ArticleThe American journal of pathology2007
Aminoacyl-tRNA synthetase-interacting multifunctional protein 1/p43 controls endoplasmic reticulum retention of heat shock protein gp96: its pathological implications in lupus-like autoimmune diseases.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- Review
- AIMP1: multifunctional regulator in physiology and pathology with therapeutic implications.PeerJ · 2025Review
- The mARS complex: a critical mediator of immune regulation and homeostasis.Frontiers in immunology · 2024Review
- The Pathophysiological Role of Heat Shock Response in Autoimmunity: A Literature Review.Cells · 2021Review
- Caspase-8 controls the secretion of inflammatory lysyl-tRNA synthetase in exosomes from cancer cells.The Journal of cell biology · 2017Article
- Chaperones in hepatitis C virus infection.World journal of hepatology · 2016Review
- Plasma membrane gp96 enhances invasion and metastatic potential of liver cancer via regulation of uPAR.Molecular oncology · 2015Article
- The N terminus of pro-endothelial monocyte-activating polypeptide II (EMAP II) regulates its binding with the C terminus, arginyl-tRNA synthetase, and neurofilament light protein.The Journal of biological chemistry · 2015Article
- Mechanisms of Translocation of ER Chaperones to the Cell Surface and Immunomodulatory Roles in Cancer and Autoimmunity.Frontiers in oncology · 2015Review
- Article
- The role of glycoprotein 96 in the persistent inflammation of rheumatoid arthritis.Archives of biochemistry and biophysics · 2013Review
- Glycoprotein 96 perpetuates the persistent inflammation of rheumatoid arthritis.Arthritis and rheumatism · 2012Article
- Modulatory role of calreticulin as chaperokine for dendritic cell-based immunotherapy.Clinical and experimental immunology · 2011Article
- Cancer-associated splicing variant of tumor suppressor AIMP2/p38: pathological implication in tumorigenesis.PLoS genetics · 2011Article
- Identification of gp96 as a novel target for treatment of autoimmune disease in mice.PloS one · 2010Article
- MSC p43 required for axonal development in motor neurons.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Heat shock protein 96 is elevated in rheumatoid arthritis and activates macrophages primarily via TLR2 signaling.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Role of chaperones and FcgammaR in immunogenic death.Current opinion in immunology · 2008Review
- Aminoacyl tRNA synthetases and their connections to disease.Proceedings of the National Academy of Sciences of the United States of America · 2008Review
- tRNA synthetase: tRNA aminoacylation and beyond.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Aminoacyl-tRNA synthetase-interacting multifunctional protein 1 (AIMP1; previously known as p43) is a multifunctional protein that was initially found in multitRNA synthetase complex. In the present study, screening of the AIMP1-binding proteins revealed that AIMP1 can form a molecular complex with heat shock protein gp96. AIMP1 enhances gp96 dimerization and the interaction between gp96 and KDEL receptor-1 (KDELR-1), which mediates the retrieval of KDEL-containing proteins from Golgi to the endoplasmic reticulum (ER). The interaction between gp96 and KDELR-1 was reduced in AIMP1-deficient cells, and this disturbed ER retention of gp96 and increased its cell surface localization. Moreover, this localization of gp96 at the cell surface was suppressed by its interaction with AIMP1 and enhanced by the depletion of endogenous AIMP1. In addition, AIMP1-deficient mice showed dendritic cell activation attributable to increased gp96 surface presentation and lupus-like autoimmune phenotypes. These results suggest that AIMP1 acts as a regulator of the ER retention of gp96 and provide a new perspective of the regulatory mechanism underlying immune stimulation by gp96.
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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.