FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3088931844> ?p ?o ?g. }

• W3088931844 abstract "Abstract Background： Hirschsprung’s disease (HSCR) is a congenital colon disease characterized by the lack of ganglion cells which is closely related to impaired migration and proliferation of enteric neural crest cells (ENCCs). Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been authenticated as an important class of regulators of biological functions. In this study, a microarray analysis was conducted and found that Rhabdomyosarcoma 2-associated transcript (RMST), a newly defined lncRNA, was down-regulated in the stenotic segment of HSCR patients. MiR-1251 is transcribed from the intron region of RMST and was also low expressed in the aganglionic tract. This study aimed to clarify the roles they played in the occurrence of HSCR. Methods： qRT-PCR was applied to validate the mRNA expression of RMST, miR-1251, SOX2 and AHNAK, while western blotting was employed to evaluate the protein level of SOX2 and AHNAK in clinical samples and cells. CCK-8 and transwell assays were used to detect cell proliferation and migration after transfection. Chromatin immunoprecipitation (CHIP) was applied to confirm SOX2 could bind to the promoter region of miR-1251. RNA binding protein immunoprecipitation (RIP) was used to demonstrate the interaction between RMST and SOX2. Dul-luciferase reporter assay was performed to confirm miR-1251 could interact with AHNAK. Results: When the expression of RMST or miR-1251 was reduced, cell proliferation and migration was attenuated. However, RMST not to influence the expression of miR-1251 directly. Through bioinformatic analysis, transcription factor SOX2 was predicted to bind to the promoter region of miR-1251 which was confirmed by CHIP assay. We also demonstrated that RMST exerted as a co-regulator of SOX2 via RIP assay. AHNAK was predicted as the downstream gene of miR-1251 confirmed by the dual-luciferase reporter assay. Furtherly, rescue experiments showed RMST functioned as a transcription co-regulator of SOX2 to upregulate the expression of downstream gene AHNAK by strengthening the regulation of SOX2 on miR-1251 in HSCR. Conclusions: These findings uncovered the role of RMST/SOX2/miR-1251/AHNAK pathway during the development of Hirschsprung's disease and presented potential therapeutic targets for HSCR." @default.
• W3088931844 created "2020-10-01" @default.
• W3088931844 creator A5004863693 @default.
• W3088931844 creator A5021169746 @default.
• W3088931844 creator A5022462605 @default.
• W3088931844 creator A5034250958 @default.
• W3088931844 creator A5053967110 @default.
• W3088931844 creator A5054175249 @default.
• W3088931844 creator A5072378052 @default.
• W3088931844 creator A5075901687 @default.
• W3088931844 date "2020-12-21" @default.
• W3088931844 modified "2023-09-27" @default.
• W3088931844 title "lncRNA-RMST Functioned as a SOX2 Transcription Co-regulator to Regulate miR-1251 in the Progression of Hirschsprung's Disease" @default.
• W3088931844 cites W1996391360 @default.
• W3088931844 cites W2002702165 @default.
• W3088931844 cites W2047222236 @default.
• W3088931844 cites W2054677853 @default.
• W3088931844 cites W2075598942 @default.
• W3088931844 cites W2086538740 @default.
• W3088931844 cites W2088662406 @default.
• W3088931844 cites W2104882581 @default.
• W3088931844 cites W2131210947 @default.
• W3088931844 cites W2135445817 @default.
• W3088931844 cites W2145931062 @default.
• W3088931844 cites W2163133855 @default.
• W3088931844 cites W2189641654 @default.
• W3088931844 cites W2253228615 @default.
• W3088931844 cites W2310459715 @default.
• W3088931844 cites W2403600548 @default.
• W3088931844 cites W2595718592 @default.
• W3088931844 cites W2613424444 @default.
• W3088931844 cites W2751847132 @default.
• W3088931844 cites W2751933285 @default.
• W3088931844 cites W2789614451 @default.
