Results 161 to 170 of about 186,664 (282)

CD44 [PDF]

open access: yesScience-Business eXchange, 2010
openaire   +1 more source

CD44 and cancer

open access: yesThe Lancet, 1993
DavidG. Jackson   +5 more
openaire   +2 more sources

NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation

open access: yesAdvanced Science, EarlyView.
NIBAN2, highly expressed in glioma stem‐like cells (GSCs), assembles with FLII and transcription factor RREB1 to form a nuclear complex. This complex transcriptionally activates stemness‐associated genes (e.g., CD44, NANOG) and metabolic enzymes (e.g., LDHA), thereby sustaining both transcriptional and metabolic stemness programs.
Liang liang Shi   +14 more
wiley   +1 more source

Integrated network analysis and experimental validation identify CCNA2, CD44, and STAT1 as clinically relevant hub genes in oral squamous cell carcinoma. [PDF]

open access: yesFront Mol Biosci
Bu M   +12 more
europepmc   +1 more source

CD3ɛ Nanobody‐Engineered Extracellular Vesicles Driving In Vivo Generation of TCE‐secreting CAR‐Ts for Solid Tumor Therapy With Memory Response and Minimal Immunogenicity

open access: yesAdvanced Science, EarlyView.
HEK‐293T‐derived CD3ε Nb‐engineered EVs to generate dual‐targeting CAR‐T cells directly in vivo. These EVs selectively deliver CAR.BiTE transgenes into T cells and reprogramed to HLA‐G/PD‐L1‐targeting effector cells with enhanced memory and persistence.
Shi‐Wei Huang   +27 more
wiley   +1 more source

CD44 [PDF]

open access: yes, 2019
openaire   +1 more source

Cellular Identity Crisis: RD3 Loss Fuels Plasticity and Immune Silence in Progressive Neuroblastoma

open access: yesAdvanced Science, EarlyView.
Researchers discovered that therapy‐induced loss of RD3 protein in neuroblastoma triggers a dangerous shift: cancer cells become more stem‐like, invasive, and resistant to treatment while evading immune detection. RD3 loss suppresses antigen presentation and boosts immune checkpoints, creating an immune‐silent environment.
Poorvi Subramanian   +7 more
wiley   +1 more source

miR‐135a‐5p Is a Promising Target to Prevent the Glomerulosclerosis Associated with Podocyte Developmental Toxicity in Offspring Induced by Prenatal Dexamethasone Exposure

open access: yesAdvanced Science, EarlyView.
Prenatal dexamethasone exposure (PDE) programs persistent podocyte developmental injury and adult glomerulosclerosis. Mechanistically, glucocorticoid receptor (GR) binds the miR‐135a‐5p promoter and recruits the histone acetyltransferase p300, increasing promoter histone acetylation and sustaining miR‐135a‐5p expression. Elevated miR‐135a‐5p suppresses
Xiaoqi Zhao   +8 more
wiley   +1 more source

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