Results 141 to 150 of about 43,794 (228)

Exosome‐mediated miR‐4660 delivery inhibits OPN promoted hepatoma cells aggression through targeting LGALS3BP

open access: yesJournal of Cell Communication and Signaling, Volume 20, Issue 2, June 2026.
miR‐4660 was found to be downregulated in exosomes derived from SMMC‐OPN cells, a stable HCC cell line that overexpresses OPN. LGALS3BP has been identified as a direct target of miR‐4660, with its expression levels elevated in both SMMC‐OPN cells and their secreted exosomes.
Cuihua Liu   +9 more
wiley   +1 more source

Physiology, pathology and therapeutic potential of microglial triggering receptor expressed on myeloid cells 2 signalling: A narrative update

open access: yesClinical and Translational Discovery, Volume 6, Issue 3, June 2026.
TREM2hi microglia and macrophages exert distinct roles in neurological diseases. Enhancing TREM2 signalling supports pathological protein or debris clearance and mitigates inflammation in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, demyelination disorders and stroke, whereas blocking TREM2 may alleviate tauopathy and ...
Zhe Kong   +3 more
wiley   +1 more source

A Dynamic Change of Microglial States Occurs During the Transition From Photoreceptor Degeneration to Regeneration in Zebrafish pde6c Mutants

open access: yesGlia, Volume 74, Issue 6, June 2026.
Zebrafish pde6c mutants undergo photoreceptor degeneration from 5 dpf, but rods regenerate from 4 wpf. scRNA‐seq of retinal microglia reveals dynamic change of states between 5 dpf and 4 wpf. Two states emerge specifically during regeneration. ABSTRACT Microglia, brain‐resident immune cells, maintain brain homeostasis.
Darshini Ravishankar   +2 more
wiley   +1 more source

Study of the Elevation of Galectin-3 Level in Plasma Patients with Inflammatory Bowel Disease in Babylon Province

open access: yesMedical Journal of Babylon
Background: Inflammatory bowel disease is a collection of illnesses that mainly affect the colon and small intestine, the most prevalent types being Crohn’s disease and ulcerative colitis. Carbohydrate-binding proteins (also known as galectins) have been
Arkan Khanjar Nasrullah   +2 more
doaj   +1 more source

Urinary galectin-3 binding protein (G3BP) as a biomarker for disease activity and renal pathology characteristics in lupus nephritis. [PDF]

open access: yesArthritis Res Ther, 2022
Ding H   +9 more
europepmc   +1 more source

Biomarkers Beyond the Natriuretic Peptides for Chronic Heart Failure: Galectin-3 and Soluble ST2. [PDF]

open access: yes, 2012
B-type natriuretic peptide (BNP) and NT-proBNP are widely used plasma biomarkers for the diagnosis of acute decompensated heart failure and prognosis for future cardiac disease.
Wu, Alan HB
core   +1 more source

Broad and thematic remodeling of the surfaceome and glycoproteome on isogenic cells transformed with driving proliferative oncogenes. [PDF]

open access: yes, 2020
The cell surface proteome, the surfaceome, is the interface for engaging the extracellular space in normal and cancer cells. Here we apply quantitative proteomics of N-linked glycoproteins to reveal how a collection of some 700 surface proteins is ...
Coon, Joshua   +5 more
core  

P022 Galectin-3, galectin-9, and galectin-3 binding protein in patients with inflammatory bowel diseases [PDF]

open access: yesJournal of Crohn's and Colitis, 2019
D Cibor, K Szczeklik, D Owczarek, T Mach
openaire   +1 more source

Inhibition of PLA2G15 Alleviates Palmitic Acid‐Induced Lysosomal Membrane Permeabilization in Human Nucleus Pulposus Cells During Intervertebral Disc Degeneration

open access: yesJOR SPINE, Volume 9, Issue 2, June 2026.
LMP is responsible for lysosomal dysfunction in IDD. The lipid composition changes in the lysosomal membrane, mediated by PLA2G15, are the cause of LMP. The C/EBPα significantly promotes PLA2G15 expression under PA overload stress. Inhibition of PLA2G15 alleviates PA‐induced LMP by inhibiting the hydrolysis of lysosomal membrane phospholipids. ABSTRACT
Liqun Duan   +7 more
wiley   +1 more source

Home - About - Disclaimer - Privacy