• W3088931844 cites W2795382323 @default.
• W3088931844 cites W2885105504 @default.
• W3088931844 cites W2886269920 @default.
• W3088931844 cites W2916099678 @default.
• W3088931844 cites W2923724699 @default.
• W3088931844 cites W2963185595 @default.
• W3088931844 cites W2968954088 @default.
• W3088931844 cites W2971198922 @default.
• W3088931844 cites W2972412282 @default.
• W3088931844 cites W2990965923 @default.
• W3088931844 cites W2996161270 @default.
• W3088931844 cites W2996658600 @default.
• W3088931844 cites W2997348366 @default.
• W3088931844 cites W3000314003 @default.
• W3088931844 cites W3000680274 @default.
• W3088931844 cites W3004108255 @default.
• W3088931844 cites W3008367627 @default.
• W3088931844 cites W3008601088 @default.
• W3088931844 cites W3013468467 @default.
• W3088931844 doi "https://doi.org/10.21203/rs.3.rs-130704/v1" @default.
• W3088931844 hasPublicationYear "2020" @default.
• W3088931844 type Work @default.
• W3088931844 sameAs 3088931844 @default.
• W3088931844 citedByCount "0" @default.
• W3088931844 crossrefType "posted-content" @default.
• W3088931844 hasAuthorship W3088931844A5004863693 @default.
• W3088931844 hasAuthorship W3088931844A5021169746 @default.
• W3088931844 hasAuthorship W3088931844A5022462605 @default.
• W3088931844 hasAuthorship W3088931844A5034250958 @default.
• W3088931844 hasAuthorship W3088931844A5053967110 @default.
• W3088931844 hasAuthorship W3088931844A5054175249 @default.
• W3088931844 hasAuthorship W3088931844A5072378052 @default.
• W3088931844 hasAuthorship W3088931844A5075901687 @default.
• W3088931844 hasBestOaLocation W30889318441 @default.
• W3088931844 hasConcept C101762097 @default.
• W3088931844 hasConcept C104317684 @default.
• W3088931844 hasConcept C134320426 @default.
• W3088931844 hasConcept C145059251 @default.
• W3088931844 hasConcept C150194340 @default.
• W3088931844 hasConcept C2777933648 @default.
• W3088931844 hasConcept C502942594 @default.
• W3088931844 hasConcept C54355233 @default.
• W3088931844 hasConcept C6929976 @default.
• W3088931844 hasConcept C71829478 @default.
• W3088931844 hasConcept C86339819 @default.
• W3088931844 hasConcept C86803240 @default.
• W3088931844 hasConcept C95444343 @default.
• W3088931844 hasConceptScore W3088931844C101762097 @default.
• W3088931844 hasConceptScore W3088931844C104317684 @default.
• W3088931844 hasConceptScore W3088931844C134320426 @default.
• W3088931844 hasConceptScore W3088931844C145059251 @default.
• W3088931844 hasConceptScore W3088931844C150194340 @default.
• W3088931844 hasConceptScore W3088931844C2777933648 @default.
• W3088931844 hasConceptScore W3088931844C502942594 @default.
• W3088931844 hasConceptScore W3088931844C54355233 @default.
• W3088931844 hasConceptScore W3088931844C6929976 @default.
• W3088931844 hasConceptScore W3088931844C71829478 @default.
• W3088931844 hasConceptScore W3088931844C86339819 @default.
• W3088931844 hasConceptScore W3088931844C86803240 @default.
• W3088931844 hasConceptScore W3088931844C95444343 @default.
• W3088931844 hasLocation W30889318441 @default.
• W3088931844 hasLocation W30889318442 @default.
• W3088931844 hasLocation W30889318443 @default.
• W3088931844 hasOpenAccess W3088931844 @default.
• W3088931844 hasPrimaryLocation W30889318441 @default.
• W3088931844 hasRelatedWork W1133482058 @default.

• next