FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2023861744> ?p ?o ?g. }

• W2023861744 abstract "Abstract Background Activation Induced cytidine Deaminase (AID) targets the immunoglobulin genes of activated B cells, where it converts cytidine to uracil to induce mutagenesis and recombination. While essential for immunoglobulin gene diversification, AID misregulation can result in genomic instability and oncogenic transformation. This is classically illustrated in Burkitt's lymphoma, which is characterized by AID-induced mutation and reciprocal translocation of the c-MYC oncogene with the IgH loci. Originally thought to be B cell-specific, AID now appears to be misexpressed in several epithelial cancers, raising the specter that AID may also participate in non-B cell carcinogenesis. Methods The mutagenic potential of AID argues for the existence of cellular regulators capable of repressing inappropriate AID expression. MicroRNAs (miRs) have this capacity, and we have examined the publically available human AID EST dataset for miR complementarities to the human AID 3'UTR. In this work, we have evaluated the capacity of two candidate miRs to repress human AID expression in MCF-7 breast carcinoma cells. Results We have discovered moderate miR-155 and pronounced miR-93 complementary target sites encoded within the human AID mRNA. Luciferase reporter assays indicate that both miR-93 and miR-155 can interact with the 3'UTR of AID to block expression. In addition, over-expression of either miR in MCF-7 cells reduces endogenous AID protein, but not mRNA, levels. Similarly indicative of AID translational regulation, depletion of either miR in MCF-7 cells increases AID protein levels without concurrent increases in AID mRNA. Conclusions Together, our findings demonstrate that miR-93 and miR-155 constitutively suppress AID translation in MCF-7 cells, suggesting widespread roles for these miRs in preventing genome cytidine deaminations, mutagenesis, and oncogenic transformation. In addition, our characterization of an obscured miR-93 target site located within the AID 3'UTR supports the recent suggestion that many miR regulations have been overlooked due to the prevalence of truncated 3'UTR annotations." @default.
• W2023861744 created "2016-06-24" @default.
• W2023861744 creator A5033599506 @default.
• W2023861744 creator A5062904702 @default.
• W2023861744 creator A5077685901 @default.
• W2023861744 date "2011-08-10" @default.
• W2023861744 modified "2023-09-27" @default.
• W2023861744 title "Repression of human activation induced cytidine deaminase by miR-93 and miR-155" @default.
• W2023861744 cites W1548106667 @default.
• W2023861744 cites W1969286968 @default.
• W2023861744 cites W1970760326 @default.
• W2023861744 cites W1972989638 @default.
• W2023861744 cites W1978598063 @default.
• W2023861744 cites W1980952225 @default.
• W2023861744 cites W1985264665 @default.
• W2023861744 cites W1988821953 @default.
• W2023861744 cites W1990060110 @default.
• W2023861744 cites W1992941735 @default.
• W2023861744 cites W2004284284 @default.
• W2023861744 cites W2024426483 @default.
• W2023861744 cites W2026304664 @default.
• W2023861744 cites W2037821015 @default.
• W2023861744 cites W2044601473 @default.
• W2023861744 cites W2049079731 @default.
• W2023861744 cites W2050434777 @default.
• W2023861744 cites W2053702192 @default.
• W2023861744 cites W2053705988 @default.
• W2023861744 cites W2056668940 @default.
• W2023861744 cites W2060236569 @default.
• W2023861744 cites W2061265134 @default.
• W2023861744 cites W2067026554 @default.
• W2023861744 cites W2067608841 @default.
• W2023861744 cites W2069408870 @default.
• W2023861744 cites W2080800490 @default.
• W2023861744 cites W2089274312 @default.
• W2023861744 cites W2091613784 @default.
• W2023861744 cites W2098309323 @default.
• W2023861744 cites W2100187123 @default.
• W2023861744 cites W2107268184 @default.
• W2023861744 cites W2108230228 @default.
• W2023861744 cites W2118133351 @default.
• W2023861744 cites W2121629705 @default.
• W2023861744 cites W2123830039 @default.
• W2023861744 cites W2126662967 @default.
• W2023861744 cites W2128100527 @default.
• W2023861744 cites W2135109966 @default.
• W2023861744 cites W2147835141 @default.
• W2023861744 cites W2149146453 @default.
• W2023861744 cites W2149584454 @default.
• W2023861744 cites W2154143786 @default.
• W2023861744 cites W2154841949 @default.
• W2023861744 cites W2155044281 @default.
• W2023861744 cites W2157577917 @default.
• W2023861744 cites W2166316790 @default.
• W2023861744 cites W2167557255 @default.
• W2023861744 cites W2170629396 @default.
• W2023861744 cites W4241570450 @default.
• W2023861744 doi "https://doi.org/10.1186/1471-2407-11-347" @default.
• W2023861744 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3163633" @default.
• W2023861744 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21831295" @default.
• W2023861744 hasPublicationYear "2011" @default.
• W2023861744 type Work @default.
• W2023861744 sameAs 2023861744 @default.
• W2023861744 citedByCount "45" @default.
• W2023861744 countsByYear W20238617442012 @default.
• W2023861744 countsByYear W20238617442013 @default.
• W2023861744 countsByYear W20238617442014 @default.
• W2023861744 countsByYear W20238617442015 @default.
• W2023861744 countsByYear W20238617442017 @default.
• W2023861744 countsByYear W20238617442018 @default.
• W2023861744 countsByYear W20238617442019 @default.
• W2023861744 countsByYear W20238617442020 @default.
• W2023861744 countsByYear W20238617442021 @default.
• W2023861744 countsByYear W20238617442022 @default.
• W2023861744 countsByYear W20238617442023 @default.
• W2023861744 crossrefType "journal-article" @default.
• W2023861744 hasAuthorship W2023861744A5033599506 @default.
• W2023861744 hasAuthorship W2023861744A5062904702 @default.
• W2023861744 hasAuthorship W2023861744A5077685901 @default.
• W2023861744 hasBestOaLocation W20238617441 @default.
• W2023861744 hasConcept C104317684 @default.
• W2023861744 hasConcept C128526571 @default.
• W2023861744 hasConcept C145059251 @default.
• W2023861744 hasConcept C153911025 @default.
• W2023861744 hasConcept C159654299 @default.
• W2023861744 hasConcept C181199279 @default.
• W2023861744 hasConcept C27082348 @default.
• W2023861744 hasConcept C2776985229 @default.
• W2023861744 hasConcept C2778453870 @default.
• W2023861744 hasConcept C2781184954 @default.
• W2023861744 hasConcept C502942594 @default.
• W2023861744 hasConcept C54355233 @default.
• W2023861744 hasConcept C55493867 @default.
• W2023861744 hasConcept C555283112 @default.
• W2023861744 hasConcept C86803240 @default.
• W2023861744 hasConcept C95444343 @default.
• W2023861744 hasConceptScore W2023861744C104317684 @default.
• W2023861744 hasConceptScore W2023861744C128526571 @default.
• W2023861744 hasConceptScore W2023861744C145059251 @default.
• W2023861744 hasConceptScore W2023861744C153911025 @default.

• next