Results 161 to 170 of about 518,432 (294)
Isolation of a fission yeast mutant cell affected in MAP kinase signaling and sterol biosynthesis.
Kiwamu Imagawa +5 more
openalex +1 more source
MAP kinase phosphorylation is dispensable for cell division, but required for cell growth in Drosophila [PDF]
Neena Majumdar +4 more
openalex +1 more source
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon +13 more
wiley +1 more source
ATRT-17. INHIBITING THE MAP KINASE PATHWAY WITH MEK INHIBITOR MIRDAMETINIB SUPPRESSES CANCER GROWTH IN ATYPICAL TERATOID/RHABDOID TUMORS [PDF]
Yiming Deng +6 more
openalex +1 more source
LDAcoop: Integrating non‐linear population dynamics into the analysis of clonogenic growth in vitro
Limiting dilution assays (LDAs) quantify clonogenic growth by seeding serial dilutions of cells and scoring wells for colony formation. The fraction of negative wells is plotted against cells seeded and analyzed using the non‐linear modeling of LDAcoop.
Nikko Brix +13 more
wiley +1 more source
Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li +10 more
wiley +1 more source
50 Hz magnetic fields activate mussel immunocyte p38 MAP kinase and induce HSP70 and 90
Davide Malagoli +3 more
openalex +2 more sources
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala +15 more
wiley +1 more source
Violaceous, hyperkeratotic plaque in a pediatric patient
Racquel A. Bitar, BS +3 more
doaj +1 more source

