ReviewOncogene2000
Janus kinases: components of multiple signaling pathways.
Review in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 1 of them a synthesis that pooled it.
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
165 citing papers in PubMed, 1 synthesis or guideline pooled it, 466 citations in OpenAlex.
- Association ofBioscience reports · 2019Pooled it
- Extracellular matrix rigidity controls breast cancer metastasis via TYK2-mediated mechanotransduction.Nature communications · 2026Article
- Exploration of Novel Chemical Spaces to Discover JAK1 Inhibitors: An Ensemble Docking-Guided Deep Learning Approach.ACS omega · 2026Article
- Extracellular matrix rigidity controls breast cancer metastasis via TYK2-mediated mechanotransduction.bioRxiv : the preprint server for biology · 2025Article
- Adverse effects of Janus kinase inhibitors with relevance for daily practice in dermatology.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025Review
- Review
- MicroRNA-204-5p Deficiency within the vmPFC Region Contributes to Neuroinflammation and Behavioral Disorders via the JAK2/STAT3 Signaling Pathway in Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Methamphetamine-induced cardiotoxicity: in search of protective transcriptional mechanisms.Herz · 2024Review
- GHRH-stimulated pituitary small extracellular vesicles inhibit hepatocyte proliferation and IGF-1 expression by its cargo miR-375-3p.Journal of nanobiotechnology · 2024Article
- Cardiovascular Risk in Philadelphia-Negative Myeloproliferative Neoplasms: Mechanisms and Implications-A Narrative Review.Current issues in molecular biology · 2024Review
- The Role of the JAK-STAT Pathway in Childhood B-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Review
- Kinase inhibitor macrocycles: a perspective on limiting conformational flexibility when targeting the kinome with small molecules.RSC medicinal chemistry · 2024Review
- Eleutheroside B alleviates oxidative stress and neuroinflammation by inhibiting the JAK2/STAT3 signaling pathway in a rat high altitude cerebral edema model.Frontiers in pharmacology · 2024Article
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- JAK inhibitors for inflammatory bowel disease: recent advances.Frontline gastroenterology · 2024Review
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Are All Janus Kinase Inhibitors for Inflammatory Bowel Disease the Same?Gastroenterology & hepatology · 2023Article
- Review
- Association between Polymorphism in the Janus Kinase 2 (Animals : an open access journal from MDPI · 2023Article
- Galectin-1 induces a tumor-associated macrophage phenotype and upregulates indoleamine 2,3-dioxygenase-1.iScience · 2023Article
105 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
Cytoplasmic Janus protein tyrosine kinases (JAKs) are crucial components of diverse signal transduction pathways that govern cellular survival, proliferation, differentiation and apoptosis. Evidence to date, indicates that JAK kinase function may integrate components of diverse signaling cascades. While it is likely that activation of STAT proteins may be an important function attributed to the JAK kinases, it is certainly not the only function performed by this key family of cytoplasmic tyrosine kinases. Emerging evidence indicates that phosphorylation of cytokine and growth factor receptors may be the primary functional attribute of JAK kinases. The JAK-triggered receptor phosphorylation can potentially be a rate-limiting event for a successful culmination of downstream signaling events. In support of this hypothesis, it has been found that JAK kinase function is required for optimal activation of the Src-kinase cascade, the Ras-MAP kinase pathway, the PI3K-AKT pathway and STAT signaling following the interaction of cytokine/interferon receptors with their ligands. Aberrations in JAK kinase activity, that may lead to derailment of one or more of the above mentioned pathways could disrupt normal cellular responses and result in disease states. Thus, over-activation of JAK kinases has been implicated in tumorigenesis. In contrast, loss of JAK kinase function has been found to result in disease states such as severe-combined immunodeficiency. In summary, optimal JAK kinase activity is a critical determinant of normal transmission of cytokine and growth factor signals.
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.