ArticleThe Journal of clinical investigation2017
EMC3 coordinates surfactant protein and lipid homeostasis required for respiration.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
42 citing papers in PubMed, 60 citations in OpenAlex.
- Machine learning-based gait classification and genome-wide association identify a QTL for gait type in Colombian paso horses.iScience · 2026Article
- Roles of ER Membrane Protein Complex in Protein Biogenesis and Quality Control in the Lung and Beyond.Cell proliferation · 2026Review
- Unlocking Alveolar Regeneration: AT2 Stem Cells, Signaling Networks, and Therapeutic Frontiers.Stem cell reviews and reports · 2026Review
- Divergent pathways of surfactant protein C maturation for disease-associated isoforms.The Journal of biological chemistry · 2026Article
- Article
- Endocan attenuates LPS-induced alveolar type II cells injury through PI3K/Akt/mTOR pathway.Upsala journal of medical sciences · 2026Article
- Reprogrammed Fibrotic Niche Fuels Lung Cancer Initiation and Reciprocal Remodeling.International journal of biological sciences · 2026Review
- Single-cell multiomics analysis reveals CTCF as a key regulator of lung morphogenesis and progenitor maintenance.Nature communications · 2025Article
- Metabolomic profiling reveals distinct lipid signatures in progressive versus stable fibrotic lung disease.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Divergent Pathways of Surfactant Protein C Maturation for Disease-Associated Isoforms.bioRxiv : the preprint server for biology · 2025Article
- Cell Population-resolved Multiomics Atlas of the Developing Lung.American journal of respiratory cell and molecular biology · 2025Article
- EMC3 is critical for CFTR function and calcium mobilization in the mouse intestinal epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- miR-624 accelerates the growth of liver cancer cells by inhibiting EMC3.Non-coding RNA research · 2023Article
- The Biogenesis of Multipass Membrane Proteins.Cold Spring Harbor perspectives in biology · 2023Review
- A toolbox for systematic discovery of stable and transient protein interactors in baker's yeast.Molecular systems biology · 2023Article
- EMC3 regulates mesenchymal cell survival via control of the mitotic spindle assembly.iScience · 2023Article
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- Article
- EMC is required for biogenesis of Xport-A, an essential chaperone of Rhodopsin-1 and the TRP channel.EMBO reports · 2022Article
- Cryo-EM structures of the endoplasmic reticulum membrane complex.The FEBS journal · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Adaptation to respiration at birth depends upon the synthesis of pulmonary surfactant, a lipid-protein complex that reduces surface tension at the air-liquid interface in the alveoli and prevents lung collapse during the ventilatory cycle. Herein, we demonstrated that the gene encoding a subunit of the endoplasmic reticulum membrane complex, EMC3, also known as TMEM111 (Emc3/Tmem111), was required for murine pulmonary surfactant synthesis and lung function at birth. Conditional deletion of Emc3 in murine embryonic lung epithelial cells disrupted the synthesis and packaging of surfactant lipids and proteins, impaired the formation of lamellar bodies, and induced the unfolded protein response in alveolar type 2 (AT2) cells. EMC3 was essential for the processing and routing of surfactant proteins, SP-B and SP-C, and the biogenesis of the phospholipid transport protein ABCA3. Transcriptomic, lipidomic, and proteomic analyses demonstrated that EMC3 coordinates the assembly of lipids and proteins in AT2 cells that is necessary for surfactant synthesis and function at birth.
Indexed as
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What OpenQuestion holds
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.