Results 171 to 180 of about 1,314,359 (264)
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
Correction: Post-transcriptional regulation of MEK-1 by polyamines through the RNA-binding protein HuR modulating intestinal epithelial apoptosis. [PDF]
Wang JY +9 more
europepmc +1 more source
RNA binding protein <i>Pcbp1</i> maintains mitochondria integrity to promote antibody production and germinal center response. [PDF]
Zhu L +8 more
europepmc +1 more source
IGFBP4 knockdown (KD) impairs preadipocyte proliferation and is associated with IGF1R protein downregulation and attenuated AKT phosphorylation. The mechanisms by which IGFBP4 KD influences the IGF1R/AKT signaling pathway involve newly synthesized proteins and lysosomal degradation pathways. Created in BioRender.
Yujia Guo +6 more
wiley +1 more source
Targeting Cold-Inducible RNA-Binding Protein Attenuates Pancreatic Fibrosis by Suppressing Pyroptosis in Chronic Pancreatitis. [PDF]
Cui Q +8 more
europepmc +1 more source
Aging Is a Key Driver for Adult Acute Myeloid Leukemia
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
RNA binding protein ZFP36L1 promotes ferroptosis in chronic rhinosinusitis by destabilizing CAMK2A mRNA and impairing mitochondrial quality control. [PDF]
Xiong J +6 more
europepmc +1 more source
Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance
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

