FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1997698927> ?p ?o ?g. }

• W1997698927 endingPage "e807" @default.
• W1997698927 startingPage "e807" @default.
• W1997698927 abstract "Thyroid iodide accumulation via the sodium/iodide symporter (NIS; SLC5A5) has been the basis for the longtime use of radio-iodide in the diagnosis and treatment of thyroid cancers. NIS is also expressed, but poorly functional, in some non-thyroid human cancers. In particular, it is much more strongly expressed in cholangiocarcinoma (CCA) and hepatocellular carcinoma (HCC) cell lines than in primary human hepatocytes (PHH). The transcription factors and signaling pathways that control NIS overexpression in these cancers is largely unknown. We identified two putative regulatory clusters of p53-responsive elements (p53REs) in the NIS core promoter, and investigated the regulation of NIS transcription by p53-family members in liver cancer cells. NIS promoter activity and endogenous NIS mRNA expression are stimulated by exogenously expressed p53-family members and significantly reduced by member-specific siRNAs. Chromatin immunoprecipitation analysis shows that the p53–REs clusters in the NIS promoter are differentially occupied by the p53-family members to regulate basal and DNA damage-induced NIS transcription. Doxorubicin strongly induces p53 and p73 binding to the NIS promoter, leading to an increased expression of endogenous NIS mRNA and protein in HCC and CCA cells, but not in PHH. Silencing NIS expression reduced doxorubicin-induced apoptosis in HCC cells, pointing to a possible role of a p53-family-dependent expression of NIS in apoptotic cell death. Altogether, these results indicate that the NIS gene is a direct target of the p53 family and suggests that the modulation of NIS by DNA-damaging agents is potentially exploitable to boost NIS upregulation in vivo." @default.
• W1997698927 created "2016-06-24" @default.
• W1997698927 creator A5024653835 @default.
• W1997698927 creator A5024747879 @default.
• W1997698927 creator A5025780107 @default.
• W1997698927 creator A5047108324 @default.
• W1997698927 creator A5049976461 @default.
• W1997698927 creator A5056673453 @default.
• W1997698927 creator A5059508363 @default.
• W1997698927 creator A5064563908 @default.
• W1997698927 creator A5078457997 @default.
• W1997698927 creator A5086068992 @default.
• W1997698927 date "2013-09-19" @default.
• W1997698927 modified "2023-10-10" @default.
• W1997698927 title "The sodium/iodide symporter NIS is a transcriptional target of the p53-family members in liver cancer cells" @default.
• W1997698927 cites W136769219 @default.
• W1997698927 cites W1491403843 @default.
• W1997698927 cites W1547551683 @default.
• W1997698927 cites W1964366490 @default.
• W1997698927 cites W1966355308 @default.
• W1997698927 cites W1968752204 @default.
• W1997698927 cites W1971598291 @default.
• W1997698927 cites W1973661184 @default.
• W1997698927 cites W1982822994 @default.
• W1997698927 cites W1992296999 @default.
• W1997698927 cites W2005013681 @default.
• W1997698927 cites W2009861669 @default.
• W1997698927 cites W2013321335 @default.
• W1997698927 cites W2014796515 @default.
• W1997698927 cites W2021129338 @default.
• W1997698927 cites W2024593733 @default.
• W1997698927 cites W2028321784 @default.
• W1997698927 cites W2034083247 @default.
• W1997698927 cites W2037674089 @default.
• W1997698927 cites W2038464222 @default.
• W1997698927 cites W2038587180 @default.
• W1997698927 cites W2038796544 @default.
• W1997698927 cites W2042245678 @default.
• W1997698927 cites W2043394193 @default.
• W1997698927 cites W2044641078 @default.
• W1997698927 cites W2045380897 @default.
• W1997698927 cites W2063665939 @default.
• W1997698927 cites W2067574516 @default.
• W1997698927 cites W2075371735 @default.
• W1997698927 cites W2076833060 @default.
• W1997698927 cites W2077019840 @default.
• W1997698927 cites W2079910956 @default.
• W1997698927 cites W2082832566 @default.
• W1997698927 cites W2084810075 @default.
• W1997698927 cites W2087008760 @default.
• W1997698927 cites W2089470253 @default.
• W1997698927 cites W2089806809 @default.
• W1997698927 cites W2090966017 @default.
• W1997698927 cites W2091923260 @default.
• W1997698927 cites W2092200570 @default.
• W1997698927 cites W2092789866 @default.
• W1997698927 cites W2095243258 @default.
• W1997698927 cites W2101888517 @default.
• W1997698927 cites W2113141752 @default.
• W1997698927 cites W2117994222 @default.
• W1997698927 cites W2126627575 @default.
• W1997698927 cites W2134781138 @default.
• W1997698927 cites W2140131559 @default.
• W1997698927 cites W2140907576 @default.
• W1997698927 cites W2144243892 @default.
• W1997698927 cites W2147545451 @default.
• W1997698927 cites W2151410031 @default.
• W1997698927 cites W2153057419 @default.
• W1997698927 cites W2154685721 @default.
• W1997698927 cites W2167379769 @default.
• W1997698927 cites W272605836 @default.
• W1997698927 doi "https://doi.org/10.1038/cddis.2013.302" @default.
• W1997698927 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3789165" @default.
• W1997698927 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24052075" @default.
• W1997698927 hasPublicationYear "2013" @default.
• W1997698927 type Work @default.
• W1997698927 sameAs 1997698927 @default.
• W1997698927 citedByCount "18" @default.
• W1997698927 countsByYear W19976989272013 @default.
• W1997698927 countsByYear W19976989272014 @default.
• W1997698927 countsByYear W19976989272015 @default.
• W1997698927 countsByYear W19976989272017 @default.
• W1997698927 countsByYear W19976989272019 @default.
• W1997698927 countsByYear W19976989272020 @default.
• W1997698927 countsByYear W19976989272022 @default.
• W1997698927 countsByYear W19976989272023 @default.
• W1997698927 crossrefType "journal-article" @default.
• W1997698927 hasAuthorship W1997698927A5024653835 @default.
• W1997698927 hasAuthorship W1997698927A5024747879 @default.
• W1997698927 hasAuthorship W1997698927A5025780107 @default.
• W1997698927 hasAuthorship W1997698927A5047108324 @default.
• W1997698927 hasAuthorship W1997698927A5049976461 @default.
• W1997698927 hasAuthorship W1997698927A5056673453 @default.
• W1997698927 hasAuthorship W1997698927A5059508363 @default.
• W1997698927 hasAuthorship W1997698927A5064563908 @default.
• W1997698927 hasAuthorship W1997698927A5078457997 @default.
• W1997698927 hasAuthorship W1997698927A5086068992 @default.
• W1997698927 hasBestOaLocation W19976989271 @default.

• next