Results 111 to 120 of about 120,191 (200)

Accessing Polyphenols Effect on Bond Strength and Dentin Enzymatic Degradation

open access: yesClinical and Experimental Dental Research, Volume 12, Issue 5, October 2026.
ABSTRACT Introduction Polyphenols have been investigated in dental materials and restorative techniques due to their interactions with metal cations, antioxidant activity, and collagen crosslinking ability, which make them a promise for reinforcing the dental substrate and improving material adhesion.
Ana Catarina Rios Castro Alves   +7 more
wiley   +1 more source

Inhibition of cruzain and cathepsins by nitrile-based cysteine protease inhibitors.

open access: yes, 2017
Inhibition of cruzain and cathepsins by nitrile-based cysteine protease inhibitors.
Andrei Leitão (769676)   +10 more
core   +1 more source

Cathepsin L in cancer: Context‐dependent functions, microenvironmental regulation and translational opportunities

open access: yesClinical and Translational Discovery, Volume 6, Issue 5, October 2026.
Cathepsin L (CTSL) acts as a context‐dependent facilitator of tumour progression rather than a universal oncogenic driver. CTSL's pro‐tumorigenic functions are critically evaluated alongside its inherent biochemical constraints and family‐wide redundancy. CTSL‐related biology may provide translational opportunities in selected contexts.
Yujun Wu   +7 more
wiley   +1 more source

Lysosomal cysteine proteinases as mediators of inflammation and tumor spread [PDF]

open access: yes, 1992
Assfalg-Machleidt, Irmgard   +4 more
core   +1 more source

E3 Ubiquitin Ligase NEDD4‐Mediated CTSB Ubiquitination Prevents Microglial Ferroptosis After Subarachnoid Hemorrhage

open access: yesJournal of Biochemical and Molecular Toxicology, Volume 40, Issue 10, October 2026.
NEDD4 attenuates secondary brain injury after SAH by ubiquitinating and degrading CTSB, thereby inhibiting microglial ferroptosis. ABSTRACT To investigate the role of cathepsin B (CTSB) in microglial ferroptosis after subarachnoid hemorrhage (SAH) and its upstream regulatory mechanisms.
Xiuyou Yan   +6 more
wiley   +1 more source

The Interplay of M1 Macrophages and Dental Pulp Stem Cells Promotes Angiogenesis Through IL‐8‐Dependent VEGF Regulation: An In Vitro Study

open access: yesInternational Endodontic Journal, Volume 59, Issue 10, Page 2143-2163, October 2026.
ABSTRACT Background Dental pulp inflammation triggers immune responses involving macrophages and dental pulp stem cells (DPSCs), which interact to regulate angiogenesis essential for tissue repair. M1 pro‐inflammatory macrophages predominate early in pulpitis, and clarifying their angiogenic role is vital in identifying inflammatory regenerative ...
Dineshi Sewvandi Thalakiriyawa   +5 more
wiley   +1 more source

LLOMe does not release cysteine cathepsins to the cytosol but inactivates them in transiently permeabilized lysosomes

open access: yes, 2017
L-leucyl-L-leucine methyl ester (LLOMe) induces apoptosis, which is thought to be mediated by release of lysosomal cysteine cathepsins from permeabilized lysosomes into the cytosol.
Cinzia Progida   +7 more
core   +1 more source

Discovery of Post‐Translationally Modified Epitopes in Autoimmunity: Someone Has to Fish so Everyone Can Eat

open access: yesImmunological Reviews, Volume 343, Issue 1, October 2026.
ABSTRACT Post‐translational modifications (PTMs) chemically diversify the ~20,000 genomically encoded proteins into millions of functional variants, and this diversity has profound consequences for T cell‐mediated immune responses. PTM‐reactive T cells have been identified across numerous autoimmune diseases and, in several cases, implicated directly ...
Sanya Arshad   +2 more
wiley   +1 more source

ASXL1 in proinflammatory macrophages attenuates inflammatory activation and macrophage‐mediated renal tubular epithelial cell damage in acute kidney injury

open access: yesPhysiological Reports, Volume 14, Issue 19, October 2026.
ASXL1 in inflammatory macrophages attenuates renal tubular cell damage through coordinated histone modification of H3K27me3 and H3K4me3 in acute kidney injury. Abstract Macrophages are major contributors to inflammatory responses in acute kidney injury (AKI) and rapidly alter their gene expression through epigenetic regulation.
Yoshiyasu Ogura   +3 more
wiley   +1 more source

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