Tag results:
CRISPR-Cas9
Prostate Cell News
Alternative Splicing of NF-YA Promotes Prostate Cancer Aggressiveness and Represents a New Molecular Marker for Clinical Stratification of Patients
[Journal of Experimental & Clinical Cancer Research] Researchers indicated that the modulation of NF-YA isoforms affected prostate pathophysiological processes and contributed to a cancer-relevant phenotype, in vitro and in vivo.
Endothelial Cell News
Locus-Conserved Circular RNA cZNF292 Controls Endothelial Cell Flow Responses
[Circulation Research] The authors identified the protein syndesmos to specifically interact with cZNF292 in endothelial cells by RNA affinity purification and subsequent mass spectrometry analysis.
Umbilical & Placental Cell News
Modeling Clonal Hematopoiesis in Umbilical Cord Blood Cells by CRISPR/Cas9
[Leukemia] Site-specific mutations were introduced in defined regions of DNMT3A, TET2, and ASXL1 in CD34+ progenitor cells that were subsequently analyzed in short-term as well as long-term in vitro culture assays to assess self-renewal and differentiation capacities.
Prostate Cell News
Anti-Metastatic Effect of GV1001 on Prostate Cancer Cells; Roles of GnRHR-Mediated Gαs-cAMP Pathway and AR-YAP1 Axis
[Cell & Bioscience] The authors revealed the potential mechanisms of which GV1001-stimulated Gαs-cAMP signaling pathway reduced the migration and metastasis of prostate cancer cells.
Neural Cell News
Loss of p53 Suppresses Replication Stress-Induced DNA Damage in ATRX-Deficient Neuroblastoma
[Oncogenesis] Researchers sugggested that alpha thalassemia mental retardation X-linked (ATRX) maintained genome integrity and p53 deficiency attenuated replication stress-induced DNA damage in neuroblastoma cells featuring inactivated ATRX by regulating DNA repair mechanisms.
ESC & iPSC News
PCSK9 Regulates the NODAL Signaling Pathway and Cellular Proliferation in hiPSCs
[Stem Cell Reports] Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibition in human iPSCs (hiPSCs) with the use of short hairpin RNA, CRISPR/cas9-mediated knockout, or endogenous PCSK9 loss-of-function mutation R104C/V114A unveiled its new role as a potential cell cycle regulator through the NODAL signaling pathway.