Results 291 to 300 of about 3,122,867 (388)

Lipopolysaccharide uptake is augmented in lipopolysaccharide‐tolerant mouse macrophage‐like cells via increased CD14 expression

open access: yesFEBS Open Bio, EarlyView.
In normal (nontolerant) cells, CD14 is crucial for both LPS uptake and LPS signaling. In LPS‐tolerant cells, in which LPS‐induced TNF‐α and IFN‐β production is suppressed, there is a dramatic increase in surface CD14 expression. The overexpressed CD14 in LPS‐tolerant cells is responsible for the enhanced LPS uptake without inducing pro‐inflammatory ...
Saeka Nishihara   +3 more
wiley   +1 more source

Proximity Labeling Reveals RNA-Binding Proteins Associating with the Human Mitochondrial Import Receptor TOMM20. [PDF]

open access: yesJ Proteome Res
Akram S   +6 more
europepmc   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Protein kinase a regulates cyclooxygenase-2 expression through the RNA-binding proteins HuR and TTP. [PDF]

open access: yesJ Biol Chem
Adame-Garcia SR   +8 more
europepmc   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

Chloroplast RNA-binding Proteins

open access: yesNippon Nōgeikagaku Kaishi, 1997
Mamoru SUGITA, Masahiro SUGIURA
openaire   +2 more sources

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