ReviewJAK-STAT2012
Comparative evolutionary genomics of the STAT family of transcription factors.
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 42 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
42 citing papers in PubMed, 62 citations in OpenAlex.
- Integrated Evolutionary and Multi-Omic Analysis of STAT Family Activation Across Solid Tumors.Genes · 2026Article
- Asymmetry and redundancy of STAT5 paralogs across CD8Communications biology · 2026Article
- Trawling the depths of gene regulation: transcription-factor families orchestrating immunity in teleost fish.Frontiers in immunology · 2026Review
- Genome-Wide Identification and Expression Analysis of the STAT Family in Reeve's Turtle (Mauremys reevesii).Biochemical genetics · 2025Article
- STAT Signature Dish: Serving Immunity with a Side of Dietary Control.Biomolecules · 2025Review
- Unlocking the dual role of autophagy: A new strategy for treating lung cancer.Journal of pharmaceutical analysis · 2025Review
- Maintenance of hematopoietic stem cells by tyrosine-unphosphorylated STAT5 and JAK inhibition.Blood advances · 2025Article
- Asymmetry of Motif Conservation Within Their Homotypic Pairs Distinguishes DNA-Binding Domains of Target Transcription Factors in ChIP-Seq Data.International journal of molecular sciences · 2025Article
- Modulation of STAT6 signaling for hepatoprotection.Frontiers in pharmacology · 2025Review
- Hemophagocytic lymphohistiocytosis: current treatment advances, emerging targeted therapy and underlying mechanisms.Journal of hematology & oncology · 2024Review
- Genetic analysis of a phenotypic loss in the mechanosensory entrainment of a circalunar clock.PLoS genetics · 2023Article
- The ups and downs of STAT3 function: too much, too little and human immune dysregulation.Clinical and experimental immunology · 2023Review
- Bow-tie architectures in biological and artificial neural networks: Implications for network evolution and assay design.iScience · 2023Article
- In vivo single-cell transcriptomics reveal Klebsiella pneumoniae skews lung macrophages to promote infection.EMBO molecular medicine · 2022Article
- STAT3 in medulloblastoma: a key transcriptional regulator and potential therapeutic target.Molecular biology reports · 2022Review
- Targeting fibrosis, mechanisms and cilinical trials.Signal transduction and targeted therapy · 2022Review
- Mechanisms of Viral Degradation of Cellular Signal Transducer and Activator of Transcription 2.International journal of molecular sciences · 2022Review
- Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function.Basic research in cardiology · 2021Review
- The Roles of Post-Translational Modifications in STAT3 Biological Activities and Functions.Biomedicines · 2021Review
- Role of intracellular signaling pathways and their inhibitors in the treatment of inflammation.Inflammopharmacology · 2021Review
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 1 country.
Funding
Abstract
The STAT signaling pathway is one of the seven common pathways that govern cell fate decisions during animal development. Comparative genomics revealed multiple incidences of stat gene duplications throughout metazoan evolutionary history. While pseudogenization is a frequent fate of duplicated genes, many of these STAT duplications evolved into novel genes through rapid sequence diversification and neofunctionalization. Additionally, the core of STAT gene regulatory networks, comprising stat1 through 4, stat5 and stat6, arose early in vertebrate evolution, probably through the two whole genome duplication events that occurred after the split of Cephalochordates but before the rise of Chondrichthyes. While another complete genome duplication event took place during the evolution of bony fish after their separation from the tetrapods about 450 million years ago (Mya), modern fish have only one set of these core stats, suggesting the rapid loss of most duplicated stat genes. The two stat5 genes in mammals likely arose from a duplication event in early Eutherian evolution, a period from about 310 Mya at the avian-mammal divergence to the separation of marsupials from other mammals about 130 Mya. These analyses indicate that whole genome duplications and gene duplications by unequal chromosomal crossing over were likely the major mechanisms underlying the evolution of STATs.
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.