Results 51 to 60 of about 86,842 (296)

Bioinformatics analysis identifies several intrinsically disordered human E3 ubiquitin-protein ligases [PDF]

open access: yesPeerJ, 2016
The ubiquitin-proteasome system targets misfolded proteins for degradation. Since the accumulation of such proteins is potentially harmful for the cell, their prompt removal is important.
Wouter Boomsma   +4 more
doaj   +2 more sources

Genetic attenuation of ALDH1A1 increases metastatic potential and aggressiveness in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Aldehyde dehydrogenase 1A1 (ALDH1A1) is a cancer stem cell marker in several malignancies. We established a novel epithelial cell line from rectal adenocarcinoma with unique overexpression of this enzyme. Genetic attenuation of ALDH1A1 led to increased invasive capacity and metastatic potential, the inhibition of proliferation activity, and ultimately ...
Martina Poturnajova   +25 more
wiley   +1 more source

E3 Ubiquitin Ligases and Their Therapeutic Applications in Cancers: Narrative Review

open access: yesJournal of Pharmacy and Bioallied Sciences
E3 ubiquitin ligases are a class of enzymes, essential for maintaining the equilibrium of cells by binding ubiquitin molecules to substrates to mark them for destruction.
Azfar Jamal
doaj   +1 more source

E3 Ubiquitin Ligases Neurobiological Mechanisms: Development to Degeneration

open access: yesFrontiers in Molecular Neuroscience, 2017
Cells regularly synthesize new proteins to replace old or damaged proteins. Deposition of various aberrant proteins in specific brain regions leads to neurodegeneration and aging.
Arun Upadhyay   +6 more
doaj   +1 more source

Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma

open access: yesMolecular Oncology, EarlyView.
The causes of central nervous system (CNS) hemangioblastoma in Von Hippel–Lindau (vHL) disease are unclear. We used Whole Exome Sequencing (WES) on familial hemangioblastoma to investigate events that underlie tumor development. Our findings suggest that VHL loss creates a permissive environment for tumor formation, while additional alterations ...
Maja Dembic   +5 more
wiley   +1 more source

Targeting TNBC: core–shell polycationic polyurea dendrimers with inherent anticancer activity

open access: yesFEBS Open Bio, EarlyView.
Core–shell polycationic PURE dendrimers were tested in TNBC‐derived tumor models. Both formulations selectively targeted TNBC and effectively reduced tumor volume. PUREG4‐OEI48 suppressed tumor growth without detectable toxicity, whereas PUREG4‐OCEI24, despite showing efficacy, induced hepatic toxicity.
Adriana Cruz   +9 more
wiley   +1 more source

A Key Role for the Ubiquitin Ligase UBR4 in Myofiber Hypertrophy in Drosophila and Mice

open access: yesCell Reports, 2019
Summary: Skeletal muscle cell (myofiber) atrophy is a detrimental component of aging and cancer that primarily results from muscle protein degradation via the proteasome and ubiquitin ligases.
Liam C. Hunt   +11 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

Evolution of DNA ligases of Nucleo-Cytoplasmic Large DNA viruses of eukaryotes: a case of hidden complexity

open access: yesBiology Direct, 2009
Background Eukaryotic Nucleo-Cytoplasmic Large DNA Viruses (NCLDV) encode most if not all of the enzymes involved in their DNA replication. It has been inferred that genes for these enzymes were already present in the last common ancestor of the NCLDV ...
Koonin Eugene V, Yutin Natalya
doaj   +1 more source

Self‐regulating ubiquitin ligases [PDF]

open access: yesThe EMBO Journal, 2017
Occasional auto‐modification of ubiquitin ligases typically leads to their proteasomal destruction, but new findings published in The EMBO Journal now show that in the case of Rsp5/Nedd4, auto‐ubiquitylation instead triggers oligomerization and concomitant reduction of ligase activity. This novel mechanism therefore creates silenced ligases that remain
Spencer Hill, Gary Kleiger
openaire   +2 more sources

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