Results 91 to 100 of about 32,418 (239)

RNA Helicase DDX21 Controls CD4+ T Cell Proliferation and Promotes Inflammatory Bowel Disease via Translational Control

open access: yesAdvanced Science, EarlyView.
ABSTRACT Inflammatory bowel disease (IBD) is characterized by dysregulated T cell responses. RNA helicases, including DExD‐box helicase 21 (DDX21), are pivotal in RNA metabolism, but their role in T cell‐mediated pathology during IBD remains unclear. Here, we demonstrate that DDX21 expression in CD4+ T cells correlates with cell cycle and translation ...
Yujuan Zhang   +11 more
wiley   +1 more source

Methods to Analyze the Contribution of Complement Evasion Factor (CEF) to Streptococcus pyogenes Virulence.

open access: yes, 2023
Group A Streptococcus (GAS, Streptococcus pyogenes) is an exclusively human pathogen that causes a range of diseases, including pharyngitis, tonsillitis, impetigo, erysipelas, necrotizing fasciitis, and toxic shock syndrome.
Aghababa, Haniyeh   +2 more
core   +1 more source

Decoding IGLL5 Mutation‐Mediated BCR Signaling: A Novel Mechanism of CD8+ T Cell Exhaustion and Ocular MALT Lymphoma Progression

open access: yesAdvanced Science, EarlyView.
OAML harbors recurrent IGLL5 mutations that reinforce CD79A/CD79B‐associated BCR signaling. Mechanistic analysis of the S47G and A54G variants reveals induction of CXCL10/CXCL11, enhanced CD8+ T‐cell recruitment, and exhaustion‐associated dysfunction, supporting an immune‐tolerant niche.
Andi Zhao   +12 more
wiley   +1 more source

Tax Progressivity and Tax Evasion [PDF]

open access: yes
More progressive income taxes raise employment in models of imperfectly competitive labour markets. However, this prediction is not robust to modifications of the analytical structure.
Laszlo Goerke
core  

Staphylococcal complement evasion by various convertase-blocking molecules.

open access: yes, 2007
To combat the human immune response, bacteria should be able to divert the effectiveness of the complement system. We identify four potent complement inhibitors in Staphylococcus aureus that are part of a new immune evasion cluster. Two are homologues of
Maartje Ruyken   +15 more
core   +1 more source

Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

open access: yesAdvanced Science, EarlyView.
Pancreatic neuroendocrine tumors frequently silence MEN1 through epigenetic mechanisms. Here, SIRT7 recruits DNMT1 to the MEN1 promoter, drives hypermethylation, and enhances DNA repair. Inhibiting SIRT7 restores MEN1, reduces MRN complex abundance, impairs double‐strand break repair, and sensitizes PanNET models to radiation, supporting SIRT7 as a ...
Jianyun Jiang   +11 more
wiley   +1 more source

Complement Evasion by S. aureus Surface Proteins [PDF]

open access: yes, 2015
The complement system, a major component of the innate immunity, is critical for combating microbial infections. It can be activated by three distinct pathways: the classical pathway, the lectin pathway and the alternative pathway.
Kang, Mingsong
core  

Recruitment of C4b-binding protein is not a complement evasion strategy employed by Staphylococcus aureus. [PDF]

open access: yesMicrobiology (Reading), 2023
Li S   +5 more
europepmc   +1 more source

Tumor‐Derived Alpha‐1 Antitrypsin Promotes Liver Metastasis of Colorectal Cancer Through the Neutrophil Extracellular Traps–CCDC25 Pathway

open access: yesAdvanced Science, EarlyView.
ABSTRACT Liver metastasis is a leading cause of mortality in colorectal cancer (CRC), where the inflammatory tumor microenvironment, specifically neutrophil infiltration, significantly promotes metastatic colonization. This study reveals a pro‐metastatic role for alpha‐1 antitrypsin (A1AT) in CRC liver metastasis via a dual mechanism involving ...
Qian Fei   +11 more
wiley   +1 more source

Tumor‐Derived LAMB3 Drives Immunosuppressive LRRC15+ Fibroblast Formation During Pancreatic Ductal Adenocarcinoma Development

open access: yesAdvanced Science, EarlyView.
A single‐cell atlas of pancreatic ductal adenocarcinoma development reveals progressive ductal‐fibroblast‐immune crosstalk. Tumor‐derived LAMB3 drives the formation of immunosuppressive LRRC15+ fibroblasts through the ITGB1/FAK/MAPK/FOSL2 signaling. Glycolytic reprogramming upregulates LAMB3 and correlates with LRRC15+ fibroblast enrichment.
Xuqing Shi   +23 more
wiley   +1 more source

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