ArticleThe Journal of experimental medicine2020
Essential cell-extrinsic requirement for PDIA6 in lymphoid and myeloid development.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Proinsulin regulators identified with CRISPR screen and in vivo mouse QTL mapping.Nature communications · 2026Article
- Protein disulfide isomerase A6 (PDIA6) is essential for acrosome biogenesis and male fertility in mice.Cell communication and signaling : CCS · 2026Article
- Identification of gene modules associated with B cell activation and tissue remodeling in primary Sjögren's syndrome.BMC immunology · 2025Article
- A multichaperone condensate enhances protein folding in the endoplasmic reticulum.Nature cell biology · 2025Article
- A hypomorphic Mpi mutation unlocks an in vivo tool for studying global N-glycosylation deficiency.JCI insight · 2025Article
- Longitudinal single cell profiling of epitope specific memory CD4+ T cell responses to recombinant zoster vaccine.Nature communications · 2025Article
- Suppression of melanoma by mice lacking MHC-II: Mechanisms and implications for cancer immunotherapy.The Journal of experimental medicine · 2024Article
- Increased ER stress by depletion of PDIA6 impairs primary ciliogenesis and enhances sensitivity to ferroptosis in kidney cells.BMB reports · 2024Article
- Essential role of MFSD1-GLMP-GIMAP5 in lymphocyte survival and liver homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- OVOL2 sustains postnatal thymic epithelial cell identity.Nature communications · 2023Article
- Essential requirement for IER3IP1 in B cell development.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Endoplasmic reticulum protein 5 attenuates platelet endoplasmic reticulum stress and secretion in a mouse model.Blood advances · 2023Article
- Population-enriched innate immune variants may identify candidate gene targets at the intersection of cancer and cardio-metabolic disease.Frontiers in endocrinology · 2023Review
- Excessive sulfur oxidation in endoplasmic reticulum drives an inflammatory reaction of chondrocytes in aging mice.Frontiers in pharmacology · 2022Article
- Germline Saturation Mutagenesis Induces Skeletal Phenotypes in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
In a forward genetic screen of N-ethyl-N-nitrosourea (ENU)-induced mutant mice for aberrant immune function, we identified mice with a syndromic disorder marked by growth retardation, diabetes, premature death, and severe lymphoid and myeloid hypoplasia together with diminished T cell-independent (TI) antibody responses. The causative mutation was in Pdia6, an essential gene encoding protein disulfide isomerase A6 (PDIA6), an oxidoreductase that functions in nascent protein folding in the endoplasmic reticulum. The immune deficiency caused by the Pdia6 mutation was, with the exception of a residual T cell developmental defect, completely rescued in irradiated wild-type recipients of PDIA6-deficient bone marrow cells, both in the absence or presence of competition. The viable hypomorphic allele uncovered in these studies reveals an essential role for PDIA6 in hematopoiesis, but one extrinsic to cells of the hematopoietic lineage. We show evidence that this role is in the proper folding of Wnt3a, BAFF, IL-7, and perhaps other factors produced by the extra-hematopoietic compartment that contribute to the development and lineage commitment of hematopoietic cells.
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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.