ArticleMolecular and cellular biology1999
hSiah2 is a new Vav binding protein which inhibits Vav-mediated signaling pathways.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- SIAH proteins: critical roles in leukemogenesis.Leukemia · 2013Review
- S-nitrosylation of B23/nucleophosmin by GAPDH protects cells from the SIAH1-GAPDH death cascade.The Journal of cell biology · 2012Article
- ARTS and Siah collaborate in a pathway for XIAP degradation.Molecular cell · 2011Article
- Distinct expression patterns of the E3 ligase SIAH-1 and its partner Kid/KIF22 in normal tissues and in the breast tumoral processes.Journal of experimental & clinical cancer research : CR · 2010Article
- The ubiquitin ligase Siah2 and the hypoxia response.Molecular cancer research : MCR · 2009Review
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- Siah-1S, a novel splice variant of Siah-1 (seven in absentia homolog), counteracts Siah-1-mediated downregulation of beta-catenin.Oncogene · 2007Article
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- Generation and analysis of Siah2 mutant mice.Molecular and cellular biology · 2003Article
- A binding motif for Siah ubiquitin ligase.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Stress-induced decrease in TRAF2 stability is mediated by Siah2.The EMBO journal · 2002Article
- Phyllopod acts as an adaptor protein to link the sina ubiquitin ligase to the substrate protein tramtrack.Molecular and cellular biology · 2002Article
- Vav1 is a component of transcriptionally active complexes.The Journal of experimental medicine · 2002Article
- The ubiquitin ligase component Siah1a is required for completion of meiosis I in male mice.Molecular and cellular biology · 2002Article
- The RING finger protein Siah-1 regulates the level of the transcriptional coactivator OBF-1.The EMBO journal · 2001Article
- Regulation of BOB.1/OBF.1 stability by SIAH.The EMBO journal · 2001Article
- SIAH-1 interacts with alpha-tubulin and degrades the kinesin Kid by the proteasome pathway during mitosis.Oncogene · 2000Article
- Vav3 mediates receptor protein tyrosine kinase signaling, regulates GTPase activity, modulates cell morphology, and induces cell transformation.Molecular and cellular biology · 2000Article
- Regulatory and signaling properties of the Vav family.Molecular and cellular biology · 2000Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hematopoietic proto-oncogene vav has been characterized as a Rac1-GDP/GTP exchanger protein which regulates cytoskeletal reorganization as well as signaling pathways leading to the activation of stress-activated protein kinases (SAPK/JNKs). Furthermore, vav overexpression enhances basal and T-cell receptor (TCR)-mediated stimulation of the nuclear factor of activated T cells (NFAT). We report here the interaction between Vav and hSiah2, a mammalian homolog of Drosophila Seven in absentia (Sina) that has been implicated in R7 photoreceptor cell formation during Drosophila eye development via the proteasome degradation pathway. Vav and hSiah2 interact in vitro and in vivo and colocalize in the cytoplasm of hematopoietic cells. The Src homology domain of Vav and the C-terminal region of hSiah2 are required for this interaction. We provide evidence for a negative regulation by hSiah2 of Vav-induced basal and TCR-mediated NFAT-dependent transcription. Overexpression of hSiah2 also inhibits the onco-Vav-induced JNK activation. Although the Vav-interacting domain is located in the C-terminal portion of hSiah2, the N-terminal region of hSiah2 is necessary for the inhibitory role that seems to be independent of the proteasome degradation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.