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- Alzheimer's Disease (1)
- As those identified in primary tauopathies (e.g. P301L and G389R) (1)
- Both enhanced vesicular release of tau in the extracellular space (1)
- Due to a process called phase separation. My Thesis tested the hypothesis that tau mutations (1)
- In both HEK293T and SHSY-5Y cells compared to wild type. However (1)
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- Into either HEK293T (1)
- It has recently been well accepted that tau is also an intrinsically disordered protein that tends to form membraneless organelles called coacervates (1)
- Might impair the phase separation properties of the protein and impact its pathological role in cells. I first tested the effect of single amino acid substitutions in vitro (1)
- Mouse (1)
- Neurodegeneration (1)
- OTX2 (1)
- OTX2ECR2 (1)
- One third is characterized by the presence of genetic mutations leading to the synthesis of tau proteins with single amino acid substitutions at specific locations and affecting protein function. While most of the initial studies have emphasize the functional role of tau as modulator of the axonal cytoskeleton (1)
- Or in SHSY-5Y neuroblastoma cells (1)
- PROX1 (1)
- Phase Separation (1)
- Retina (1)
- SecretionTau is a protein expressed exclusively in glia and neurons in the central nervous system and implicated in several neurogenerative diseases called “tauopathies”. Among all the tauopathies (1)
- Tau (1)
- The expression of tau mutants did not affect cell viability in response to oxidative stress. While the relationship between the biophysical properties of tau and its function in cells remain to be elucidated (1)
- This study suggest potential mechanisms by which specific mutations of tau may induce its release in the extracellular space and suggest a potential role in spreading of the pathology. (1)
- Transgenic (1)
- Using recombinant tau and the results revealed that the tau pathogenic mutations P301L and G389R increased the propensity of tau to phase separate and form coacervates with higher viscosity than wild type. I then hypothesized that tau mutants and wild type tau may also differentially impact cell function. This was studied by transfecting tau and its two mutants P301L and G389R (1)
- Via calcium-dependent membrane blebbing (1)
- We determined that tau P301L and G389R (1)
- We used a bimolecular fluorescence complementation assay based on the formation of tau dimers fused with either the N or C terminus of the reporter VENUS fluorescent protein. Using live imaging (1)
- Which do not express endogenous tau (1)
- Which endogenously express tau. For the experiments (1)
Articles 1 - 2 of 2
Full-Text Articles in Life Sciences
Characterization Of Pathological Tau Mutants, Charles J. Mcdonald
Characterization Of Pathological Tau Mutants, Charles J. Mcdonald
Dissertations, Theses, and Capstone Projects
Tau is a protein expressed exclusively in glia and neurons in the central nervous system and implicated in several neurogenerative diseases called “tauopathies”. Among all the tauopathies, one third is characterized by the presence of genetic mutations leading to the synthesis of tau proteins with single amino acid substitutions at specific locations and affecting protein function. While most of the initial studies have emphasize the functional role of tau as modulator of the axonal cytoskeleton, it has recently been well accepted that tau is also an intrinsically disordered protein that tends to form membraneless organelles called coacervates, due to a …
Effects Of The Otx2ecr2 Enhancer & Prox1 Overexpression In Murine Retina Development, Erick J. Subillaga
Effects Of The Otx2ecr2 Enhancer & Prox1 Overexpression In Murine Retina Development, Erick J. Subillaga
Dissertations and Theses
There is a large subset of retinal progenitor cells that upregulate the OTX2 gene in the developing retina of the mouse. OTX2 is a homeobox transcription factor important for the development of photoreceptors and bipolar cells. If OTX2 is knocked out, photoreceptors and bipolar cells fail to differentiate. In order for OTX2 to be activated in certain retinal populations, it requires the activity of an enhancer called OTX2ECR2. Past studies demonstrated that retinal progenitor cells that had activity of OTX2ECR2 turned into horizontal cells, which require OTX2 for cell genesis and survival, and photoreceptors which require OTX2 for cell …