A5022022696- Cellular transport and secretion
- Alzheimer's disease research and treatments
- Biotin and Related Studies
- Advanced Proteomics Techniques and Applications
- RNA Research and Splicing
- S100 Proteins and Annexins
- Cell Adhesion Molecules Research
- Neurogenetic and Muscular Disorders Research
- Ubiquitin and proteasome pathways
- Amyotrophic Lateral Sclerosis Research
- Lipid Membrane Structure and Behavior
- interferon and immune responses
- RNA modifications and cancer
- Cellular Mechanics and Interactions
- Receptor Mechanisms and Signaling
- Epigenetics and DNA Methylation
- Retinal Development and Disorders
- Parkinson's Disease Mechanisms and Treatments
- Protein Kinase Regulation and GTPase Signaling
- Endoplasmic Reticulum Stress and Disease
- Hereditary Neurological Disorders
- Advanced Fluorescence Microscopy Techniques
- Genetic Neurodegenerative Diseases
- Muscle Physiology and Disorders
- Cancer Genomics and Diagnostics
Mayo Clinic in Florida
2018-2025
WinnMed
2022-2024
Institute of Molecular Biology and Genetics
2009-2017
The critical point for successful treatment of cancer is diagnosis at early stages tumor development. Cancer cell-specific methylated DNA has been found in the blood patients, indicating that cell-free (cfDNA) circulating a convenient tumor-associated marker. Therefore cfDNA can be used as minimally invasive diagnostic We analysed concentration plasma and methylation six suppressor genes samples 27 patients with renal 15 healthy donors controls. concentrations from was measured using two...
Abstract The most common inherited cause of two genetically and clinico-pathologically overlapping neurodegenerative diseases, amyotrophic lateral sclerosis (ALS) frontotemporal dementia (FTD), is the presence expanded GGGGCC intronic hexanucleotide repeats in C9orf72 gene. Aside from haploinsufficiency toxic RNA foci, another non-exclusive disease mechanism non-canonical translation repeat into five different dipeptide proteins (DPRs), which form neuronal inclusions affected patient brains....
Abstract Background Cytoplasmic mislocalization and aggregation of TAR DNA-binding protein-43 (TDP-43) is a hallmark the amyotrophic lateral sclerosis frontotemporal dementia (ALS/FTD) disease spectrum, causing both nuclear loss-of-function cytoplasmic toxic gain-of-function phenotypes. While TDP-43 proteinopathy has been associated with defects in nucleocytoplasmic transport, this process still poorly understood. Here we study role karyopherin-β1 (KPNB1) other import receptors regulating...
Intersectins (ITSNs) are a family of highly conserved proteins with orthologs from nematodes to mammals. In vertebrates, ITSNs encoded by two genes (itsn1 and itsn2), which act as scaffolds that were initially discovered involved in endocytosis. Further investigation demonstrated ITSN1 is also implicated several other processes including regulated exocytosis, thereby suggesting role for the coupling between exocytosis endocytosis excitatory cells. Despite high degree conservation amongst...
Abstract Background Tauopathies represent a diverse group of neurodegenerative disorders characterized by the abnormal aggregation microtubule-associated protein tau. Despite extensive research, mechanisms underlying diversity neuronal and glial tau pathology in different tauopathies are poorly understood. While there is growing understanding tauopathy-specific differences isoforms fibrillar structures, specific composition heterogenous lesions remains unknown. Here we study aggregates four...
Glioblastoma (GBM) is the most prevalent and aggressive malignant primary brain tumor. GBM proximal to lateral ventricles (LVs) more aggressive, potentially because of subventricular zone contact. Despite this, cross-talk between neural stem/progenitor cells (NSC/NPCs) not well understood. Using cell-specific proteomics, we show that LV-proximal prevents neuronal maturation NSCs through induction senescence. In addition, tumor-initiating (BTICs) increase expression cathepsin B (CTSB) upon...
Adaptor/scaffold proteins of the intersectin (ITSN) family are important components endocytic and signalling complexes.They coordinate trafficking events with actin cytoskeleton rearrangements modulate activity a variety pathways.In this review, we present our results as part recent findings on function ITSNs, role alternative splicing in generation ITSN1 diversity potential relevance ITSNs for neurodegenerative diseases cancer.
