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neurodegenerative diseases/arabidopsis

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Modeling human neurodegenerative diseases in transgenic systems.

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Transgenic systems are widely used to study the cellular and molecular basis of human neurodegenerative diseases. A wide variety of model organisms have been utilized, including bacteria (Escherichia coli), plants (Arabidopsis thaliana), nematodes (Caenorhabditis elegans), arthropods (Drosophila
Failure to maintain organelle genome stability has been linked to numerous phenotypes, including variegation and cytosolic male sterility (CMS) in plants, as well as cancer and neurodegenerative diseases in mammals. Here we describe a next-generation sequencing approach that precisely maps and

The value of Arabidopsis research in understanding human disease states.

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Although Arabidopsis thaliana is traditionally viewed as the key model organism for plant biology it is becoming increasingly clear that Arabidopsis represents an invaluable tool in our efforts to understand molecular mechanisms that underpin human disease states. A comparison of the annotated

Arabidopsis AtPARK13, which confers thermotolerance, targets misfolded proteins.

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Mutations in HTRA2/Omi/PARK13 have been implicated in Parkinson disease (PD). PARK13 is a neuroprotective serine protease; however, little is known about how PARK13 confers stress protection and which protein targets are directly affected by PARK13. We have reported that Arabidopsis thaliana

The phosphatase laforin crosses evolutionary boundaries and links carbohydrate metabolism to neuronal disease.

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Lafora disease (LD) is a progressive myoclonic epilepsy resulting in severe neurodegeneration followed by death. A hallmark of LD is the accumulation of insoluble polyglucosans called Lafora bodies (LBs). LD is caused by mutations in the gene encoding the phosphatase laforin, which reportedly exists

Background-dependent effects of polyglutamine variation in the Arabidopsis thaliana gene ELF3.

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Tandem repeats (TRs) have extremely high mutation rates and are often considered to be neutrally evolving DNA. However, in coding regions, TR copy number mutations can significantly affect phenotype and may facilitate rapid adaptation to new environments. In several human genes, TR copy number
Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS or SACS) is an early onset neurodegenerative disease with high prevalence (carrier frequency 1/22) in the Charlevoix-Saguenay-Lac-Saint-Jean (CSLSJ) region of Quebec. We previously mapped the gene responsible for ARSACS to chromosome
Eukaryotes contain a ubiquitous family of autophagy-associated Atg8 proteins. In animal cells, these proteins have multiple functions associated with growth, cancer, and degenerative diseases, but their functions in plants are still largely unknown. To search for novel functions of Atg8 in plants,
Alzheimer's disease (AD) is the most common neurodegenerative disorder and the primary form of dementia in the elderly. One of the main features of AD is the increase in amyloid-beta (Aβ) peptide production and aggregation, leading to oxidative stress, neuroinflammation and neurodegeneration.

Arabidopsis Bax inhibitor-1: A rheostat for ER stress-induced programmed cell death.

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Unfolded and misfolded proteins in the endoplasmic reticulum (ER) of eukaryotic cells elicit a highly conserved unfolded protein response (UPR) that leads to an increase in the capacity of the ER to deal with protein folding by hightened expression of enzymes such as chaperone and protein disulfide

An Arabidopsis mutant hypersensitive to red and far-red light signals.

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A new mutant called psi2 (for phytochrome signaling) was isolated by screening for elevated activity of a chlorophyll a/b binding protein-luciferase (CAB2-LUC) transgene in Arabidopsis. This mutant exhibited hypersensitive induction of CAB1, CAB2, and the small subunit of ribulose-1,5-bisphosphate

Optical Activation of TrkB Signaling

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Brain-derived neurotrophic factor, via activation of tropomyosin receptor kinase B (TrkB), plays a critical role in neuronal proliferation, differentiation, survival, and death. Dysregulation of TrkB signaling is implicated in neurodegenerative disorders and cancers. Precise activation of TrkB
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