Results 81 to 90 of about 22,445 (222)

Increased ERK signalling promotes inflammatory signalling in primary airway epithelial cells expressing Z α1-antitrypsin. [PDF]

open access: yes, 2013
Overexpression of Z α1-antitrypsin is known to induce polymer formation, prime the cells for endoplasmic reticulum stress and initiate nuclear factor kappa B (NF-κB) signalling. However, whether endogenous expression in primary bronchial epithelial cells
Adriana Ordóñez   +61 more
core   +1 more source

Proteolysis at the extracellular matrix interface: Molecular architects and regulators in health and disease

open access: yesThe FEBS Journal, EarlyView.
The extracellular matrix (ECM) is a dynamic scaffold that orchestrates tissue architecture and cellular communication. A critical but underexplored interplay between proteases and cluster of differentiation molecules (CD) governs ECM turnover and directs cell fate.
David Jurnečka   +3 more
wiley   +1 more source

ADAM17 cleaves CD16b (FcγRIIIb) in human neutrophils

open access: yesBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2013
CD16b (FcγRIIIb) is exclusively expressed by human neutrophils and binds IgG in immune complexes. Cell surface CD16b undergoes efficient ectodomain shedding upon neutrophil activation and apoptosis. Indeed, soluble CD16b is present at high levels in the plasma of healthy individuals, which appears to be maintained by the daily turnover of apoptotic ...
Wang, Yue   +5 more
openaire   +2 more sources

The metalloprotease ADM-4/ADAM17 promotes axonal repair

open access: yesScience Advances, 2022
Axonal fusion is an efficient means of repair following axonal transection, whereby the regenerating axon fuses with its own separated axonal fragment to restore neuronal function. Despite being described over 50 years ago, its molecular mechanisms remain poorly understood.
Xue Yan Ho   +4 more
openaire   +2 more sources

ADAM17 and its proteolytic targets in disease pathogenesis

open access: yesThe FEBS Journal, EarlyView.
ADAM17 as a multifunctional sheddase with contrasting roles across inflammatory, metabolic, cardiovascular, and neoplastic diseases. Through regulated activation by iRhom, iTAP/FRMD8, and tetraspanins, ADAM17 cleaves diverse membrane ligands and receptors, thereby promoting inflammation, fibrosis, obesity, insulin resistance, and tumor progression ...
Abdulbasit Amin, Marina Badenes
wiley   +1 more source

Upregulation of polycistronic microRNA-143 and microRNA-145 in colonocytes suppresses colitis and inflammation-associated colon cancer

open access: yesEpigenetics, 2021
Because ADAM17 promotes colonic tumorigenesis, we investigated potential miRNAs regulating ADAM17; and examined effects of diet and tumorigenesis on these miRNAs.
Urszula Dougherty   +24 more
doaj   +1 more source

ADAM17, shedding, TACE as therapeutic targets

open access: yesPharmacological Research, 2013
ADAM17 has been molecularly cloned as the enzyme responsible for cleavage of the transmembrane protein TNFα (TNFα converting enzyme, TACE). Later it was realized that ADAM17 was also responsible for the processing of cell adhesion proteins, cytokine and growth factor receptors and many ligands of the EGF receptor.
openaire   +2 more sources

ADAM17 as a Therapeutic Target in Multiple Diseases [PDF]

open access: yesCurrent Pharmaceutical Design, 2009
As a metalloproteinase specialized in releasing membrane-tethered proteins, A Disintegrin and A Metalloproteinase 17 (ADAM17), also known as Tumor necrosis factor-alpha Converting Enzyme (TACE) or less commonly CD156q, has received more than its share of attention.
Arribas, Joaquin, Esselens, Carl
openaire   +3 more sources

Biogenesis of TNF‐α‐insights into proteostasis and inflammation

open access: yesThe FEBS Journal, EarlyView.
TNF‐α biogenesis, trafficking, and signalling are tightly and reciprocally coupled to cellular proteostasis systems, including ER chaperones and endoplasmic reticulum‐associated degradation. This bidirectional crosstalk determines whether TNF‐α responses are adaptive or proteotoxic.
Bailasan Haidar   +3 more
wiley   +1 more source

P38 MAPK activated ADAM17 mediates ACE2 shedding and promotes cardiac remodeling and heart failure after myocardial infarction

open access: yesCell Communication and Signaling, 2023
Background Heart failure (HF) after myocardial infarction (MI) is a prevalent disease with a poor prognosis. Relieving pathological cardiac remodeling and preserving cardiac function is a critical link in the treatment of post-MI HF.
Qi Chen   +7 more
doaj   +1 more source

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