Results 61 to 70 of about 423,991 (315)

Mutant GGGGCC RNA prevents YY1 from binding to Fuzzy promoter which stimulates Wnt/β-catenin pathway in C9ALS/FTD

open access: yesNature Communications, 2023
The GGGGCC hexanucleotide repeat expansion mutation in the chromosome 9 open reading frame 72 (C9orf72) gene is a major genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia (C9ALS/FTD).
Zhefan Stephen Chen   +6 more
doaj   +1 more source

Bringing synapses into focus: Recent advances in synaptic imaging and mass-spectrometry for studying synaptopathy

open access: yesFrontiers in Synaptic Neuroscience, 2023
Synapses are integral for healthy brain function and are becoming increasingly recognized as key structures in the early stages of brain disease.
Nicole Hindley   +4 more
doaj   +1 more source

EMT‐associated bias in the Parsortix® system observed with pancreatic cancer cell lines

open access: yesMolecular Oncology, EarlyView.
The Parsortix® system was tested for CTC enrichment using pancreatic cancer cell lines with different EMT phenotypes. Spike‐in experiments showed lower recovery of mesenchymal‐like cells. This was confirmed with an EMT‐inducible breast cancer cell line.
Nele Vandenbussche   +8 more
wiley   +1 more source

Stasimon Contributes to the Loss of Sensory Synapses and Motor Neuron Death in a Mouse Model of Spinal Muscular Atrophy

open access: yesCell Reports, 2019
Summary: Reduced expression of the survival motor neuron (SMN) protein causes the neurodegenerative disease spinal muscular atrophy (SMA). Here, we show that adeno-associated virus serotype 9 (AAV9)-mediated delivery of Stasimon—a gene encoding an ...
Christian M. Simon   +7 more
doaj   +1 more source

Decrypting cancer's spatial code: from single cells to tissue niches

open access: yesMolecular Oncology, EarlyView.
Spatial transcriptomics maps gene activity across tissues, offering powerful insights into how cancer cells are organised, switch states and interact with their surroundings. This review outlines emerging computational, artificial intelligence (AI) and geospatial approaches to define cell states, uncover tumour niches and integrate spatial data with ...
Cenk Celik   +4 more
wiley   +1 more source

Neuronal cell culture from transgenic zebrafish models of neurodegenerative disease

open access: yesBiology Open, 2018
We describe a protocol for culturing neurons from transgenic zebrafish embryos to investigate the subcellular distribution and protein aggregation status of neurodegenerative disease-causing proteins.
Jamie R. Acosta   +11 more
doaj   +1 more source

Investigating the cell of origin and novel molecular targets in Merkel cell carcinoma: a historic misnomer

open access: yesMolecular Oncology, EarlyView.
This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian   +10 more
wiley   +1 more source

Proteomics Approaches for Biomarker and Drug Target Discovery in ALS and FTD

open access: yesFrontiers in Neuroscience, 2019
Neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are increasing in prevalence but lack targeted therapeutics. Although the pathological mechanisms behind these diseases remain unclear, both ALS and
Thomas J. Hedl   +11 more
doaj   +1 more source

ALS IMPLICATED PROTEIN TDP-43 SUSTAINS LEVELS OF STMN2 A MEDIATOR OF MOTOR NEURON GROWTH AND REPAIR

open access: yesNature Neuroscience, 2019
The findings that amyotrophic lateral sclerosis (ALS) patients almost universally display pathological mislocalization of the RNA-binding protein TDP-43 and that mutations in its gene cause familial ALS have nominated altered RNA metabolism as a disease ...
Joseph R. Klim   +15 more
semanticscholar   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

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