ArticleJournal of cell science2015
Ubiquitylation of CD98 limits cell proliferation and clonal expansion.
Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 30 citations in OpenAlex.
- SNHG family lncRNAs promote Ewing sarcoma cell fitness through intronic snoRNA-guided rRNA modifications.NAR cancer · 2026Article
- A proximity ligation screen identifies SNAT2 as a novel target of the MARCH1 E3 ubiquitin ligase.Biology open · 2026Article
- Review
- MARCH1, transcriptionally regulated by POU2F2, facilitates acute myeloid leukemia progression via inducing MYCT1 degradation.Oncogene · 2025Article
- Anaplastic Lymphoma Kinase signaling stabilizes SLC3A2 expression via MARCH11 to promote neuroblastoma cell growth.Cell death and differentiation · 2024Article
- Regulation of MHC class II and CD86 expression by March-I in immunity and disease.Current opinion in immunology · 2023Review
- CD98 heavy chain as a prognostic biomarker and target for cancer treatment.Frontiers in oncology · 2023Review
- Oncogenic RAS commandeers amino acid sensing machinery to aberrantly activate mTORC1 in multiple myeloma.Nature communications · 2022Article
- Article
- Heteromeric Solute Carriers: Function, Structure, Pathology and Pharmacology.Advances in experimental medicine and biology · 2021Review
- Targeting SLC1A5 and SLC3A2/SLC7A5 as a Potential Strategy to Strengthen Anti-Tumor Immunity in the Tumor Microenvironment.Frontiers in immunology · 2021Review
- Physiological substrates and ontogeny-specific expression of the ubiquitin ligases MARCH1 and MARCH8.Current research in immunology · 2021Article
- MARCH Proteins Mediate Responses to Antitumor Antibodies.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- The E3 ubiquitin ligase MARCH1 regulates antimalaria immunity through interferon signaling and T cell activation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Lack of the E3 Ubiquitin Ligase March1 Affects CD8 T Cell Fate and Exacerbates Insulin Resistance in Obese Mice.Frontiers in immunology · 2020Article
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
- Review
- FOXO1 transcription factor plays a key role in T cell-HIV-1 interaction.PLoS pathogens · 2019Article
- MARCH1 encourages tumour progression of hepatocellular carcinoma via regulation of PI3K-AKT-β-catenin pathways.Journal of cellular and molecular medicine · 2019Article
- Soluble CD137 Ameliorates Acute Type 1 Diabetes by Inducing T Cell Anergy.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
CD98 heavy chain (SLC3A2) facilitates lymphocyte clonal expansion that enables adaptive immunity; however, increased expression of CD98 is also a feature of both lymphomas and leukemias and represents a potential therapeutic target in these diseases. CD98 is transcriptionally regulated and ectopic expression of the membrane-associated RING-CH (MARCH) E3 ubiquitin ligases MARCH1 or MARCH8 leads to ubiquitylation and lysosomal degradation of CD98. Here, we examined the potential role of ubiquitylation in regulating CD98 expression and cell proliferation. We report that blocking ubiquitylation by use of a catalytically inactive MARCH or by creating a ubiquitylation-resistant CD98 mutant, prevents MARCH-induced CD98 downregulation in HeLa cells. March1-null T cells display increased CD98 expression. Similarly, T cells expressing ubiquitylation-resistant CD98 manifest increased proliferation in vitro and clonal expansion in vivo. Thus, ubiquitylation and the resulting downregulation of CD98 can limit cell proliferation and clonal expansion.
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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.