FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3132335794> ?p ?o ?g. }

• W3132335794 abstract "The SALL2 transcription factor, an evolutionarily conserved gene through vertebrates, is involved in normal development and neuronal differentiation. In disease, SALL2 is associated with eye, kidney, and brain disorders, but mainly is related to cancer. Some studies support a tumor suppressor role and others an oncogenic role for SALL2, which seems to depend on the cancer type. An additional consideration is tissue-dependent expression of different SALL2 isoforms. Human and mouse SALL2 gene loci contain two promoters, each controlling the expression of a different protein isoform (E1 and E1A). Also, several improvements on the human genome assembly and gene annotation through next-generation sequencing technologies reveal correction and annotation of additional isoforms, obscuring dissection of SALL2 isoform-specific transcriptional targets and functions. We here integrated current data of normal/tumor gene expression databases along with ChIP-seq binding profiles to analyze SALL2 isoforms expression distribution and infer isoform-specific SALL2 targets. We found that the canonical SALL2 E1 isoform is one of the lowest expressed, while the E1A isoform is highly predominant across cell types. To dissect SALL2 isoform-specific targets, we analyzed publicly available ChIP-seq data from Glioblastoma tumor-propagating cells and in-house ChIP-seq datasets performed in SALL2 wild-type and E1A isoform knockout HEK293 cells. Another available ChIP-seq data in HEK293 cells (ENCODE Consortium Phase III) overexpressing a non-canonical SALL2 isoform (short_E1A) was also analyzed. Regardless of cell type, our analysis indicates that the SALL2 long E1 and E1A isoforms, but not short_E1A, are mostly contributing to transcriptional control, and reveals a highly conserved network of brain-specific transcription factors (i.e., SALL3, POU3F2, and NPAS3). Our data integration identified a conserved molecular network in which SALL2 regulates genes associated with neural function, cell differentiation, development, and cell adhesion between others. Also, we identified PODXL as a gene that is likely regulated by SALL2 across tissues. Our study encourages the validation of publicly available ChIP-seq datasets to assess a specific gene/isoform’s transcriptional targets. The knowledge of SALL2 isoforms expression and function in different tissue contexts is relevant to understanding its role in disease." @default.
• W3132335794 created "2021-03-01" @default.
• W3132335794 creator A5008319799 @default.
• W3132335794 creator A5022475487 @default.
• W3132335794 creator A5032796532 @default.
• W3132335794 creator A5035082677 @default.
• W3132335794 creator A5053048184 @default.
• W3132335794 creator A5057332775 @default.
• W3132335794 creator A5065184098 @default.
• W3132335794 creator A5069220234 @default.
• W3132335794 creator A5089812167 @default.
• W3132335794 date "2021-02-22" @default.
• W3132335794 modified "2023-10-03" @default.
• W3132335794 title "Characterization of SALL2 Gene Isoforms and Targets Across Cell Types Reveals Highly Conserved Networks" @default.
• W3132335794 cites W1608481248 @default.
• W3132335794 cites W1963553964 @default.
• W3132335794 cites W1968962291 @default.
• W3132335794 cites W1982290479 @default.
• W3132335794 cites W1983150473 @default.
• W3132335794 cites W1984248139 @default.
• W3132335794 cites W2010122622 @default.
• W3132335794 cites W2017688631 @default.
• W3132335794 cites W2018838463 @default.
• W3132335794 cites W2019267788 @default.
• W3132335794 cites W2021341670 @default.
• W3132335794 cites W2036870885 @default.
• W3132335794 cites W2043398720 @default.
• W3132335794 cites W2045362835 @default.
• W3132335794 cites W2064406354 @default.
• W3132335794 cites W2076534093 @default.
• W3132335794 cites W2088338354 @default.
• W3132335794 cites W2096690683 @default.
• W3132335794 cites W2097812689 @default.
• W3132335794 cites W2099915768 @default.
• W3132335794 cites W2108234281 @default.
• W3132335794 cites W2114302716 @default.
• W3132335794 cites W2118527670 @default.
• W3132335794 cites W2119324444 @default.
• W3132335794 cites W2120772060 @default.
• W3132335794 cites W2124954099 @default.
• W3132335794 cites W2136292095 @default.
• W3132335794 cites W2147231609 @default.
• W3132335794 cites W2158485828 @default.
• W3132335794 cites W2161645441 @default.
• W3132335794 cites W2162496698 @default.
• W3132335794 cites W2170551349 @default.
• W3132335794 cites W2170830174 @default.
• W3132335794 cites W2341539131 @default.
• W3132335794 cites W2346613849 @default.
• W3132335794 cites W2517548108 @default.
• W3132335794 cites W2528543174 @default.
• W3132335794 cites W2579217144 @default.
• W3132335794 cites W2606905591 @default.
• W3132335794 cites W2612932943 @default.
• W3132335794 cites W2757783981 @default.
• W3132335794 cites W2775755225 @default.
• W3132335794 cites W2801410246 @default.
• W3132335794 cites W2805281510 @default.
• W3132335794 cites W2892863317 @default.
• W3132335794 cites W2944381397 @default.
• W3132335794 cites W2945883683 @default.
• W3132335794 cites W2946191579 @default.
• W3132335794 cites W2950495754 @default.
• W3132335794 cites W2964393626 @default.
• W3132335794 cites W2982143550 @default.
• W3132335794 cites W3005174906 @default.
• W3132335794 cites W3012149288 @default.
• W3132335794 cites W3025534357 @default.
• W3132335794 cites W872810040 @default.
• W3132335794 doi "https://doi.org/10.3389/fgene.2021.613808" @default.
• W3132335794 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7937961" @default.
• W3132335794 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33692826" @default.
• W3132335794 hasPublicationYear "2021" @default.
• W3132335794 type Work @default.
• W3132335794 sameAs 3132335794 @default.
• W3132335794 citedByCount "3" @default.
• W3132335794 countsByYear W31323357942021 @default.
• W3132335794 countsByYear W31323357942022 @default.
• W3132335794 countsByYear W31323357942023 @default.
• W3132335794 crossrefType "journal-article" @default.
• W3132335794 hasAuthorship W3132335794A5008319799 @default.
• W3132335794 hasAuthorship W3132335794A5022475487 @default.
• W3132335794 hasAuthorship W3132335794A5032796532 @default.
• W3132335794 hasAuthorship W3132335794A5035082677 @default.
• W3132335794 hasAuthorship W3132335794A5053048184 @default.
• W3132335794 hasAuthorship W3132335794A5057332775 @default.
• W3132335794 hasAuthorship W3132335794A5065184098 @default.
• W3132335794 hasAuthorship W3132335794A5069220234 @default.
• W3132335794 hasAuthorship W3132335794A5089812167 @default.
• W3132335794 hasBestOaLocation W31323357941 @default.
• W3132335794 hasConcept C104317684 @default.
• W3132335794 hasConcept C150194340 @default.
• W3132335794 hasConcept C174510640 @default.
• W3132335794 hasConcept C53345823 @default.
• W3132335794 hasConcept C54355233 @default.
• W3132335794 hasConcept C70721500 @default.
• W3132335794 hasConcept C86803240 @default.
• W3132335794 hasConceptScore W3132335794C104317684 @default.
• W3132335794 hasConceptScore W3132335794C150194340 @default.
• W3132335794 hasConceptScore W3132335794C174510640 @default.

• next