ArticleThe Biochemical journal2007
STAT5 isoforms: controversies and clarifications.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
6 citing papers in PubMed, 12 citations in OpenAlex.
- Get Spliced: Uniting Alternative Splicing and Arthritis.International journal of molecular sciences · 2024Review
- Protein tyrosine phosphatases as wardens of STAT signaling.JAK-STAT · 2014Review
- Tuning of alternative splicing--switch from proto-oncogene to tumor suppressor.International journal of biological sciences · 2013Article
- Mechanisms of unphosphorylated STAT3 transcription factor binding to DNA.The Journal of biological chemistry · 2012Article
- GM-CSF induces STAT5 binding at epigenetic regulatory sites within the Csf2 promoter of non-obese diabetic (NOD) mouse myeloid cells.Journal of autoimmunity · 2008Article
- The different functions of Stat5 and chromatin alteration through Stat5 proteins.Frontiers in bioscience : a journal and virtual library · 2008Review
Corrections and comments
- Comment on
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
STAT (signal transducer and activator of transcription) family transcription factors are critical regulators of the development and differentiation of many cell types. STAT isoforms are generated by alternative splicing, but have also been suggested to be generated post-transcriptionally. In this issue of the Biochemical Journal, Schuster and colleagues have identified cathepsin G as the protease that cleaves full-length STAT5 (STAT5alpha) to generate a C-terminally truncated form in immature myeloid cells. However, the authors argue that this proteolytically generated isoform does not occur naturally in vivo; rather, it is artificially generated by cathepsin G during the preparation of cell extracts. This new evidence calls into question the physiological significance of this putative isoform and forces the general re-examination of proteolytically generated STAT isoforms.
Indexed as
Identifiers
17447893PMC1868835W2119819670What 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.