ArticleThe EMBO journal2000
A small amphipathic alpha-helical region is required for transcriptional activities and proteasome-dependent turnover of the tyrosine-phosphorylated Stat5.
Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 121 citations in OpenAlex.
- Unexpected functional role of the transactivation domain for nuclear import of STAT5.Communications biology · 2026Article
- GTN Enhances Antitumor Effects of Doxorubicin in TNBC by Targeting the Immunosuppressive Activity of PMN-MDSC.Cancers · 2023Article
- The implications of alternative pre-mRNA splicing in cell signal transduction.Experimental & molecular medicine · 2023Review
- A Narrative Review of STAT Proteins in Diabetic Retinopathy: From Mechanisms to Therapeutic Prospects.Ophthalmology and therapy · 2022Review
- Impact of STAT Proteins in Tumor Progress and Therapy Resistance in Advanced and Metastasized Prostate Cancer.Cancers · 2021Review
- Proteasome α6 Subunit Negatively Regulates the JAK/STAT Pathway and Blood Cell Activation inFrontiers in immunology · 2021Article
- Kras-Deficient T Cells Attenuate Graft-versus-Host Disease but Retain Graft-versus-Leukemia Activity.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- FBXW7-mediated stability regulation of signal transducer and activator of transcription 2 in melanoma formation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Regulation of murine skeletal muscle growth by STAT5B is age- and sex-specific.Skeletal muscle · 2019Article
- Calreticulin-mutant proteins induce megakaryocytic signaling to transform hematopoietic cells and undergo accelerated degradation and Golgi-mediated secretion.Journal of hematology & oncology · 2016Article
- Dual-Specificity Phosphatase 4 Regulates STAT5 Protein Stability and Helper T Cell Polarization.PloS one · 2015Article
- STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.Oncotarget · 2012Article
- Quantification of degeneracy in biological systems for characterization of functional interactions between modules.Journal of theoretical biology · 2012Article
- Leptin signaling and Alzheimer's disease.American journal of neurodegenerative disease · 2012Article
- PARP-1 deficiency blocks IL-5 expression through calpain-dependent degradation of STAT-6 in a murine asthma model.Allergy · 2011Article
- The tumor suppressor hTid1 inhibits STAT5b activity via functional interaction.The Journal of biological chemistry · 2011Article
- Stat5a serine 725 and 779 phosphorylation is a prerequisite for hematopoietic transformation.Blood · 2010Article
- Signal transducer and activation of transcription (STAT) 4beta, a shorter isoform of interleukin-12-induced STAT4, is preferentially activated by estrogen.Endocrinology · 2009Article
- Inteferons pen the JAK-STAT pathway.Seminars in cell & developmental biology · 2008Review
- Osteopontin mediates Stat1 degradation to inhibit iNOS transcription in a cecal ligation and puncture model of sepsis.Surgery · 2008Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Cytokines induce the tyrosine phosphorylation and associated activation of signal transducers and activators of transcription (Stat). The mechanisms by which this response is terminated are largely unknown. Among a variety of inhibitors examined, the proteasome inhibitors MG132 and lactacystin affected Stat4, Stat5 and Stat6 turnover by significantly stabilizing the tyrosine-phosphorylated form. However, these proteasome inhibitors did not affect downregulation of the tyrosine-phosphorylated Stat1, Stat2 and Stat3. With Stat5 isoforms, we have observed that tyrosine-phosphorylated carboxyl-truncated forms of Stat5 proteins were considerably more stable than phosphorylated wild-type forms of the protein. Also, the C-terminal region of Stat5 could confer proteasome-dependent downregulation to Stat1. With a series of C-terminal deletion mutants, we have defined a relatively small, potentially amphipathic alpha-helical region that is required for the rapid turnover of the phosphorylated Stat5 proteins. The region is also required for transcriptional activation, suggesting that the functions are linked. The results are consistent with a model in which the transcriptional activation domain of activated Stat5 is required for its transcriptional activity and downregulation through a proteasome-dependent pathway.
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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.