{"id":{"repo_id":"nus","oai_identifier":"oai:scholarbank.nus.edu.sg:10635/213217"},"canonical_url":"https://search.dev.ndltd.org/etd/nus/oai:scholarbank.nus.edu.sg:10635/213217","repository":{"repo_id":"nus","name":"National University of Singapore","base_url":"https://scholarbank.nus.edu.sg/oai/request"},"display":{"title":"THE ROLE OF ADARS-INTERACTING RNA HELICASES IN SHAPING THE RNA EDITOME IN CANCER","abstract":"Adenosine-to-inosine (A-to-I) RNA editing, primarily catalysed by the ADAR family of proteins, is oftentimes dysregulated in cancers. However, the regulatory mechanisms controlling editing frequency in cancer cells remain largely elusive. Besides factors affecting the expression and activity of ADAR proteins, ADARs-interacting proteins are known to orchestrate editing regulation. From our co-immunoprecipitation coupled with mass spectrometry analysis, we identified 23 RNA helicases as ADARs interactors, most having an unknown role in A-to-I editing. Employing an unbiased transcriptome-wide A-to-I editing analysis, I unravelled that 6 of these ADARs-interacting RNA helicases could reshape the A-to-I editome in a bidirectional, enhancive, or repressive fashion in cancer cells. I further investigated two bidirectional regulators DHX9 and DDX21, with oncogenic functions, that regulate distinct subsets of editing sites plausibly via RNA-binding dependent and independent mechanisms respectively. My findings illustrate crucial insights about the mechanistic underpinnings of A-to-I editing regulation mediated by ADARs-interacting RNA helicases.","abstract_html":"Adenosine-to-inosine (A-to-I) RNA editing, primarily catalysed by the ADAR family of proteins, is oftentimes dysregulated in cancers. However, the regulatory mechanisms controlling editing frequency in cancer cells remain largely elusive. Besides factors affecting the expression and activity of ADAR proteins, ADARs-interacting proteins are known to orchestrate editing regulation. From our co-immunoprecipitation coupled with mass spectrometry analysis, we identified 23 RNA helicases as ADARs interactors, most having an unknown role in A-to-I editing. Employing an unbiased transcriptome-wide A-to-I editing analysis, I unravelled that 6 of these ADARs-interacting RNA helicases could reshape the A-to-I editome in a bidirectional, enhancive, or repressive fashion in cancer cells. I further investigated two bidirectional regulators DHX9 and DDX21, with oncogenic functions, that regulate distinct subsets of editing sites plausibly via RNA-binding dependent and independent mechanisms respectively. My findings illustrate crucial insights about the mechanistic underpinnings of A-to-I editing regulation mediated by ADARs-interacting RNA helicases.","abstract_has_math":false,"creators":["PRIYANKAA PITCHESHWAR"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2021,"date_issued":"2021-08-05","date_published":"2021-08-05","updated_at":"2026-07-24T03:33:34Z","subjects":["A-to-I RNA editing, bidirectional regulators, cancer"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":null,"outbound_label":null,"outbound_source":null},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["PRIYANKAA PITCHESHWAR"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.issued","label":"Date","values":["2021-08-05"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://scholarbank.nus.edu.sg/handle/10635/213217"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["A-to-I RNA editing, bidirectional regulators, cancer"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://scholarbank.nus.edu.sg/bitstreams/aa2a5721-0b99-487b-9517-76b0fc81f94e/download"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Adenosine-to-inosine (A-to-I) RNA editing, primarily catalysed by the ADAR family of proteins, is oftentimes dysregulated in cancers. However, the regulatory mechanisms controlling editing frequency in cancer cells remain largely elusive. Besides factors affecting the expression and activity of ADAR proteins, ADARs-interacting proteins are known to orchestrate editing regulation. From our co-immunoprecipitation coupled with mass spectrometry analysis, we identified 23 RNA helicases as ADARs interactors, most having an unknown role in A-to-I editing. Employing an unbiased transcriptome-wide A-to-I editing analysis, I unravelled that 6 of these ADARs-interacting RNA helicases could reshape the A-to-I editome in a bidirectional, enhancive, or repressive fashion in cancer cells. I further investigated two bidirectional regulators DHX9 and DDX21, with oncogenic functions, that regulate distinct subsets of editing sites plausibly via RNA-binding dependent and independent mechanisms respectively. My findings illustrate crucial insights about the mechanistic underpinnings of A-to-I editing regulation mediated by ADARs-interacting RNA helicases."]},{"key":"dc:format.checksum.md5","label":"Dc Format Checksum Md5","values":["08e1823ed4062702df18e87d2e30dab6","18c4038ba5dbdebf594423a384b3f731"]},{"key":"dc:title","label":"Title","values":["THE ROLE OF ADARS-INTERACTING RNA HELICASES IN SHAPING THE RNA EDITOME IN CANCER"]}]}],"canonical_facts":{"dc:creator":["PRIYANKAA PITCHESHWAR"],"dc:date.issued":["2021-08-05"],"dc:description.abstract":["Adenosine-to-inosine (A-to-I) RNA editing, primarily catalysed by the ADAR family of proteins, is oftentimes dysregulated in cancers. However, the regulatory mechanisms controlling editing frequency in cancer cells remain largely elusive. Besides factors affecting the expression and activity of ADAR proteins, ADARs-interacting proteins are known to orchestrate editing regulation. From our co-immunoprecipitation coupled with mass spectrometry analysis, we identified 23 RNA helicases as ADARs interactors, most having an unknown role in A-to-I editing. Employing an unbiased transcriptome-wide A-to-I editing analysis, I unravelled that 6 of these ADARs-interacting RNA helicases could reshape the A-to-I editome in a bidirectional, enhancive, or repressive fashion in cancer cells. I further investigated two bidirectional regulators DHX9 and DDX21, with oncogenic functions, that regulate distinct subsets of editing sites plausibly via RNA-binding dependent and independent mechanisms respectively. My findings illustrate crucial insights about the mechanistic underpinnings of A-to-I editing regulation mediated by ADARs-interacting RNA helicases."],"dc:format.checksum.md5":["08e1823ed4062702df18e87d2e30dab6","18c4038ba5dbdebf594423a384b3f731"],"dc:identifier.uri":["https://scholarbank.nus.edu.sg/bitstreams/aa2a5721-0b99-487b-9517-76b0fc81f94e/download"],"dc:relation.isreferencedby":["https://scholarbank.nus.edu.sg/handle/10635/213217"],"dc:subject":["A-to-I RNA editing, bidirectional regulators, cancer"],"dc:title":["THE ROLE OF ADARS-INTERACTING RNA HELICASES IN SHAPING THE RNA EDITOME IN CANCER"],"dc:type":["Thesis"]},"updated_at":"2026-07-24T03:33:34Z"}