Home > Publications database > VEGF-A isoforms differentially regulate ATF-2-dependent VCAM-1 gene expression and endothelial-leukocyte interactions. > print |
001 | 119924 | ||
005 | 20240228135001.0 | ||
024 | 7 | _ | |a 10.1091/mbc.E14-05-0962 |2 doi |
024 | 7 | _ | |a pmid:24966171 |2 pmid |
024 | 7 | _ | |a pmc:PMC4142621 |2 pmc |
024 | 7 | _ | |a 1044-2030 |2 ISSN |
024 | 7 | _ | |a 1059-1524 |2 ISSN |
024 | 7 | _ | |a 1939-4586 |2 ISSN |
024 | 7 | _ | |a altmetric:2797603 |2 altmetric |
037 | _ | _ | |a DKFZ-2017-00515 |
041 | _ | _ | |a eng |
082 | _ | _ | |a 570 |
100 | 1 | _ | |a Fearnley, Gareth W |b 0 |
245 | _ | _ | |a VEGF-A isoforms differentially regulate ATF-2-dependent VCAM-1 gene expression and endothelial-leukocyte interactions. |
260 | _ | _ | |a Bethesda, Md. |c 2014 |b American Society for Cell Biology |
336 | 7 | _ | |a article |2 DRIVER |
336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1490276916_30632 |2 PUB:(DE-HGF) |
336 | 7 | _ | |a ARTICLE |2 BibTeX |
336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
520 | _ | _ | |a Vascular endothelial growth factor A (VEGF-A) regulates many aspects of vascular physiology. VEGF-A stimulates signal transduction pathways that modulate endothelial outputs such as cell migration, proliferation, tubulogenesis, and cell-cell interactions. Multiple VEGF-A isoforms exist, but the biological significance of this is unclear. Here we analyzed VEGF-A isoform-specific stimulation of VCAM-1 gene expression, which controls endothelial-leukocyte interactions, and show that this is dependent on both ERK1/2 and activating transcription factor-2 (ATF-2). VEGF-A isoforms showed differential ERK1/2 and p38 MAPK phosphorylation kinetics. A key feature of VEGF-A isoform-specific ERK1/2 activation and nuclear translocation was increased phosphorylation of ATF-2 on threonine residue 71 (T71). Using reverse genetics, we showed ATF-2 to be functionally required for VEGF-A-stimulated endothelial VCAM-1 gene expression. ATF-2 knockdown blocked VEGF-A-stimulated VCAM-1 expression and endothelial-leukocyte interactions. ATF-2 was also required for other endothelial cell outputs, such as cell migration and tubulogenesis. In contrast, VCAM-1 was essential only for promoting endothelial-leukocyte interactions. This work presents a new paradigm for understanding how soluble growth factor isoforms program complex cellular outputs and responses by modulating signal transduction pathways. |
536 | _ | _ | |a 313 - Cancer risk factors and prevention (POF3-313) |0 G:(DE-HGF)POF3-313 |c POF3-313 |f POF III |x 0 |
588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
650 | _ | 7 | |a ATF2 protein, human |2 NLM Chemicals |
650 | _ | 7 | |a Activating Transcription Factor 2 |2 NLM Chemicals |
650 | _ | 7 | |a Protein Isoforms |2 NLM Chemicals |
650 | _ | 7 | |a VEGFA protein, human |2 NLM Chemicals |
650 | _ | 7 | |a Vascular Cell Adhesion Molecule-1 |2 NLM Chemicals |
650 | _ | 7 | |a Vascular Endothelial Growth Factor A |2 NLM Chemicals |
650 | _ | 7 | |a KDR protein, human |0 EC 2.7.10.1 |2 NLM Chemicals |
650 | _ | 7 | |a Vascular Endothelial Growth Factor Receptor-2 |0 EC 2.7.10.1 |2 NLM Chemicals |
700 | 1 | _ | |a Odell, Adam F |b 1 |
700 | 1 | _ | |a Latham, Antony M |b 2 |
700 | 1 | _ | |a Mughal, Nadeem A |b 3 |
700 | 1 | _ | |a Bruns, Alexander F |b 4 |
700 | 1 | _ | |a Burgoyne, Nicholas J |b 5 |
700 | 1 | _ | |a Homer-Vanniasinkam, Shervanthi |b 6 |
700 | 1 | _ | |a Zachary, Ian C |b 7 |
700 | 1 | _ | |a Hollstein, Monica |0 P:(DE-He78)f3bec70c95e9e3dce0f39d54b3843118 |b 8 |u dkfz |
700 | 1 | _ | |a Wheatcroft, Stephen B |b 9 |
700 | 1 | _ | |a Ponnambalam, Sreenivasan |b 10 |
773 | _ | _ | |a 10.1091/mbc.E14-05-0962 |g Vol. 25, no. 16, p. 2509 - 2521 |0 PERI:(DE-600)1474922-1 |n 16 |p 2509 - 2521 |t Molecular biology of the cell |v 25 |y 2014 |x 1059-1524 |
909 | C | O | |o oai:inrepo02.dkfz.de:119924 |p VDB |
910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 8 |6 P:(DE-He78)f3bec70c95e9e3dce0f39d54b3843118 |
913 | 1 | _ | |a DE-HGF |l Krebsforschung |1 G:(DE-HGF)POF3-310 |0 G:(DE-HGF)POF3-313 |2 G:(DE-HGF)POF3-300 |v Cancer risk factors and prevention |x 0 |4 G:(DE-HGF)POF |3 G:(DE-HGF)POF3 |b Gesundheit |
914 | 1 | _ | |y 2014 |
915 | _ | _ | |a JCR |0 StatID:(DE-HGF)0100 |2 StatID |b MOL BIOL CELL : 2015 |
915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0200 |2 StatID |b SCOPUS |
915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0300 |2 StatID |b Medline |
915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0310 |2 StatID |b NCBI Molecular Biology Database |
915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0199 |2 StatID |b Thomson Reuters Master Journal List |
915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0110 |2 StatID |b Science Citation Index |
915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0150 |2 StatID |b Web of Science Core Collection |
915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0111 |2 StatID |b Science Citation Index Expanded |
915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1030 |2 StatID |b Current Contents - Life Sciences |
915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1050 |2 StatID |b BIOSIS Previews |
915 | _ | _ | |a IF < 5 |0 StatID:(DE-HGF)9900 |2 StatID |
920 | 1 | _ | |0 I:(DE-He78)C016-20160331 |k C016 |l Genetische Veränderungen bei der Karzinogenese |x 0 |
980 | _ | _ | |a journal |
980 | _ | _ | |a VDB |
980 | _ | _ | |a I:(DE-He78)C016-20160331 |
980 | _ | _ | |a UNRESTRICTED |
Library | Collection | CLSMajor | CLSMinor | Language | Author |
---|