ArticleCell1992
A brefeldin A-like phenotype is induced by the overexpression of a human ERD-2-like protein, ELP-1.
Article in Cell, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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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
71 citing papers in PubMed, 152 citations in OpenAlex.
- Pyra-metho-carnil disrupts cancer cell proteostasis and induces apoptosis by binding to KDEL receptors.Scientific reports · 2026Article
- A regulatory circuit operated by KDELR1 and KDELR3 fine-tunes the composition of the early secretory pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Excitotoxic glutamate levels cause the secretion of resident endoplasmic reticulum proteins.Journal of neurochemistry · 2024Article
- Exploring the potential biological significance of KDELR family genes in lung adenocarcinoma.Scientific reports · 2024Article
- KDELR2 promotes bone marrow mesenchymal stem cell osteogenic differentiation via GSK3β/β-catenin signaling pathway.Cell and tissue research · 2024Article
- Reply to: Does the KDEL receptor cycle between the Golgi and the ER?Nature communications · 2024Article
- The K/HDEL receptor does not recycle but instead acts as a Golgi-gatekeeper.Nature communications · 2023Article
- KDELR2 as a diagnostic and prognostic biomarker of bladder urothelial carcinoma and its correlation with immune infiltration.Genetics and molecular biology · 2023Article
- KDEL Receptors: Pathophysiological Functions, Therapeutic Options, and Biotechnological Opportunities.Biomedicines · 2022Review
- Shared and specific functions of Arfs 1-5 at the Golgi revealed by systematic knockouts.The Journal of cell biology · 2022Article
- A novel endoplasmic stress mediator, Kelch domain containing 7B (KLHDC7B), increased Harakiri (HRK) in the SubAB-induced apoptosis signaling pathway.Cell death discovery · 2021Article
- KDELR2 promotes breast cancer proliferation via HDAC3-mediated cell cycle progression.Cancer communications (London, England) · 2021Article
- Computational Modeling of C-Terminal Tails to Predict the Calcium-Dependent Secretion of Endoplasmic Reticulum Resident Proteins.Frontiers in chemistry · 2021Article
- Article
- Rab5b-Associated Arf1 GTPase Regulates Export of N-Myristoylated Adenylate Kinase 2 From the Endoplasmic Reticulum inFrontiers in cellular and infection microbiology · 2020Article
- KDELR2 Promotes Glioblastoma Tumorigenesis Targeted by HIF1a via mTOR Signaling Pathway.Cellular and molecular neurobiology · 2019Article
- Article
- KDEL Receptors Are Differentially Regulated to Maintain the ER Proteome under Calcium Deficiency.Cell reports · 2018Article
- Predominant Golgi Residency of the Plant K/HDEL Receptor Is Essential for Its Function in Mediating ER Retention.The Plant cell · 2018Article
- Identification and characterization of a Golgi retention signal in feline coronavirus accessory protein 7b.The Journal of general virology · 2017Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brefeldin A (BFA) is a unique drug affecting the molecular mechanisms that regulate membrane traffic and organelle structure. BFA's ability to alter retrograde traffic from the Golgi to the endoplasmic reticulum (ER) led us to ask whether the ERD-2 retrieval receptor, proposed to return escaped ER resident proteins from the Golgi, might either interfere with or mimic the effects of the drug. When either human ERD-2 or a novel human homolog (referred to as ELP-1) is overexpressed in a variety of cell types, the effects are phenotypically indistinguishable from the addition of BFA. These include the redistribution of the Golgi coat protein, beta-COP, to the cytosol, the loss of the Golgi apparatus as a distinct organelle, the mixing of this organelle with the ER, the addition of complex oligosaccharides to resident ER glycoproteins, and the block of anterograde traffic. Thus, these receptors may provide signals that regulate retrograde traffic between the Golgi and the ER.
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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.