ArticleCell stress & chaperones2010
Plasma cell differentiation initiates a limited ER stress response by specifically suppressing the PERK-dependent branch of the unfolded protein response.
Article in Cell stress & chaperones, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 139 citations in OpenAlex.
- Cell intrinsic versus cell extrinsic control of plasma cell longevity.Trends in immunology · 2026Review
- IFNγ-induced IRF1 synergizes with TLR7 signals to tune the IRF4-IRF8 axis and drive pathogenic effector B cell fate.bioRxiv : the preprint server for biology · 2026Article
- Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.bioRxiv : the preprint server for biology · 2026Article
- Secretory IgA dysfunction underlies poor prognosis inGut microbes · 2025Article
- Macrophage DNases Limit Neutrophil Extracellular Trap-Mediated Defective Efferocytosis in Atherosclerosis.Circulation research · 2025Article
- Autophagy, ER-phagy and ER Dynamics During Cell Differentiation.Journal of molecular biology · 2025Review
- Endoplasmic Reticulum Stress in Cancer Progression: A Comprehensive Review of Its Role and Mechanisms.International journal of medical sciences · 2025Review
- BiP/GRP78 is a pro-viral factor for diverse dsDNA viruses that promotes the survival and proliferation of cells upon KSHV infection.PLoS pathogens · 2024Article
- Super enhancer acquisition drives expression of oncogenic PPP1R15B that regulates protein homeostasis in multiple myeloma.Nature communications · 2024Article
- Hemin treatment drives viral reactivation and plasma cell differentiation of EBV latently infected B cells.PLoS pathogens · 2023Article
- Myogenesis in C2C12 Cells Requires Phosphorylation of ATF6α by p38 MAPK.Biomedicines · 2023Article
- Article
- Sec22b is a critical and nonredundant regulator of plasma cell maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- ER stress: an emerging regulator in GVHD development.Frontiers in immunology · 2023Review
- Looking into Endoplasmic Reticulum Stress: The Key to Drug-Resistance of Multiple Myeloma?Cancers · 2022Review
- Reshaping endoplasmic reticulum quality control through the unfolded protein response.Molecular cell · 2022Review
- In Vitro Stimulation of IRE1α/XBP1-Deficient B Cells with LPS.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Model Identifies Genetic Predisposition of Alzheimer's Disease as Key Decider in Cell Susceptibility to Stress.International journal of molecular sciences · 2021Article
- Plasma cell survival: The intrinsic drivers, migratory signals, and extrinsic regulators.Immunological reviews · 2021Review
- Biochemical coordination of plasma cell genesis.Immunological reviews · 2021Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In response to terminal differentiation signals that enable B cells to produce vast quantities of antibodies, a dramatic expansion of the secretory pathway and a corresponding increase in the molecular chaperones and folding enzymes that aid and monitor immunoglobulin synthesis occurs. Recent studies reveal that the unfolded protein response (UPR), which is normally activated by endoplasmic reticulum (ER) stress, plays a critical role in this process. Although B cells activate all three branches of the UPR in response to pharmacological inducers of the pathway, plasma cell differentiation elicits only a partial UPR in which components of the PKR-like ER kinase (PERK) branch are not expressed. This prompted us to further characterize UPR activation during plasma cell differentiation. We found that in response to lipopolysaccharides (LPS)-induced differentiation of the I.29 micro(+) B cell line, Ire1 was activated early, which led to splicing of XBP-1. PERK was partially phosphorylated with similar kinetics, but this was not sufficient to activate its downstream target eIF-2alpha, which initiates translation arrest, or to induce other targets like CHOP or GADD34. Both of these events preceded increased Ig synthesis, arguing this is not the signal for activating these two transducers. Targets of activating transcription factor 6 (ATF6) were up-regulated considerably later, arguing that the ATF6 branch is activated by a distinct signal. Pretreatment with LPS inhibited activation of the PERK branch by pharmacological inducers of the UPR, suggesting that differentiation-induced signals specifically silence this branch. This unique ability to differentially regulate various branches of the UPR allows B cells to accomplish distinct outcomes via the same UPR machinery.
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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.