ArticleFEBS open bio2017
A new role for human dyskerin in vesicular trafficking.
Article in FEBS open bio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- A working model for cytoplasmic assembly of H/ACA snoRNPs.FEBS letters · 2025Review
- New Insights into Dyskerin-CypA Interaction: Implications for X-Linked Dyskeratosis Congenita and Beyond.Genes · 2023Article
- Loss of dyskerin facilitates the acquisition of metastatic traits by altering the mevalonate pathway.Life science alliance · 2023Article
- Dyskerin Downregulation Can Induce ER Stress and Promote Autophagy via AKT-mTOR Signaling Deregulation.Biomedicines · 2022Article
- Understanding inborn errors of immunity: A lens into the pathophysiology of monogenic inflammatory bowel disease.Frontiers in immunology · 2022Review
- Lithium chloride increases sensitivity to photon irradiation treatment in primary mesenchymal colon cancer cells.Molecular medicine reports · 2020Article
- Article
- Characterisation of mesenchymal colon tumour-derived cells in tumourspheres as a model for colorectal cancer progression.International journal of oncology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dyskerin is an essential, conserved, multifunctional protein found in the nucleolus, whose loss of function causes the rare genetic diseases X-linked dyskeratosis congenita and Hoyeraal-Hreidarsson syndrome. To further investigate the wide range of dyskerin's biological roles, we set up stable cell lines able to trigger inducible protein knockdown and allow a detailed analysis of the cascade of events occurring within a short time frame. We report that dyskerin depletion quickly induces cytoskeleton remodeling and significant alterations in endocytic Ras-related protein Rab-5A/Rab11 trafficking. These effects arise in different cell lines well before the onset of telomere shortening, which is widely considered the main cause of dyskerin-related diseases. Given that vesicular trafficking affects many homeostatic and differentiative processes, these findings add novel insights into the molecular mechanisms underlining the pleiotropic manifestation of the dyskerin loss-of-function phenotype.
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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.