Effects of macro- and micronutrient intake on bone mineral density, osteoporotic fracture risk, inflammation, and functional rehabilitation outcomes in orthopedic patients: a systematic review and meta-analysis. [PDF]
Lv C, Xiao X, He R.
europepmc +1 more source
Evaluating the involvement of autolysosomes in the nuclear translocation of fluorescent proteins
Endogenously expressed fluorescent proteins can be degraded by autophagy and transported to cell nuclei via the nuclear pore complex. But in some cell lines, for example, HeLa cells which are positive for immunoreactivity of a receptor ligand, such as UCN I, in cell nuclei, fusion of autolysosome with the nuclear envelope is involved in the nuclear ...
Keiichi Ikeda
wiley +1 more source
Draft genome data analysis and pathogenicity profiling of <i>Staphylococcus aureus</i> strain IHS3A with antibiotic resistance genes isolated from a hospital in Jordan. [PDF]
Abushattal S +3 more
europepmc +1 more source
Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells
Loss of AMBRA1 in melanoma cells activates multiple oncogenic pathways associated with tumor progression. Transcriptomic and protein network analyses revealed that AMBRA1 depletion enhances MAPK/ERK signaling, angiogenesis, TGF‐β/EMT signaling, and Wnt/axon guidance pathways.
Milad Ibrahim +4 more
wiley +1 more source
Unplanned Emergency Room Visits following Hip Arthroscopy. [PDF]
Sacklow JE +5 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
Pharmacological and device-based interventions for paraplegia: A ClinicalTrials.gov-based analysis. [PDF]
Alorfi NM +7 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

