ArticleJAK-STAT2012
Acetylation and sumoylation control STAT5 activation antagonistically.
Article in JAK-STAT, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Role of TLRs in HIV-1 Infection and Potential of TLR Agonists in HIV-1 Vaccine Development and Treatment Strategies.Pathogens (Basel, Switzerland) · 2023Review
- STAT proteins: a kaleidoscope of canonical and non-canonical functions in immunity and cancer.Journal of hematology & oncology · 2021Review
- Review
- Pharmacological Inhibition of Oncogenic STAT3 and STAT5 Signaling in Hematopoietic Cancers.Cancers · 2020Review
- Cell Metabolism Control Through O-GlcNAcylation of STAT5: A Full or Empty Fuel Tank Makes a Big Difference for Cancer Cell Growth and Survival.International journal of molecular sciences · 2019Review
- Review
- O-GlcNAcylation of STAT5 controls tyrosine phosphorylation and oncogenic transcription in STAT5-dependent malignancies.Leukemia · 2017Article
- Granulocyte colony-stimulating factor receptor signaling in severe congenital neutropenia, chronic neutrophilic leukemia, and related malignancies.Experimental hematology · 2017Review
- Article
- Article
- Review
- STAT5 acetylation: Mechanisms and consequences for immunological control and leukemogenesis.JAK-STAT · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STAT5 proteins are activated by tyrosine phosphorylation, but recently further post-translation modifications such as serine/threonine phosphorylation, acetylation at lysine residues or sumoylation in close vicinity of the critical tyrosine residue have been reported. Here, we discuss new findings on impaired STAT5 signaling in lymphocytes isolated from a SUMO-specific protease knockout mouse (SENP1(-/-)), which results in sumoylated STAT5 and abolishes tyrosine phosphorylation. Van Nguyen and colleagues examined acetylation and sumoylation of STAT5 and found that both modifications act antagonistically to control tyrosine phosphorylation of STAT5.
Indexed as
Identifiers
What OpenQuestion holds
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.