ITSN1 adaptor/scaffold protein takes part in a variety of physiological and pathological cellular processes.It has complex expression regulation many partners.Aim.Characterization the functio ning control is important for understanding its role cell.Methods.Bioinformatic analysis, semiquantitative analysis by RTPCR, immunoprecipitation.Results.We have described ana lyzed promoter regions, detected alternatively spliced isoforms at mRNA levels different cancer specimens.Using bioinformatic...
ITSN1 is an endocytic scaffold protein with a prominent function in synaptic transmission.It known that Ca 2+ signaling crucial for the regulation of proteins functioning.Aim.Checking possibility /calmodulin-dependent phosphorylation ITSN1.Methods.Affinity chromatography, vitro kinase reaction, Western blotting, gel staining fluorescent stains.Results.We show fraction calmodulin-binding able to phosphorylate recombinant fragments encoding coiled-coil region and SH3 domain-containing presence...
Glioblastoma (GBM) is the most prevalent and aggressive malignant primary brain tumor. GBM proximal to lateral ventricles (LVs) more aggressive, potentially due subventricular zone (SVZ) contact. Despite this, crosstalk between neural stem/progenitor cells (NSC/NPCs) not well understood. Using cell-specific proteomics, we show that LV-proximal prevents neuronal maturation of NSCs through induction senescence. Additionally, tumor initiating (BTICs) increase expression CTSB upon interaction...
Tauopathies represent a diverse group of neurodegenerative disorders characterized by the abnormal aggregation microtubule-associated protein tau. Despite extensive research, precise mechanisms underlying complexity different types tau pathology remain incompletely understood. Here we describe an approach for proteomic profiling aggregate-associated proteomes on slides with formalin-fixed, paraffin-embedded (FFPE) tissue that utilizes proximity labelling upon high preservation aggregate...
Abstract Background Neuropathologic inclusions formed by hyperphosphorylated protein tau in the brain are a hallmark of Alzheimer’s disease and other human neurodegenerative disorders commonly referred to as tauopathies. Tau lesions differ their disease‐specific morphological presentations, affected cell type, subcellular compartments isoforms present inclusions. In addition, filaments isolated from different tauopathies have distinct fibrillar structures that potentially underlie diversity...
ITSN1 is a scaffold protein involved in endocytosis, signal transduction and cytoskeleton regulation.It has been previously shown that undergoes Ca 2+ /calmodulin-dependent phosphorylation vitro.Aim.We intend to identify these sites.Methods.In vitro kinase reaction; liquid chromatography-tandem mass spectrometry (LC/MS/MS).Results.We identified five sites of the recombinant fragments ITSN1.Conclusions.We have coiled-coil region (CCR) interdomain linkers between EH2 CCR, SH3A SH3B, SH3B SH3C...
ITSN1 is an endocytic scaffold protein implicated in synaptic functioning.Ca 2+ known to be important for endocytosis both pre-and post-synaptic terminals.ITSN1 contains two EH (Eps15 homology) domains which possess putative Ca -binding EF-hand motifs.Aim.To test the effect of on domain binding properties.Methods.His-tag pulldown, Western blotting.Results.Addition 1.5 mM does not affect C-terminal fragment Epsin 1. Conclusions.The data obtained indicate that has no properties domains.
Abstract Background Alzheimer’s disease (AD) is characterized by the accumulation of neurofibrillary tangles (NFTs), comprised primarily microtubule‐associated protein tau. NFTs are defining hallmarks AD and its into pathological oligomers fibrils has been associated with cognitive decline in other tauopathies. Despite pivotal role process, we still have a poor understanding how their formation, toxicity, spread across brain regions regulated via tau‐associated proteins that regulate...
Abstract Background Alzheimer's disease (AD) and related neurodegenerative diseases are characterized by the accumulation of abnormal protein aggregates. A defining hallmark AD is formation neurofibrillary tangles (NFTs) aggregation microtubule‐associated tau into pathological oligomers fibrils. Although NFTs believed to play a pivotal role in process, we have poor understanding how their formation, toxicity, spread across brain regions regulated. Recent data suggest that seeding behavior...