ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Stress-regulated targeting of the NKG2D ligand Mult1 by a membrane-associated RING-CH family E3 ligase.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. 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.
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Who cites it
26 citing papers in PubMed, 57 citations in OpenAlex.
- Review
- MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026Article
- Molecular cloning, characterization, and functional analysis of the uncharacterized C11orf96 gene.BMC veterinary research · 2022Article
- Engineering Tolerance toward Allogeneic CAR-T Cells by Regulation of MHC Surface Expression with Human Herpes Virus-8 Proteins.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Review
- Negative regulation of NEMO signaling by the ubiquitin E3 ligase MARCH2.The EMBO journal · 2020Article
- Membrane-associated RING-CH (MARCH) 1 and 2 are MARCH family members that inhibit HIV-1 infection.The Journal of biological chemistry · 2019Article
- A serine in the first transmembrane domain of the human E3 ubiquitin ligase MARCH9 is critical for down-regulation of its protein substrates.The Journal of biological chemistry · 2019Article
- Post-translational Mechanisms Regulating NK Cell Activating Receptors and Their Ligands in Cancer: Potential Targets for Therapeutic Intervention.Frontiers in immunology · 2019Review
- The Membrane-Associated MARCH E3 Ligase Family: Emerging Roles in Immune Regulation.Frontiers in immunology · 2019Review
- New Insights Into the Regulation of Natural-Killer Group 2 Member D (NKG2D) and NKG2D-Ligands: Endoplasmic Reticulum Stress and CEA-Related Cell Adhesion Molecule 1.Frontiers in immunology · 2018Review
- The NKG2D/NKG2DL Axis in the Crosstalk Between Lymphoid and Myeloid Cells in Health and Disease.Frontiers in immunology · 2018Review
- Dysregulated cellular functions and cell stress pathways provide critical cues for activating and targeting natural killer cells to transformed and infected cells.Immunological reviews · 2017Review
- MARCH9-mediated ubiquitination regulates MHC I export from the TGN.Immunology and cell biology · 2017Article
- Tracing the dynamics of gene transcripts after organismal death.Open biology · 2017Article
- Immunosurveillance and immunotherapy of tumors by innate immune cells.Current opinion in immunology · 2016Review
- Molecular mechanism and cellular function of MHCII ubiquitination.Immunological reviews · 2015Review
- MCMV avoidance of recognition and control by NK cells.Seminars in immunopathology · 2014Review
- N-glycosylation of asparagine 8 regulates surface expression of major histocompatibility complex class I chain-related protein A (MICA) alleles dependent on threonine 24.The Journal of biological chemistry · 2014Article
- The Membrane Associated RING-CH Proteins: A Family of E3 Ligases with Diverse Roles through the Cell.International scholarly research notices · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
NKG2D is a stimulatory receptor expressed by NK cells and some T cell subsets. Expression of the self-encoded ligands for NKG2D is presumably tightly regulated to prevent autoimmune disorders while allowing detection of infected cells and developing tumors. The NKG2D ligand Mult1 is regulated at multiple levels, with a final layer of regulation controlling protein stability. In this article, we report that Mult1 cell-surface expression was prevented by two closely related E3 ubiquitin ligases membrane-associated RING-CH (MARCH)4 and MARCH9, members of an E3 family that regulates other immunologically active proteins. Lysines within the cytoplasmic domain of Mult1 were essential for this repression by MARCH4 or MARCH9. Downregulation of Mult1 by MARCH9 was reversed by heat-shock treatment, which resulted in the dissociation of the two proteins and increased the amount of Mult1 at the cell surface. These results identify Mult1 as a target for the MARCH family of E3 ligases and show that induction of Mult1 in response to heat shock is due to regulated association with its E3 ligases.
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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.