FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2593235722> ?p ?o ?g. }

• W2593235722 abstract "To investigate the role of chromosome region maintenance-1 (CRM1) in Crohn's disease (CD) and its potential pathological mechanisms.The expression and distribution of CRM1 in mucosal biopsies from patients with active CD and normal controls were detected by immunohistochemistry (IHC). We established a murine model of acute colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). Western blot was performed to investigate the expression levels of CRM1, apoptotic markers (active caspase-3 and cleaved PARP), p27kip1 and p-p27ser10. IHC was performed to evaluate the distribution of CRM1, and double immunofluorescence (IF) was performed to evaluate the co-localization of CRM1 and active capase-3. Cells of the human intestinal epithelial cell line HT-29 were incubated with tumor necrosis factor-α (TNF-α) to establish an apoptotic in vitro model. Western blot was performed to determine the expression levels of CRM1, active caspase-3, cleaved PARP and p-p27ser10. Cytoplasmic and nuclear extracts were assessed to examine the translocation of CRM1. The interaction between CRM1 and p27kip1 was assessed by co-immunoprecipitation (co-IP) assays. Furthermore, we used small interfering RNA (siRNA) to knock down the protein expression of CRM1 in HT-29 cells and then measured the expression of active caspase-3, cleaved PARP and p-p27ser10. Flow cytometry was used to determine the effect of CRM1 on intestinal epithelial cell (IEC) apoptosis.We observed up-regulation of CRM1 accompanied by elevated levels of IEC apoptotic markers (active caspase-3 and cleaved PARP) and p-p27ser10 in IECs of patients with active CD and in TNBS-induced colitis model cells. However, the expression of p27kip1 was negatively correlated with the expression patterns of CRM1, p-p27ser10 and apoptotic biochemical markers. Co-localization of CRM1 and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of CRM1 in IEC apoptosis. By employing TNF-α-treated HT-29 cells as an in vitro IEC apoptosis model, we found that the expression levels of CRM1 and p-p27ser10 were in accordance with active caspase-3 and cleaved PARP. In addition, immunoprecipitation confirmed the physical interaction between CRM1 and p27kip1. siRNA knockdown of CRM1 significantly inhibited the phosphorylation of p27kip1 and the expression of active caspase-3 and cleaved PARP. In addition, flow cytometry analysis also showed that silencing CRM1 by siRNA inhibited TNF-α-induced cellular apoptosis in HT-29 cells.Up-regulated CRM1 may facilitate IEC apoptosis possibly through p27kip1 in CD, indicating an important role of CRM1 in the pathophysiology of CD." @default.
• W2593235722 created "2017-03-16" @default.
• W2593235722 creator A5009562280 @default.
• W2593235722 creator A5011692149 @default.
• W2593235722 creator A5020296251 @default.
• W2593235722 creator A5021793023 @default.
• W2593235722 creator A5023242949 @default.
• W2593235722 creator A5047499885 @default.
• W2593235722 creator A5075733288 @default.
• W2593235722 creator A5083646645 @default.
• W2593235722 creator A5084682327 @default.
• W2593235722 date "2017-09-01" @default.
• W2593235722 modified "2023-09-26" @default.
• W2593235722 title "Chromosome region maintenance-1 (CRM1) regulates apoptosis of intestinal epithelial cells via p27kip1 in Crohn's disease" @default.
• W2593235722 cites W142985249 @default.
• W2593235722 cites W1569868450 @default.
• W2593235722 cites W1977532087 @default.
• W2593235722 cites W1991611148 @default.
• W2593235722 cites W1995240167 @default.
• W2593235722 cites W1998486262 @default.
• W2593235722 cites W2004136552 @default.
• W2593235722 cites W2006639479 @default.
• W2593235722 cites W2009094983 @default.
• W2593235722 cites W2009386327 @default.
• W2593235722 cites W2011698244 @default.
• W2593235722 cites W2022912279 @default.
• W2593235722 cites W2025400851 @default.
• W2593235722 cites W2027424540 @default.
• W2593235722 cites W2031682344 @default.
