ReviewJAK-STAT2012
Alternative ways of modulating JAK-STAT pathway: Looking beyond phosphorylation.
Review in JAK-STAT, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Understanding the structural features of JAK2 inhibitors: a combined 3D-QSAR, DFT and molecular dynamics study.Molecular diversity · 2019Article
- Structural Biology of STAT3 and Its Implications for Anticancer Therapies Development.International journal of molecular sciences · 2018Review
- Suppression of STAT3 NHMolecular carcinogenesis · 2018Article
- Article
- Impact of the N-Terminal Domain of STAT3 in STAT3-Dependent Transcriptional Activity.Molecular and cellular biology · 2015Article
- Involvement of the janus kinase/signal transducer and activator of transcription signaling pathway in multiple sclerosis and the animal model of experimental autoimmune encephalomyelitis.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Molecular aspects of development and regulation of endometriosis.Reproductive biology and endocrinology : RB&E · 2014Review
- STAT3 suppresses transcription of proapoptotic genes in cancer cells with the involvement of its N-terminal domain.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Targeting STATs for cancer therapy: "Undruggable" no more.JAK-STAT · 2012Article
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.
Funding
Abstract
Most attempts to develop inhibitors of STAT transcription factors target either activating phosphorylation of tyrosine residue or SH2 domains. However, all six domains of STATs are highly conserved between the species and play important roles in the function of this family of transcription factors. STATs are involved in numerous protein-protein interactions that are likely to regulate and fine tune transcriptional activity. Targeting these interactions can provide plentiful opportunities for the discovery of novel drug candidates and powerful chemical biology tools. Using N-terminal domains as an example we describe alternative rational approaches to the development of modulators of JAK-STAT signaling.
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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.