ArticleHuman molecular genetics2015
Loss of the thyroid hormone-binding protein Crym renders striatal neurons more vulnerable to mutant huntingtin in Huntington's disease.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- CRYM suppresses glioblastoma progression by inhibiting the TGFβ1/Smad-EMT signaling pathway.Journal of neuro-oncology · 2026Article
- Emerging Roles, Mechanisms, and Therapeutic Potential of Thyroid Hormones in Neurodegenerative Diseases: A Review.Brain sciences · 2026Review
- The Role of Thyroid Hormones in Neurodegenerative Disorders: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Therapeutic Options of Crystallin Mu and Protein Disulfide Isomerase A3 for Cuprizone-Induced Demyelination in Mouse Hippocampus.Neurochemical research · 2024Article
- Article
- Thyroid hormone action in adult neurogliogenic niches: the known and unknown.Frontiers in endocrinology · 2024Review
- Cannabinoids modulate the microbiota-gut-brain axis in HIV/SIV infection by reducing neuroinflammation and dysbiosis while concurrently elevating endocannabinoid and indole-3-propionate levels.Journal of neuroinflammation · 2023Article
- Thyroid Disorders and Movement Disorders-A Systematic Review.Movement disorders clinical practice · 2023Review
- Empirical comparison and recent advances of computational prediction of hormone binding proteins using machine learning methods.Computational and structural biotechnology journal · 2023Review
- Crystallin Mu in Medial Amygdala Mediates the Effect of Social Experience on Cocaine Seeking in Males but Not in Females.Biological psychiatry · 2022Article
- Cerebral Organoids Derived from a Parkinson's Patient Exhibit Unique Pathogenesis from Chikungunya Virus Infection When Compared to a Non-Parkinson's Patient.Pathogens (Basel, Switzerland) · 2021Article
- The C-Terminal Domain of LRRK2 with the G2019S Substitution Increases Mutant A53T α-Synuclein Toxicity in Dopaminergic Neurons In Vivo.International journal of molecular sciences · 2021Article
- µ-Crystallin: A thyroid hormone binding protein.Endocrine regulations · 2021Review
- Thyroid hormone: sex-dependent role in nervous system regulation and disease.Biology of sex differences · 2021Review
- Proteome profiling in cerebrospinal fluid reveals novel biomarkers of Alzheimer's disease.Molecular systems biology · 2020Article
- Moderate-Intensity Exercise Induces Neurogenesis and Improves Cognition in Old Mice by Upregulating Hippocampal Hippocalcin, Otub1, and Spectrin-α.Molecular neurobiology · 2019Article
- Astrocyte Heterogeneity: Impact to Brain Aging and Disease.Frontiers in aging neuroscience · 2019Review
- The striatal kinase DCLK3 produces neuroprotection against mutant huntingtin.Brain : a journal of neurology · 2018Article
- Neurobiology: Diversity reaches the stars.Nature · 2017Article
- Neural Circuit-Specialized Astrocytes: Transcriptomic, Proteomic, Morphological, and Functional Evidence.Neuron · 2017Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms underlying preferential atrophy of the striatum in Huntington's disease (HD) are unknown. One hypothesis is that a set of gene products preferentially expressed in the striatum could determine the particular vulnerability of this brain region to mutant huntingtin (mHtt). Here, we studied the striatal protein µ-crystallin (Crym). Crym is the NADPH-dependent p38 cytosolic T3-binding protein (p38CTBP), a key regulator of thyroid hormone (TH) T3 (3,5,3'-triiodo-l-thyronine) transportation. It has been also recently identified as the enzyme that reduces the sulfur-containing cyclic ketimines, which are potential neurotransmitters. Here, we confirm the preferential expression of the Crym protein in the rodent and macaque striatum. Crym expression was found to be higher in the macaque caudate than in the putamen. Expression of Crym was reduced in the BACHD and Knock-in 140CAG mouse models of HD before onset of striatal atrophy. We show that overexpression of Crym in striatal medium-size spiny neurons using a lentiviral-based strategy in mice is neuroprotective against the neurotoxicity of an N-terminal fragment of mHtt in vivo. Thus, reduction of Crym expression in HD could render striatal neurons more susceptible to mHtt suggesting that Crym may be a key determinant of the vulnerability of the striatum. In addition our work points to Crym as a potential molecular link between striatal degeneration and the THs deregulation reported in HD patients.
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