A5011077993- Parkinson's Disease Mechanisms and Treatments
- Cellular transport and secretion
- 14-3-3 protein interactions
- Ubiquitin and proteasome pathways
- Alzheimer's disease research and treatments
- Nerve injury and regeneration
- RNA regulation and disease
- Neurological disorders and treatments
- Ginkgo biloba and Cashew Applications
- Mitochondrial Function and Pathology
- Biochemical and biochemical processes
- Genetics and Neurodevelopmental Disorders
- Fungal and yeast genetics research
- Diabetes and associated disorders
- Photoreceptor and optogenetics research
- Genetic Neurodegenerative Diseases
- Nuclear Receptors and Signaling
- Zebrafish Biomedical Research Applications
- Mechanisms of cancer metastasis
- Signaling Pathways in Disease
- Pancreatic function and diabetes
University of Alabama at Birmingham
2015-2022
Civitan International
2022
Center for Neuro-Oncology
2018
Nikon (United Kingdom)
2006
Abstract α‐Synuclein (α‐syn) is an abundant presynaptic protein that the primary constituent of inclusions define Lewy body diseases (LBDs). In these inclusions, α‐syn phosphorylated at serine‐129 residue. Antibodies directed to this phosphorylation site are used measure inclusion abundance and stage disease progression in preclinical models as well postmortem tissues LBDs. While it critical reliably identify phospho‐specific antibodies often cross‐react with nonspecific antigens. Four...
α-Synuclein (αsyn) is the key protein that forms neuronal aggregates in neurodegenerative disorders Parkinson's disease (PD) and dementia with Lewy bodies. Recent evidence points to prion-like spread of αsyn from one brain region another. Propagation likely dependent on release, uptake, misfolding. Under normal circumstances, this highly expressed functions normally without promoting pathology, yet underlying endogenous mechanisms prevent are not understood. 14-3-3 proteins have chaperone...
Alpha-synuclein (αsyn) is the key component of proteinaceous aggregates termed Lewy Bodies that pathologically define a group disorders known as synucleinopathies, including Parkinson's Disease (PD) and Dementia with Bodies. αSyn hypothesized to misfold spread throughout brain in prion-like fashion. Transmission αsyn necessitates release misfolded from one cell uptake by another, which it can template misfolding endogenous upon internalization. 14-3-3 proteins are family highly expressed...
α-Synuclein (αsyn) is the primary component of proteinaceous aggregates termed Lewy bodies that pathologically define synucleinopathies including Parkinson's disease (PD) and dementia with (DLB). αsyn hypothesized to spread through brain in a prion-like fashion by misfolded protein forming template for aggregation endogenous αsyn. The cell-to-cell release uptake are considered important processes its spread. Rab27b one several GTPases essential endosomal-lysosomal pathway implicated...
Abstract Islet-1 (Isl1) is a Lin11, Isl1, Mec3 (LIM)-homeodomain transcription factor important for pancreatic islet cell development, maturation, and function, which largely requires interaction with the LIM domain-binding protein 1 (Ldb1) coregulator. In other tissues, Ldb1 Isl1 interact additional factors to mediate target gene transcription, yet few partners are known in β-cells. Therefore, we hypothesize that participate larger regulatory complexes impact β-cell expression. To test...
SUMMARY Parkinson’s disease and Dementia with Lewy Bodies are two common neurodegenerative disorders marked by proteinaceous aggregates composed primarily of the protein α-synuclein. α-Synuclein is hypothesized to have prion-like properties, which misfolded α-synuclein induces pathological aggregation endogenous neuronal loss. Rab27a Rab27b highly homologous Rab GTPases that regulate secretion, clearance, toxicity in vitro . In this study, we tested impact Rab27a/b on transmission pathogenic...
Abstract Alpha-synuclein (αsyn) is the key component of proteinaceous aggregates termed Lewy Bodies (LBs) that pathologically define a group disorders known as synucleinopathies, including Parkinson’s Disease (PD) and Dementia with (DLB). αSyn hypothesized to misfold spread throughout brain in prion-like fashion. Transmission αsyn necessitates release misfolded from one cell uptake by another, which it can template misfolding endogenous upon internalization. 14-3-3 proteins are family highly...
Abstract We report an incidental 358.5 kb deletion spanning the region encoding for alpha-synuclein (αsyn) and multimerin1 (Mmrn1) in Rab27a/Rab27b double knockout (DKO) mouse line previously developed by Tolmachova colleagues 2007. Western blot RT-PCR studies revealed lack of αsyn expression at either mRNA or protein level Rab27a/b DKO mice. PCR genomic DNA from mice demonstrated least partial Snca locus using primers targeted to exon 4 6. Most genes located proximity locus, including Atoh1...
The human brain is an organ of extraordinary complexity. Understanding how the develops not only intrinsically interesting, but also has great significance in understanding, and possibly treating, neurological disorders CNS injury. At MRC Centre for Developmental Neurobiology, King's College, London, Dr. Steffen Scholpp, working with Professor Andrew Lumsden, interested early development thalamus. In humans, this size shape egg located centre brain.
ABSTRACT Alpha synuclein (αsyn) is the primary component of proteinaceous aggregates termed Lewy Bodies that pathologically define synucleinopathies including Parkinson’s disease (PD) and Dementia with (DLB). αSyn hypothesized to spread through brain in a prion-like fashion by misfolded protein forming template for aggregation endogenous αsyn. The release uptake αsyn from cell are considered important processes this spread. Rab27b one several GTPases essential endosomal-lysosomal pathway...