Results 211 to 220 of about 13,866,076 (358)

A Swedish family with de novo α-synuclein A53T mutation: Evidence for early cortical dysfunction

open access: green, 2009
Andreas Puschmann   +17 more
openalex   +2 more sources

LDAcoop: Integrating non‐linear population dynamics into the analysis of clonogenic growth in vitro

open access: yesMolecular Oncology, EarlyView.
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

Development and Validation of the Family ICU Delirium Detection Instrument. [PDF]

open access: yesCrit Care Explor
Krewulak KD   +17 more
europepmc   +1 more source

Predictors of Later–Generation Family Members’ Commitment to Family Enterprises

open access: green, 2013
Alexandra Dawson   +4 more
openalex   +2 more sources

A never-ending story: the steadily growing family of the FA and FA-like genes [PDF]

open access: gold, 2017
Anna Gueiderikh   +2 more
openalex   +1 more source

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

open access: yesMolecular Oncology, EarlyView.
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

The MAPKKK and MAPKK gene families in banana: identification, phylogeny and expression during development, ripening and abiotic stress [PDF]

open access: gold, 2017
Lianzhe Wang   +10 more
openalex   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
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

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