Results 191 to 200 of about 401,671 (363)

ACSS2/AATF Drives Soluble FasL‐Mediated CD8+ T Cell Apoptosis in Pancreatic Neuroendocrine Tumors

open access: yesAdvanced Science, EarlyView.
This study unveils that ACSS2‐driven acetate metabolism fuels histone pan‐acetylation in pancreatic neuroendocrine tumors (PNETs), remodeling the epigenetic landscape. The ACSS2/AATF axis transcriptionally activates soluble FasL (sFasL), which engages Fas receptors on infiltrating CD8+ T cells to trigger caspase‐8/3‐mediated apoptosis.
Qin Dang   +14 more
wiley   +1 more source

Prediction of KIR3DL1 and human leukocyte antigen binding. [PDF]

open access: yesJ Biol Chem
Maiers M   +6 more
europepmc   +1 more source

KLK1 as an Epithelial‐Specific Brake Inhibits Colorectal Tumorigenesis by Suppressing B1R‐Mediated Fibroblast Phenotypic Transition

open access: yesAdvanced Science, EarlyView.
KLK1 downregulation disrupts the intestinal mucosal barrier and impairs kallikrein‐kinin signaling, thereby reducing Lys‐des‐Arg9‐BK production. This enhances B1R activation on ADAMDEC1⁺ fibroblasts, promoting inflammation and extracellular matrix (ECM) remodeling. The resulting iCAFs promote colorectal cancer progression, highlighting a novel KLK1‐B1R
Lisha Zhou   +14 more
wiley   +1 more source

RIPK1 Drives JAK1‐STAT3 Signaling to Promote CXCL1‐Mediated Neutrophil Recruitment in Sepsis‐Induced Lung Injury

open access: yesAdvanced Science, EarlyView.
This article examines the central role of RIPK1 in the pathogenesis of sepsis‐induced lung injury. It elucidates how RIPK1 initiates an inflammatory cascade by activating JAK1‐STAT3 signaling, leading to CXCL1‐mediated neutrophil infiltration. Importantly, it demonstrates that pharmacological inhibition of RIPK1 effectively attenuates inflammation and ...
Hao Sun   +15 more
wiley   +1 more source

Association of Human Leukocyte Antigen Polymorphisms With Moderate-to-Severe Dry Eye With and Without Sjögren's Syndrome. [PDF]

open access: yesInvest Ophthalmol Vis Sci
Chen Z   +10 more
europepmc   +1 more source

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