Trial reportThe Journal of biological chemistry2013
Transgenic expression of microRNA-185 causes a developmental arrest of T cells by targeting multiple genes including Mzb1.
Trial report in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 40 citations in OpenAlex.
- Role of MZB1 in disease pathogenesis: current insights and future directions.Clinical and experimental medicine · 2026Review
- The systemic effects of 22q11.2 deletion syndrome on immunity.Journal of human immunity · 2026Review
- Research progress on the role of MZB1 in immune regulation.Frontiers in immunology · 2026Review
- MZB1-Driven Endoplasmic reticulum stress model as a predictor of breast cancer progression and survival.Functional & integrative genomics · 2025Article
- Understanding the Variability of 22q11.2 Deletion Syndrome: The Role of Epigenetic Factors.Genes · 2024Review
- StemDriver: a knowledgebase of gene functions for hematopoietic stem cell fate determination.Nucleic acids research · 2024Article
- Comprehensive phenotypic analysis of diverse FOXN1 variants.The Journal of allergy and clinical immunology · 2023Article
- Downregulation of miR-185 is a common pathogenic event in 22q11.2 deletion syndrome-related and idiopathic schizophrenia.Metabolic brain disease · 2022Article
- MZB1 expression indicates poor prognosis in estrogen receptor-positive breast cancer.Oncology letters · 2020Article
- High Mobility Group A (HMGA): Chromatin Nodes Controlled by a Knotty miRNA Network.International journal of molecular sciences · 2020Review
- FOXN1 compound heterozygous mutations cause selective thymic hypoplasia in humans.The Journal of clinical investigation · 2019Article
- Endogenous reduction of miR-185 accelerates cardiac function recovery in mice following myocardial infarction via targeting of cathepsin K.Journal of cellular and molecular medicine · 2019Article
- The Genetics and Epigenetics of 22q11.2 Deletion Syndrome.Frontiers in genetics · 2019Review
- Beyond mRNA: The role of non-coding RNAs in normal and aberrant hematopoiesis.Molecular genetics and metabolism · 2017Review
- MicroRNA-205 Maintains T Cell Development following Stress by Regulating Forkhead Box N1 and Selected Chemokines.The Journal of biological chemistry · 2016Article
- Original Research: Analysis of hepatic microRNA alterations in response to hepatitis B virus infection and pegylated interferon alpha-2a treatment.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Circulating miR-185 might be a novel biomarker for clinical outcome in patients with dilated cardiomyopathy.Scientific reports · 2016Article
- Immune cell-specific transcriptional profiling highlights distinct molecular pathways controlled by Tob1 upon experimental autoimmune encephalomyelitis.Scientific reports · 2016Article
- Increased complexin-1 and decreased miR-185 expression levels in Behçet's disease with and without neurological involvement.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016Article
- MicroRNA Mechanisms of Action: What have We Learned from Mice?Frontiers in genetics · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
miR-185 is a microRNA (miR) that targets Bruton's tyrosine kinase in B cells, with reductions in miR-185 linked to B cell autoantibody production. In hippocampal neurons, miR-185 targets both sarcoplasmic/endoplasmic reticulum calcium ATPase 2 and a novel Golgi inhibitor. This miR is haploinsufficient in 90-95% of individuals with chromosome 22q11.2 deletion syndrome, patients who can present with immune, cardiac, and parathyroid problems, learning disorders, and a high incidence of schizophrenia in adults. The reduced levels of miR-185 in neurons cause presynaptic neurotransmitter release. Many of the 22q11.2 deletion syndrome patients have a thymic hypoplasia, which results in a peripheral T cell lymphopenia and unusual T helper cell skewing. The molecular targets of miR-185 in thymocytes are unknown. Using an miR-185 T cell transgenic approach, increasing levels of miR-185 attenuated T cell development at the T cell receptor β (TCRβ) selection checkpoint and during positive selection. This caused a peripheral T cell lymphopenia. Mzb1, Nfatc3, and Camk4 were identified as novel miR-185 targets. Elevations in miR-185 enhanced TCR-dependent intracellular calcium levels, whereas a knockdown of miR-185 diminished these calcium responses. These effects concur with reductions in Mzb1, an endoplasmic reticulum calcium regulator. Consistent with their haploinsufficiency of miR-185, Mzb1 levels were elevated in thymocyte extracts from several 22q11.2 deletion syndrome patients. Our findings indicate that miR-185 regulates T cell development through its targeting of several mRNAs including Mzb1.
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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.