001     299000
005     20250318095036.0
024 7 _ |a 10.1016/j.canlet.2025.217581
|2 doi
024 7 _ |a pmid:39983894
|2 pmid
024 7 _ |a 0304-3835
|2 ISSN
024 7 _ |a 1872-7980
|2 ISSN
037 _ _ |a DKFZ-2025-00410
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Abooali, Maryam
|b 0
245 _ _ |a Intracellular and extracellular activities of V-domain Ig-containing suppressor of T cell activation (VISTA) modulated by immunosuppressive factors of tumour microenvironment.
260 _ _ |a Amsterdam [u.a.]
|c 2025
|b Elsevier Science
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 1742287798_3582
|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
500 _ _ |a 2025 Apr 28;616:217581
520 _ _ |a V-domain Ig-containing suppressor of T cell activation (VISTA) is a unique immune checkpoint protein, which was reported to display both receptor and ligand activities. However, the mechanisms of regulation of VISTA activity and functions by factors of tumour microenvironment (TME) remain unclear and understanding these processes is required in order to develop successful personalised cancer immunotherapeutic strategies and approaches. Here we report for the very first time that VISTA interacts with another immune checkpoint protein galectin-9 inside the cell most likely facilitating its interaction with TGF-β-activated kinase 1 (TAK1). This process is required for protection of lysosomes, which is crucial for many cell types and tissues. We found that VISTA expression can be differentially controlled by crucial factors present in TME, such as transforming growth factor beta type 1 (TGF-β) and hypoxia as well as other factors activating hypoxic signalling. We confirmed that involvement of these important pathways modulated by TME differentially influences VISTA expression in different cell types. These networks include: TGF-β-Smad3 pathway, TAK1 (TGF-β-activated kinase 1) or apoptosis signal-regulating kinase 1 (ASK1)-induced activation of activating transcription factor 2 (ATF-2) and hypoxic signalling pathway. Based on this work we determined the five critical functions of VISTA and the role of TME factors in controlling (modulating or downregulating) VISTA expression.
536 _ _ |a 311 - Zellbiologie und Tumorbiologie (POF4-311)
|0 G:(DE-HGF)POF4-311
|c POF4-311
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
700 1 _ |a Schlichtner, Stephanie
|0 P:(DE-He78)0b6e32bf4b6d335c6b11d5edaef8bfd3
|b 1
|u dkfz
700 1 _ |a Lei, Xi
|b 2
700 1 _ |a Aliu, Nijas
|b 3
700 1 _ |a Ruggiero, Sabrina
|b 4
700 1 _ |a Loges, Sonia
|0 P:(DE-HGF)0
|b 5
700 1 _ |a Ziegler, Martin
|0 P:(DE-He78)62a3cc13c7db450aa0e711ce99b43d7b
|b 6
|u dkfz
700 1 _ |a Hertel, Franziska
|0 P:(DE-He78)470d596989d1c5c31fdaa5a2b638e5ae
|b 7
|u dkfz
700 1 _ |a Volckmar, Anna-Lena
|b 8
700 1 _ |a Stenzinger, Albrecht
|b 9
700 1 _ |a Christopoulos, Petros
|b 10
700 1 _ |a Thomas, Michael
|b 11
700 1 _ |a Klenova, Elena
|b 12
700 1 _ |a Meyer, N Helge
|b 13
700 1 _ |a Boussios, Stergios
|b 14
700 1 _ |a Heaton, Nigel
|b 15
700 1 _ |a Zen, Yoh
|b 16
700 1 _ |a Zamalloa, Ane
|b 17
700 1 _ |a Chokshi, Shilpa
|b 18
700 1 _ |a Urbani, Luca
|b 19
700 1 _ |a Richard, Sophie
|b 20
700 1 _ |a Kirubendran, Kavitha
|b 21
700 1 _ |a Hussain, Rohanah
|b 22
700 1 _ |a Siligardi, Giuliano
|b 23
700 1 _ |a Cholewa, Dietmar
|b 24
700 1 _ |a Berger, Steffen M
|b 25
700 1 _ |a Yasinska, Inna M
|b 26
700 1 _ |a Fasler-Kan, Elizaveta
|b 27
700 1 _ |a Sumbayev, Vadim V
|b 28
773 _ _ |a 10.1016/j.canlet.2025.217581
|g p. 217581 -
|0 PERI:(DE-600)2004212-7
|p 217581
|t Cancer letters
|v 616
|y 2025
|x 0304-3835
909 C O |p VDB
|o oai:inrepo02.dkfz.de:299000
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 1
|6 P:(DE-He78)0b6e32bf4b6d335c6b11d5edaef8bfd3
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 5
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 6
|6 P:(DE-He78)62a3cc13c7db450aa0e711ce99b43d7b
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 7
|6 P:(DE-He78)470d596989d1c5c31fdaa5a2b638e5ae
913 1 _ |a DE-HGF
|b Gesundheit
|l Krebsforschung
|1 G:(DE-HGF)POF4-310
|0 G:(DE-HGF)POF4-311
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Zellbiologie und Tumorbiologie
|x 0
914 1 _ |y 2025
915 _ _ |a Nationallizenz
|0 StatID:(DE-HGF)0420
|2 StatID
|d 2024-12-16
|w ger
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b CANCER LETT : 2022
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2024-12-16
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2024-12-16
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2024-12-16
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b CANCER LETT : 2022
|d 2024-12-16
920 1 _ |0 I:(DE-He78)A420-20160331
|k A420
|l Personalisierte Medizinische Onkologie
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)A420-20160331
980 _ _ |a UNRESTRICTED


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21