Results 101 to 110 of about 22,445 (222)

Lipid‐Facilitated Opening of the ADAM10 Sheddase Revealed by Enhanced Sampling Simulations

Advanced Science, Volume 13, Issue 19, 2 April 2026.
Phosphatidylserine acts as a lipid trigger to enhance activation of the sheddase ADAM10. By integrating fluorescence spectroscopy assays with enhanced sampling molecular dynamics simulations, this study shows that phosphatidylserine promotes ADAM10 catalytic activity along with expansion of its extracellular domains, enhancing accessibility to scaffold
Adrien Schahl, Nandan Haloi, Marta Carroni, Shengpan Zhang, Quentin James Sattentau, Erdinc Sezgin, Lucie Delemotte, Rebecca J. Howard   +7 more
wiley   +1 more source

ADAM17 selectively activates the IL‐6 trans‐signaling/ERK MAPK axis in KRAS‐addicted lung cancer

EMBO Molecular Medicine, 2019
Oncogenic KRAS mutations are major drivers of lung adenocarcinoma (LAC), yet the direct therapeutic targeting of KRAS has been problematic. Here, we reveal an obligate requirement by oncogenic KRAS for the ADAM17 protease in LAC.
Mohamed I Saad, Sultan Alhayyani, Louise McLeod, Liang Yu, Mohammad Alanazi, Virginie Deswaerte, Ke Tang, Thierry Jarde, Julian A Smith, Zdenka Prodanovic, Michelle D Tate, Jesse J Balic, D Neil Watkins, Jason E Cain, Steven Bozinovski, Elizabeth Algar, Tomohiro Kohmoto, Hiromichi Ebi, Walter Ferlin, Christoph Garbers, Saleela Ruwanpura, Irit Sagi, Stefan Rose‐John, Brendan J Jenkins   +23 more
doaj   +1 more source

The role of ADAM17 in the T-cell response against bacterial pathogens.

PLoS ONE, 2017
ADAM17 is a member of the A Disintegrin And Metalloproteinase family of proteases. It is ubiquitously expressed and causes the shedding of a broad spectrum of surface proteins such as adhesion molecules, cytokines and cytokine receptors.
Moritz Andreas Link, Karsten Lücke, Joanna Schmid, Valéa Schumacher, Thomas Eden, Stefan Rose-John, Hans-Willi Mittrücker   +6 more
doaj   +1 more source

Structural basis for inflammation-driven shedding of CD163 ectodomain and tumor necrosis factor-α in macrophages

, 2013
The haptoglobin-hemoglobin receptor CD163 and proTNF-α are transmembrane macrophage proteins subjected to cleavage by the inflammation-responsive protease ADAM17. This leads to release of soluble CD163 (sCD163) and bioactive TNF-α. Sequence comparison of
Chalaris, Athena, Etzerodt, Anders, Galea, Ian, Moestrup, Søren Kragh, Møller, Holger Jon, Rasmussen, Mie Rostved, Schwarz, Jeanette, Svendsen, Pia   +7 more
core   +1 more source

Protein Kinase C: Targets to Regenerate Brain Injuries? [PDF]

, 2019
Acute or chronic injury to the central nervous system (CNS), causes neuronal death and irreversible cognitive deficits or sensory-motor alteration. Despite the capacity of the adult CNS to generate new neurons from neural stem cells (NSC), neuronal ...
Alfonso, Anton, Arvidsson, Baldwin, Barker, Basu, Baxter, Benner, Black, Blennow, Blobel, Bogard, Braun, Buffo, Cabodi, Chen, Codega, Corbit, Dang, Dang, Deleers, Dempsey, Doetsch, Doetsch, Doetsch, Du, Einat, Fallon, Fatope, García-Bernal, Geraldes, Geribaldi-Doldan, Geribaldi-Doldan, Ghashghaei, Gonzalez-Perez, Gouveia, Grade, Guo, Hansra, Huang, Inagaki, Jin, Kandasamy, Kirby, Konopatskaya, Kraft, Kuhn, Kuhn, Lee, Lesyk, Lim, Liu, Liu, Liu, Lucke-Wold, Luzzati, Ma, Magavi, Malla, Mellor, Minami, Murillo-Carretero, Murphy, Márquez, Newton, Newton, Newton, Ou, Parent, Pascale, Puls, Reyland, Reynolds, Romero-Grimaldi, Rosse, Saha, Saito, Schmidt, Singh, Sledge, Steinhart, Sun, Sunnarborg, Susarla, Sweitzer, Szallasi, Tang, Torroglosa, Van Kolen, Wang, Wang, Wang, Wang, Watanabe, Zanin-Zhorov, Zhang   +95 more
core   +5 more sources

