ReviewInternational journal of biological sciences2025
FAM134B in Cellular Homeostasis: Bridging Endoplasmic Reticulum-Phagy to Human Diseases.
Review in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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
3 citing papers in PubMed.
- Intracellular pathogen manipulation of ER-phagy: direct receptor targeting and indirect pathway perturbation.Medical microbiology and immunology · 2026Review
- RETREG1-Mediated Reticulophagy is Essential for Dendritic Cell Maturation and Function in Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The multifaceted functions of selective autophagy in cancer: molecular basis, consequences, and clinical prospects.Molecular cancer · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FAM134B, originally characterized as an oncogene in esophageal squamous carcinoma, has also been implicated in the pathogenesis of hereditary sensory and autonomic neuropathy type IIB (HSAN2B). It is recognized as the inaugural endoplasmic reticulum (ER)-phagy receptor in mammals containing an LC3-interacting region, which facilitates its interaction with LC3 and GABARAP proteins in the autophagosome. ER-phagy, a critical process involved in ER quality control, selectively degrades superfluous or damaged ER fragments in lysosomes, thereby maintaining ER and protein homeostasis. This review offers an in-depth analysis of FAM134B's structure, function, and regulation, emphasizing its role in infectious diseases, neuropathies, cancer, metabolic disorders, degenerative conditions, and cardiovascular diseases. The evidence presented highlights the need for further research on FAM134B as a potential therapeutic target in human diseases.
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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.