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We also determine the distribution of caspase 9 activity in HA14-1-treated immortalized Jurkat T-cell leukemia cells, using a multiparameter flow cytometry assay based on FAM-LEHD-FMK (caspase 9 FLICA) reagent which binds to the activated caspase 9, TMRM which labels energized mitochondria, and plasma membrane integrity marker 7-AAD (Fig. 2b).
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Notch1 signaling pathway was found to directly activate a feed-forward-loop transcriptional network and induce c-MYC gene expression to promot the growth of human T cell lymphoblastic leukemia cells, using an integrative systems biology approach which integrated gene expression array and ChIP-on-chip data [24].
Total RNA was extracted from leukemia cells using RNAiso plus (TaKaRa BIO Inc, Otsu, Japan), and the first strand cDNA synthesis was performed using a TIANScript RT Kit (TIANGEN, Beijing, China) and Oligo dT 15 primer from 2 μg total RNA according to the manufacturer's instructions.
Here, we have chronicled the dynamics of protein and mRNA expression levels across a minimally perturbed cell cycle in human myeloid leukemia cells using centrifugal elutriation combined with mass spectrometry-based proteomics and RNA-Seq, avoiding artificial synchronization procedures.
The ability of voreloxin to poison human topoisomerase II was evaluated in CCRF-CEM acute lymphocytic leukemia cells using the ICE bioassay [39].
This finding was in agreement with those reported in previous studies on leukemia cells using chemically related P2Et tannins.
Total cellular RNA was extracted from homogenized lysate samples of leukemia cells using the Qiagen RNeasy Plus Mini Kit (catalog no. 74134) (Qiagen, Santa Clarita, CA).
Inhibition of the driving TK in leukemia cells (using IM or dasatinib in BCR-ABL-driven leukemias, quizartinib in FLT3-driven leukemia, and IM in KIT-driven leukemia) makes these cells exquisitely sensitive to low doses of oligomycin-A, an inhibitor of mitochondrial ATP synthase, highlighting particular druggable dependencies in leukemic cells that are exposed to TK inhibition [ 1].
Its first target was the regulatory network involved in controlling the differentiation of THP-1 cells, a line of human leukemia cells used in laboratory experiments.
B-cell precursor acute lymphoblastic leukemia cells use tunneling nanotubes to orchestrate their microenvironment.
Importantly, our previous studies of the actions of indomethacin against myeloid leukemia cells used conventional culture conditions that do not reflect the hypoxic conditions present in the malignant bone marrow.
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