• W2593235722 cites W2033004457 @default.
• W2593235722 cites W2042598897 @default.
• W2593235722 cites W2046072152 @default.
• W2593235722 cites W2056384821 @default.
• W2593235722 cites W2058710858 @default.
• W2593235722 cites W2062520391 @default.
• W2593235722 cites W2065644803 @default.
• W2593235722 cites W2067005914 @default.
• W2593235722 cites W2072582894 @default.
• W2593235722 cites W2077511764 @default.
• W2593235722 cites W2082739624 @default.
• W2593235722 cites W2087050697 @default.
• W2593235722 cites W2092104789 @default.
• W2593235722 cites W2096890855 @default.
• W2593235722 cites W2099655761 @default.
• W2593235722 cites W2113855055 @default.
• W2593235722 cites W2114915170 @default.
• W2593235722 cites W2131766686 @default.
• W2593235722 cites W2141679700 @default.
• W2593235722 cites W2154748714 @default.
• W2593235722 cites W2156025284 @default.
• W2593235722 cites W2161015371 @default.
• W2593235722 cites W2165122599 @default.
• W2593235722 cites W2170056941 @default.
• W2593235722 cites W2325707043 @default.
• W2593235722 doi "https://doi.org/10.1016/j.clinre.2017.01.012" @default.
• W2593235722 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28286054" @default.
• W2593235722 hasPublicationYear "2017" @default.
• W2593235722 type Work @default.
• W2593235722 sameAs 2593235722 @default.
• W2593235722 citedByCount "2" @default.
• W2593235722 countsByYear W25932357222020 @default.
• W2593235722 crossrefType "journal-article" @default.
• W2593235722 hasAuthorship W2593235722A5009562280 @default.
• W2593235722 hasAuthorship W2593235722A5011692149 @default.
• W2593235722 hasAuthorship W2593235722A5020296251 @default.
• W2593235722 hasAuthorship W2593235722A5021793023 @default.
• W2593235722 hasAuthorship W2593235722A5023242949 @default.
• W2593235722 hasAuthorship W2593235722A5047499885 @default.
• W2593235722 hasAuthorship W2593235722A5075733288 @default.
• W2593235722 hasAuthorship W2593235722A5083646645 @default.
• W2593235722 hasAuthorship W2593235722A5084682327 @default.
• W2593235722 hasConcept C104317684 @default.
• W2593235722 hasConcept C12519072 @default.
• W2593235722 hasConcept C153911025 @default.
• W2593235722 hasConcept C159654299 @default.
• W2593235722 hasConcept C182979987 @default.
• W2593235722 hasConcept C190283241 @default.
• W2593235722 hasConcept C203014093 @default.
• W2593235722 hasConcept C22615655 @default.
• W2593235722 hasConcept C2776415932 @default.
• W2593235722 hasConcept C2778236600 @default.
• W2593235722 hasConcept C31573885 @default.
• W2593235722 hasConcept C502942594 @default.
• W2593235722 hasConcept C54009773 @default.
• W2593235722 hasConcept C54355233 @default.
• W2593235722 hasConcept C552990157 @default.
• W2593235722 hasConcept C553184892 @default.
• W2593235722 hasConcept C55493867 @default.
• W2593235722 hasConcept C81885089 @default.
• W2593235722 hasConcept C82381507 @default.
• W2593235722 hasConcept C86803240 @default.
• W2593235722 hasConceptScore W2593235722C104317684 @default.
• W2593235722 hasConceptScore W2593235722C12519072 @default.
• W2593235722 hasConceptScore W2593235722C153911025 @default.
• W2593235722 hasConceptScore W2593235722C159654299 @default.
• W2593235722 hasConceptScore W2593235722C182979987 @default.
• W2593235722 hasConceptScore W2593235722C190283241 @default.
• W2593235722 hasConceptScore W2593235722C203014093 @default.
• W2593235722 hasConceptScore W2593235722C22615655 @default.
• W2593235722 hasConceptScore W2593235722C2776415932 @default.

• next