Results 51 to 60 of about 138,674 (288)

Homologous expression and purification of human HAX‐1 for structural studies

open access: yesFEBS Open Bio, EarlyView.
This research protocol provides detailed instructions for cloning, expressing, and purifying large quantities of the intrinsically disordered human HAX‐1 protein, N‐terminally fused to a cleavable superfolder GFP, from mammalian cells. HAX‐1 is predicted to undergo posttranslational modifications and to interact with membranes, various cellular ...
Mariana Grieben
wiley   +1 more source

Overview of molecular signatures of senescence and associated resources: pros and cons

open access: yesFEBS Open Bio, EarlyView.
Cells can enter a stress response state termed cellular senescence that is involved in various diseases and aging. Detecting these cells is challenging due to the lack of universal biomarkers. This review presents the current state of senescence identification, from biomarkers to molecular signatures, compares tools and approaches, and highlights ...
Orestis A. Ntintas   +6 more
wiley   +1 more source

A flow cytometry-based screen of nuclear envelope transmembrane proteins identifies NET4/Tmem53 as involved in stress-dependent cell cycle withdrawal.

open access: yesPLoS ONE, 2011
Disruption of cell cycle regulation is one mechanism proposed for how nuclear envelope protein mutation can cause disease. Thus far only a few nuclear envelope proteins have been tested/found to affect cell cycle progression: to identify others, 39 novel
Nadia Korfali   +6 more
doaj   +1 more source

BMI‐1 modulation and trafficking during M phase in diffuse intrinsic pontine glioma

open access: yesFEBS Open Bio, EarlyView.
The schematic illustrates BMI‐1 phosphorylation during M phase, which triggers its translocation from the nucleus to the cytoplasm. In cycling cells, BMI‐1 functions within the PRC1 complex to mediate H2A K119 monoubiquitination. Following PTC596‐induced M phase arrest, phosphorylated BMI‐1 dissociates from PRC1 and is exported to the cytoplasm via its
Banlanjo Umaru   +6 more
wiley   +1 more source

CDK1 controls CHMP7-dependent nuclear envelope reformation

open access: yeseLife, 2021
Through membrane sealing and disassembly of spindle microtubules, the Endosomal Sorting Complex Required for Transport-III (ESCRT-III) machinery has emerged as a key player in the regeneration of a sealed nuclear envelope (NE) during mitotic exit, and in
Alberto T Gatta   +5 more
doaj   +1 more source

Nuclear pore links Fob1‐dependent rDNA damage relocation to lifespan control

open access: yesFEBS Open Bio, EarlyView.
Damaged rDNA accumulates at a specific perinuclear interface that couples nucleolar escape with nuclear envelope association. Nuclear pores at this site help inhibit Fob1‐induced rDNA instability. This spatial organization of damage handling supports a functional link between nuclear architecture, rDNA stability, and replicative lifespan in yeast.
Yamato Okada   +5 more
wiley   +1 more source

The ESCRT-III complex is required for nuclear pore complex sequestration and regulates gamete replicative lifespan in budding yeast meiosis

open access: yesNucleus, 2020
Cellular aging occurs as a cell loses its ability to maintain homeostasis. Aging cells eliminate damaged cellular compartments and other senescence factors via self-renewal.
Bailey A. Koch   +3 more
doaj   +1 more source

Dystonia and the Nuclear Envelope [PDF]

open access: yesNeuron, 2005
Mutations in torsinA cause dominantly inherited early-onset torsion dystonia in humans. In this issue of Neuron, Goodchild et al. show that torsinA knockout and knockin mice have similar phenotypes, which suggests that the mutant torsinA allele causes disease because it has decreased function. The experiments also highlight the possible role of nuclear
Cookson, Mark R., Clarimon, Jordi
openaire   +2 more sources

SNUPN‐Related Muscular Dystrophy: Novel Phenotypic, Pathological and Functional Protein Insights

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective SNUPN‐related muscular dystrophy or LGMDR29 is a new entity that covers from a congenital or childhood onset pure muscular dystrophy to more complex phenotypes combining neurodevelopmental features, cataracts, or spinocerebellar ataxia. So far, 12 different variants have been described.
Nuria Muelas   +18 more
wiley   +1 more source

A multistage sequencing strategy pinpoints novel candidate alleles for Emery-Dreifuss muscular dystrophy and supports gene misregulation as its pathomechanism

open access: yesEBioMedicine, 2020
Background: As genome-wide approaches prove difficult with genetically heterogeneous orphan diseases, we developed a new approach to identify candidate genes.
Peter Meinke   +12 more
doaj   +1 more source

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