ArticleMolecular neurodegeneration2015
Calcium-responsive transactivator (CREST) protein shares a set of structural and functional traits with other proteins associated with amyotrophic lateral sclerosis.
Article in Molecular neurodegeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Paraspeckle condensation is controlled via TDP-43 polymerization and linked to neuroprotection.Nature cell biology · 2026Article
- The nBAF complex subunit CREST/SS18L1 regulates hippocampal memory processes via tyrosine 397 and histone acetyltransferase CBP.Cell reports · 2026Article
- Artemisinin Stimulates Neuronal Cell Viability and Possess a Neuroprotective Effect In Vitro.Molecules (Basel, Switzerland) · 2025Article
- Article
- SHARK enables sensitive detection of evolutionary homologs and functional analogs in unalignable and disordered sequences.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Modelling amyotrophic lateral sclerosis in rodents.Nature reviews. Neuroscience · 2022Review
- ALS-linked cytoplasmic FUS assemblies are compositionally different from physiological stress granules and sequester hnRNPA3, a novel modifier of FUS toxicity.Neurobiology of disease · 2022Article
- Transcription factor SS18L1 regulates the proliferation, migration and differentiation of Schwann cells in peripheral nerve injury.Frontiers in veterinary science · 2022Article
- Long non-coding RNA NEAT1_1 ameliorates TDP-43 toxicity in in vivo models of TDP-43 proteinopathy.RNA biology · 2021Article
- Long non-coding RNA Neat1 regulates adaptive behavioural response to stress in mice.Translational psychiatry · 2020Article
- Stress granules regulate stress-induced paraspeckle assembly.The Journal of cell biology · 2019Article
- Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies.PLoS genetics · 2019Article
- ALS-linked FUS mutations confer loss and gain of function in the nucleus by promoting excessive formation of dysfunctional paraspeckles.Acta neuropathologica communications · 2019Article
- Loss of CREST leads to neuroinflammatory responses and ALS-like motor defects in mice.Translational neurodegeneration · 2019Article
- NEAT1 and paraspeckles in neurodegenerative diseases: A missing lnc found?Non-coding RNA research · 2018Review
- Protective paraspeckle hyper-assembly downstream of TDP-43 loss of function in amyotrophic lateral sclerosis.Molecular neurodegeneration · 2018Article
- Chronically stressed or stress-preconditioned neurons fail to maintain stress granule assembly.Cell death & disease · 2017Article
- Modulation of p-eIF2α cellular levels and stress granule assembly/disassembly by trehalose.Scientific reports · 2017Article
- Review
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundMutations in calcium-responsive transactivator (CREST) encoding gene have been recently linked to ALS. Similar to several proteins implicated in ALS, CREST contains a prion-like domain and was reported to be a component of paraspeckles.
resultsWe demonstrate that CREST is prone to aggregation and co-aggregates with FUS but not with other two ALS-linked proteins, TDP-43 and TAF15, in cultured cells. Aggregation of CREST affects paraspeckle integrity, probably by trapping other paraspeckle proteins within aggregates. Like several other ALS-associated proteins, CREST is recruited to induced stress granules. Neither of the CREST mutations described in ALS alters its subcellular localization, stress granule recruitment or detergent solubility; however Q388stop mutation results in elevated steady-state levels and more frequent nuclear aggregation of the protein. Both wild-type protein and its mutants negatively affect neurite network complexity of unstimulated cultured neurons when overexpressed, with Q388stop mutation being the most deleterious. When overexpressed in the fly eye, wild-type CREST or its mutants lead to severe retinal degeneration without obvious differences between the variants.
conclusionsOur data indicate that CREST and certain other ALS-linked proteins share several features implicated in ALS pathogenesis, namely the ability to aggregate, be recruited to stress granules and alter paraspeckle integrity. A change in CREST levels in neurons which might occur under pathological conditions would have a profound negative effect on neuronal homeostasis.
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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.