Macrophage Cluster of Differentiation 163 promotes post‐infarction cardiac repair and preserves left ventricular function via osteopontin

Clinical and Translational Medicine, Volume 16, Issue 4, April 2026.
• Circulating soluble CD163 is elevated in ischaemic cardiomyopathy and correlates with systolic dysfunction severity and ventricular dilation. • Macrophage CD163 protects against post‐infarction systolic dysfunction and left ventricular dilation in mice. • Loss of CD163 decreases macrophage osteopontin expression.
Jingyu Chen, Linjian Chen, Wei Huang, Gang Wang, Lin Wang, Wanchun Mei, Wei Ni, Yang Liu, Licheng Ding, Xiaofeng Ge, Zhaokai Li, Jing Yu, Shufen Huang, Jiayi Lin, Yifan Chen, Binni Cai, Peng Zhang, Cuilian Dai, Binbin Liu   +18 more
wiley   +1 more source

Progress of ADAM17 in Fibrosis‐Related Diseases

Mediators of Inflammation
Fibrosis leads to structural damage and functional decline and is characterized by an accumulation of fibrous connective tissue and a reduction in parenchymal cells. Because of its extremely poor prognosis, organ fibrosis poses a significant economic burden.
Suyan Yan, Yaqi Zhao, Yuyu Yang, Baocheng Liu, Wei Xu, Zhenzhen Ma, Qingrui Yang   +6 more
openaire   +3 more sources

ADAM10‐Mediated Proteolytic Remodelling of Signalling and Adhesion Proteins on Brain Cell‐Derived Small Extracellular Vesicles

Journal of Extracellular Biology, Volume 5, Issue 4, April 2026.
ABSTRACT Proteases are common components of extracellular vesicles (EVs), yet the extent and functional relevance of ongoing proteolytic activity on EV surfaces remain largely unexplored. Such activity could significantly influence EV function and identity, with likely implications for EV‐mediated signalling, recipient cell targeting, cargo delivery ...
Christopher C. Reimann, Hermann C. Altmeppen, Tomas Koudelka, Michaela Schweizer, Andreas Tholey, Behnam Mohammadi, Julia Bär, Lesley Cheng, Markus Glatzel, Marina Mikhaylova, Andrew F. Hill   +10 more
wiley   +1 more source

MicroRNA-145 Targets the Metalloprotease ADAM17 and Is Suppressed in Renal Cell Carcinoma Patients

Neoplasia: An International Journal for Oncology Research, 2013
A disintegrin and metalloproteinase 17 (ADAM17) is a metalloprotease that is overexpressed in many cancer types, including renal cancers. However, the regulatory mechanisms of ADAM17 in cancer development and progression are poorly understood.
Kai Doberstein, Nico Steinmeyer, Ann-Kathrin Hartmetz, Wolfgang Eberhardt, Michel Mittelbronn, Patrick N. Harter, Eva Juengel, Roman Blaheta, Josef Pfeilschifter, Paul Gutwein   +9 more
doaj   +1 more source

Soluble Sema4D From γδ T Cells Exerts Osteoblast Inhibition via Plexin‐B/mTOR Signalling Contributing to Pathogenesis of Bisphosphonate‐Related Osteonecrosis of the Jaws

Cell Proliferation, Volume 59, Issue 4, April 2026.
Schematic summarizing the pathway of sSema4D from γδ T cells inhibiting osteoblast differentiation in BRONJ. ABSTRACT Bisphosphonate‐related osteonecrosis of the jaw (BRONJ) is a severe complication in patients undergoing long‐term bisphosphonate therapy, while our knowledge on the pathogenesis of BRONJ is far from sufficient.
Lingling Ou, Shijia Qiao, Zhuoyi Liao, Xiner Tan, Hui Huang, Zhiyan Zhou, Ruhui Luo, Weijun Zeng, Yan Yang, Zhongxuan Zhang, Jingchen Chen, Shengli Wang, Yiqin Jiang, Jianlei Hao, Yuqin Shen, Longquan Shao   +15 more
wiley   +1 more source