ArticleThe European journal of neuroscience2010
BimEL as a possible molecular link between proteasome dysfunction and cell death induced by mutant huntingtin.
Article in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Navigating the cholesterol maze: Key insights on use of statins in neurodegenerative disorders.Neuroprotection (Chichester, England) · 2026Review
- Significance of Programmed Cell Death Pathways in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Mutant-Huntingtin Molecular Pathways Elucidate New Targets for Drug Repurposing.International journal of molecular sciences · 2023Review
- RNA-seq analysis reveals significant transcriptome changes in huntingtin-null human neuroblastoma cells.BMC medical genomics · 2021Article
- Molecular mechanisms of cell death in neurological diseases.Cell death and differentiation · 2021Review
- The pro-apoptotic domain of BIM protein forms toxic amyloid fibrils.Cellular and molecular life sciences : CMLS · 2021Article
- The Parkinson's disease gene product DJ-1 modulates miR-221 to promote neuronal survival against oxidative stress.Redox biology · 2018Article
- Aberrant subcellular localization of SQSTM1/p62 contributes to increased vulnerability to proteotoxic stress recovery in Huntington's disease.Molecular and cellular neurosciences · 2018Article
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- The Unfolded Protein Response and the Role of Protein Disulfide Isomerase in Neurodegeneration.Frontiers in cell and developmental biology · 2015Review
- Caspase-2 is essential for c-Jun transcriptional activation and Bim induction in neuron death.The Biochemical journal · 2013Article
- Defining the role of the Bcl-2 family proteins in Huntington's disease.Cell death & disease · 2013Review
- Palmitoylation and trafficking of GAD65 are impaired in a cellular model of Huntington's disease.The Biochemical journal · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) is a devastating neurodegenerative disorder caused by an expanded polyglutamine repeat within the N-terminus of the huntingtin protein. It is characterized by a selective loss of medium spiny neurons in the striatum. It has been suggested that impaired proteasome function and endoplasmic reticulum (ER) stress play important roles in mutant huntingtin (mHtt)-induced cell death. However, the molecular link involved is poorly understood. In the present study, we identified the essential role of the extra long form of Bim (Bcl-2 interacting mediator of cell death), BimEL, in mHtt-induced cell death. BimEL protein expression level was significantly increased in cell lines expressing the N-terminus of mHtt and in a mouse model of HD. Although quantitative RT-PCR analysis indicated that BimEL mRNA was increased in cells expressing mHtt, we provided evidence showing that, at the post-translational level, phosphorylation of BimEL played a more important role in regulating BimEL expression. Up-regulation of BimEL facilitated the translocation of Bax to the mitochondrial membrane, which further led to cytochrome c release and cell death. On the other hand, knocking down BimEL expression prevented mHtt-induced cell death. Taken together, these findings suggest that BimEL is a key element in regulating mHtt-induced cell death. A model depicting the role of BimEL in linking mHtt-induced ER stress and proteasome dysfunction to cell death is proposed.
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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.