ReviewJAK-STAT2012
The JAK-STAT pathway and hematopoietic stem cells from the JAK2 V617F perspective.
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 37 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
37 citing papers in PubMed, 67 citations in OpenAlex.
- Role of Flow Cytometric Enumeration of Circulating hMICL (CD371) Positive Leukemic Stem Cells in Diagnosis and Prognostication of BCR::ABL1-Negative Myeloproliferative Neoplasms.International journal of laboratory hematology · 2026Article
- Nucleotide Substitution Biases in Related Cancer Driver Genes.International journal of molecular sciences · 2025Article
- Unfolded protein response signaling promotes myeloid cell production and cooperates with oncogenic mutation.bioRxiv : the preprint server for biology · 2025Article
- JAK2 46/1 (GGCC) Haplotype in Oncogenesis, as Risk Stratifier, and Indicator for Drug Resistance in Myeloproliferative Neoplasms.International journal of molecular sciences · 2025Review
- Dibenzo [a, c] phenazin-11-yl(phenyl) methanone (SBLJ23), a novel selective inhibitor targeting JAK2Oncology research · 2025Article
- Use of Transcriptomics to Identify Candidate Genes for Hematopoietic Differences Between Wujin and Duroc Pigs.Animals : an open access journal from MDPI · 2024Article
- Analysis of action of 1,4-naphthoquinone scaffold-derived compounds against acute myeloid leukemia based on network pharmacology, molecular docking and molecular dynamics simulation.Scientific reports · 2024Article
- The application of JAK inhibitors in the peri-transplantation period of hematopoietic stem cell transplantation for myelofibrosis.Annals of hematology · 2024Review
- Step by step analysis on gene datasets of growth phases in hematopoietic stem cells.Biochemistry and biophysics reports · 2024Article
- The JAK-STAT pathway: from structural biology to cytokine engineering.Signal transduction and targeted therapy · 2024Review
- PU-H71 (NSC 750424): a molecular masterpiece that targets HSP90 in cancer and beyond.Frontiers in pharmacology · 2024Review
- Exploring the JAK/STAT Signaling Pathway in Hepatocellular Carcinoma: Unraveling Signaling Complexity and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Mutations, inflammation and phenotype of myeloproliferative neoplasms.Frontiers in oncology · 2023Review
- The Contribution ofInternational journal of molecular sciences · 2022Review
- Conversion of a False Virtual Screen Hit into Selective JAK2 JH2 Domain Binders Using Convergent Design Strategies.ACS medicinal chemistry letters · 2022Article
- Design, Synthesis and Structure-Activity Relationship Studies of Meridianin Derivatives as Novel JAK/STAT3 Signaling Inhibitors.International journal of molecular sciences · 2022Article
- Review
- Gene expression profiling of CD34(+) cells from patients with myeloproliferative neoplasms.Oncology letters · 2021Article
- Colloidal Self-Assembled Patterns Maintain the Pluripotency and Promote the Hemopoietic Potential of Human Embryonic Stem Cells.Frontiers in cell and developmental biology · 2021Article
- Role of the JAK/STAT Pathway in Cervical Cancer: Its Relationship with HPV E6/E7 Oncoproteins.Cells · 2020Review
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
Janus kinases (JAKs) are non-receptor tyrosine kinases essential for activation of signaling mediated by cytokine receptors that lack catalytic activity, including receptors for erythropoietin, thrombopoietin, most interleukins and interferon. Upon hormone binding, JAKs phosphorylate tyrosine residues in the receptor cytoplasmic domains and in JAKs themselves leading to recruitment and activation of downstream signaling proteins such as signal transducer and activator of transcription (STAT). The JAK-STAT pathway is important for functional hematopoiesis and several activating mutations in JAK proteins have recently been described as underlying cause of blood disorders. One of the best studied examples is the JAK2 V617F mutant which is found in 95% of polycythemia vera patients and 50% of patients suffering from essential thrombocythemia and primary myelofibrosis. Much effort has been made to understand how the JAK2 V617F affects hematopoietic stem cell (HSC) renewal and lineage differentiation, since convincing evidence has been provided to support the notion that the mutation is acquired at the HSC level. We discuss several in vivo models that support contrary conclusions with respect to the advantage given to HSCs by JAK2 V617F. Moreover, we provide the current knowledge about STAT5 activation and its link to HSC expansion as well as amplification of the erythroid compartment. Evidence for both JAK2 V617F mutated HSCs exhibiting skewed differentiation potential and for amplification occurring after erythroid commitment has been provided, and we will discuss whether this evidence is relevant for the disease.
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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.