Results 31 to 40 of about 22,577 (244)

Evaluation of Engineered CRISPR-Cas-Mediated Systems for Site-Specific RNA Editing

open access: yesCell Reports, 2020
Summary: Site-directed RNA editing approaches offer great potential to correct genetic mutations in somatic cells while avoiding permanent off-target genomic edits.
Ryan J. Marina   +4 more
doaj   +1 more source

Peripheral lysosomes recruit PLEKHG3 to focal adhesions and restrain protrusion dynamics

open access: yesFEBS Letters, EarlyView.
Proximity‐dependent labeling at the LAMTOR complex revealed the Rho GEF PLEKHG3 as a lysosome‐proximal protein directing the study toward the influence of lysosome positioning on actin dynamics and cell motility. We show that PLEKHG3 colocalizes with lysosomes at focal adhesion sites and observe that forced peripheral dispersion of lysosomes hinders ...
Rainer Ettelt   +8 more
wiley   +1 more source

IMPDH inhibition enhances cytarabine efficacy in SAMHD1‐expressing leukaemia cells via guanine nucleotide depletion

open access: yesMolecular Oncology, EarlyView.
Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla   +9 more
wiley   +1 more source

Targeted gene deletions in the dimorphic fungal pathogen Histoplasma using an optimized episomal CRISPR/Cas9 system

open access: yesmSphere, 2023
The rapid development of CRISPR/CRISPR-associated (Cas) systems has revolutionized the ability to produce genetic mutations in a desired locus, particularly in organisms with low rates of homologous recombination.
Chad A. Rappleye
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

CRISPR Content Correlates with the Pathogenic Potential of Escherichia coli. [PDF]

open access: yesPLoS ONE, 2015
Guide RNA molecules (crRNA) produced from clustered regularly interspaced short palindromic repeat (CRISPR) arrays, altogether with effector proteins (Cas) encoded by cognate cas (CRISPR associated) genes, mount an interference mechanism (CRISPR-Cas ...
Enriqueta García-Gutiérrez   +4 more
doaj   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

open access: yesMolecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir   +13 more
wiley   +1 more source

Expanding the Microbial Genomic Landscape and Biotechnological Applications of CRISPR-Cas Systems

open access: yesBiology
The CRISPR-Cas systems, identified initially as adaptive immune mechanisms in bacteria and archaea against viral threats, have rapidly evolved into transformative tools in genetic engineering and biotechnology.
Swati Singh   +5 more
doaj   +1 more source

Identification of the EH CRISPR‐Cas9 system on a metagenome and its application to genome engineering

open access: yesMicrobial Biotechnology, 2023
Non‐coding RNAs (crRNAs) produced from clustered regularly interspaced short palindromic repeats (CRISPR) loci and CRISPR‐associated (Cas) proteins of the prokaryotic CRISPR‐Cas systems form complexes that interfere with the spread of transmissible ...
Belen Esquerra‐Ruvira   +5 more
doaj   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

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