Results 101 to 110 of about 248,138 (311)

Large‐scale bidirectional arrayed genetic screens identify OXR1 and EMC4 as modifiers of αSynuclein aggregation

open access: yesFEBS Open Bio, EarlyView.
Activation of the mitochondrial protein OXR1 increases pSyn129 αSynuclein aggregation by lowering ATP levels and altering mitochondrial membrane potential, particularly in response to MSA‐derived fibrils. In contrast, ablation of the ER protein EMC4 enhances autophagic flux and lysosomal clearance, broadly reducing α‐synuclein aggregates.
Sandesh Neupane   +11 more
wiley   +1 more source

Splicing therapeutics in SMN2 and APOB

open access: yes, 2009
Splicing therapeutics are defined as the deliberate modification of RNA splicing to achieve therapeutic goals. Various techniques for splicing therapeutics have been described, and most of these involve the use of antisense oligonucleotide-based ...
Krainer, AR   +3 more
core  

iCLIP predicts the dual splicing effects of TIA-RNA interactions

open access: yes, 2010
The regulation of alternative splicing involves interactions between RNA-binding proteins and pre-mRNA positions close to the splice sites. T-cell intracellular antigen 1 (TIA1) and TIA1-like 1 (TIAL1) locally enhance exon inclusion by recruiting U1 ...
Nicholas M. Luscombe   +27 more
core   +1 more source

Evidence for a nuclear compartment of transcription and splicing located at chromosome domain boundaries [PDF]

open access: yes, 1993
The nuclear topography of splicing snRNPs, mRNA transcripts and chromosome domains in various mammalian cell types are described. The visualization of splicing snRNPs, defined by the Sm antigen, and coiled bodies, revealed distinctly different ...
R. M. Zirbel   +9 more
core   +1 more source

Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells

open access: yesFEBS Open Bio, EarlyView.
Loss of AMBRA1 in melanoma cells activates multiple oncogenic pathways associated with tumor progression. Transcriptomic and protein network analyses revealed that AMBRA1 depletion enhances MAPK/ERK signaling, angiogenesis, TGF‐β/EMT signaling, and Wnt/axon guidance pathways.
Milad Ibrahim   +4 more
wiley   +1 more source

Structural basis for the sequence-specific RNA-recognition mechanism of human CUG-BP1 RRM3

open access: yes, 2009
The CUG-binding protein 1 (CUG-BP1) is a member of the CUG-BP1 and ETR-like factors (CELF) family or the Bruno-like family and is involved in the control of splicing, translation and mRNA degradation.
Kanako Kuwasako   +27 more
core   +1 more source

C16orf57, a gene mutated in poikiloderma with neutropenia, encodes a putative phosphodiesterase responsible for the U6 snRNA 3′ end modification. [PDF]

open access: yes, 2012
C16orf57 encodes a human protein of unknown function, and mutations in the gene occur in poikiloderma with neutropenia (PN), which is a rare, autosomal recessive disease.
Krwawicz, Joanna   +6 more
core   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Detecting differential usage of exons from RNA-Seq data

open access: yes, 2012
RNA-Seq is a powerful tool for the study of alternative splicing and other forms of alternative isoform expression. Understanding the regulation of these processes requires comparisons between treatments, tissues or conditions.
Simon Anders   +2 more
core   +1 more source

Operon conservation and the evolution of trans-splicing in the phylum Nematoda [PDF]

open access: yes, 2006
The nematode Caenorhabditis elegans is unique among model animals in that many of its genes are cotranscribed as polycistronic pre-mRNAs from operons.
Mark L Blaxter   +5 more
core   +1 more source

Home - About - Disclaimer - Privacy