cites W2047287528 @default.
• W1781293224 cites W2056697413 @default.
• W1781293224 cites W2059680252 @default.
• W1781293224 cites W2063894714 @default.
• W1781293224 cites W2064883021 @default.
• W1781293224 cites W2067928516 @default.
• W1781293224 cites W2074512079 @default.
• W1781293224 cites W2078794107 @default.
• W1781293224 cites W2083397512 @default.
• W1781293224 cites W2086406618 @default.
• W1781293224 cites W2086782603 @default.
• W1781293224 cites W2091414871 @default.
• W1781293224 cites W2092124807 @default.
• W1781293224 cites W2096273281 @default.
• W1781293224 cites W2096317294 @default.
• W1781293224 cites W2097202436 @default.
• W1781293224 cites W2098808575 @default.
• W1781293224 cites W2117047064 @default.
• W1781293224 cites W2125036060 @default.
• W1781293224 cites W2127049690 @default.
• W1781293224 cites W2130614040 @default.
• W1781293224 cites W2134340975 @default.
• W1781293224 cites W2141809186 @default.
• W1781293224 cites W2144314191 @default.
• W1781293224 cites W2145876349 @default.
• W1781293224 cites W2146527682 @default.
• W1781293224 cites W2149250424 @default.
• W1781293224 cites W2149902537 @default.
• W1781293224 cites W2150483305 @default.
• W1781293224 cites W2158842878 @default.
• W1781293224 cites W2163885294 @default.
• W1781293224 cites W2164773432 @default.
• W1781293224 cites W2172093498 @default.
• W1781293224 cites W2028914814 @default.
• W1781293224 doi "https://doi.org/10.1016/j.jbior.2015.09.001" @default.
• W1781293224 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26429117" @default.
• W1781293224 hasPublicationYear "2016" @default.
• W1781293224 type Work @default.
• W1781293224 sameAs 1781293224 @default.
• W1781293224 citedByCount "116" @default.
• W1781293224 countsByYear W17812932242016 @default.
• W1781293224 countsByYear W17812932242017 @default.
• W1781293224 countsByYear W17812932242018 @default.
• W1781293224 countsByYear W17812932242019 @default.
• W1781293224 countsByYear W17812932242020 @default.
• W1781293224 countsByYear W17812932242021 @default.
• W1781293224 countsByYear W17812932242022 @default.
• W1781293224 countsByYear W17812932242023 @default.
• W1781293224 crossrefType "journal-article" @default.
• W1781293224 hasAuthorship W1781293224A5018753334 @default.
• W1781293224 hasAuthorship W1781293224A5023834954 @default.
• W1781293224 hasAuthorship W1781293224A5034750261 @default.
• W1781293224 hasAuthorship W1781293224A5037164805 @default.
• W1781293224 hasAuthorship W1781293224A5060561968 @default.
• W1781293224 hasAuthorship W1781293224A5068117615 @default.
• W1781293224 hasAuthorship W1781293224A5080970040 @default.
• W1781293224 hasAuthorship W1781293224A5081910376 @default.
• W1781293224 hasAuthorship W1781293224A5083844423 @default.

• next