Results 141 to 150 of about 13,242,063 (338)
Small extracellular vesicles are a promising source of diagnostic molecules. We conducted a comprehensive study, including transcriptome profiling and RT‐qPCR validation on large cohorts of samples. Diagnostic panels enabling sensitive detection of colorectal cancer and precancerous lesions were established. Some molecules were differentially expressed
Petra Vychytilova‐Faltejskova +26 more
wiley +1 more source
Stemness properties, including quiescence, self‐renewal, and chemoresistance, are closely associated with leukemia relapse. Here, we demonstrate that DNA damage‐inducible transcript 4 (DDIT4) is induced in the hypoxic bone marrow niche and is essential for maintaining the stemness of AML1‐ETO9a leukemia cells.
Yishuang Li +12 more
wiley +1 more source
Development and Applications of CRISPR-Cas9 for Genome Engineering
P. Hsu, E. Lander, Feng Zhang
semanticscholar +1 more source
Author Correction: Optimizing ternary hybrid nanofluids using neural networks, gene expression programming, and multi-objective particle swarm optimization: a computational intelligence strategy. [PDF]
Hai T +9 more
europepmc +1 more source
Proteomic and phosphoproteomic analyses were performed on lung adenocarcinoma (LUAD) tumors with EGFR, KRAS, or EML4–ALK alterations and wild‐type cases. Distinct protein expression and phosphorylation patterns were identified, especially in EGFR‐mutated tumors. Key altered pathways included vesicle transport and RNA splicing.
Fanni Bugyi +12 more
wiley +1 more source
Computing Concrete Pullout Strength [PDF]
Beseler, Jan W., , \u2788 +1 more
core +1 more source
Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs
In HGSOC with normal KRAS expression, high PTP4A3 expression regulates autophagy activation. Conversely, in HGSOC with high KRAS expression, KRAS dictates autophagy control, and PTP4A3 is not required. When high PTP4A3 expression is inhibited, HGSOC cells are preferentially sensitised towards DNA‐damaging agents.
Ana López‐Garza +3 more
wiley +1 more source

