Results 191 to 200 of about 125,259 (249)

Discovery and Optimization of AMT‐676, a CDH17‐Targeting ADC for the Treatment of Advanced Gastrointestinal Cancers

Advanced Science, EarlyView.
AMT‐676 is a novel antibody‐drug conjugate targeting CDH17, an adhesion molecule uniquely exposed on gastrointestinal tumor surfaces. Engineered with an optimized exatecan payload, it demonstrates profound tumor regression and a robust bystander effect across diverse preclinical models.
Ying‐nan Wang, Dan‐yun Ruan, Jing Shi, Yue Huang, Hui Sheng, Ya‐ling Huang, Linjie Ma, Lijun Wang, Caiwei Chen, Yixuan Wang, Yue Zhang, Yi Shen, Qing Zhang, Jianjian Zhang, Yanfang Tang, Jin‐ling Zhang, Jia‐jia Hu, Chen‐yi Wu, Jia‐ying Chen, Xun Meng, Shu‐Hui Liu, Feng Wang   +21 more
wiley   +1 more source

Epigenetic Reactivation of TNFRSF19 Suppresses Mitophagy and Sensitizes Triple‐Negative Breast Cancer to Doxorubicin

Advanced Science, EarlyView.
TNFRSF19 is an epigenetically silenced regulator of mitophagy in triple‐negative breast cancer. TNFRSF19 deficiency activates the TGFBR1–SMAD3–PINK1 axis to promote mitophagy and confer doxorubicin resistance, whereas decitabine‐mediated restoration of TNFRSF19 suppresses mitophagy and enhances doxorubicin sensitivity, revealing a targetable epigenetic–
Shiyang Liu, Chenguang Liu, Weihong Zheng, Xiaofei Tong, Zhengwei Gui, Zonghong Lu, Sun Ieong, Lin Zhang   +7 more
wiley   +1 more source

Interleukin‐1α Mediates Pancreatic Fibroblast Activation, Regulates Immune Cell Recruitment and Fibrosis in Acute and Chronic Pancreatitis

Advanced Science, EarlyView.
During pancreatitis, IL‐1α is released from necrotic acinar cells. In response to IL‐1α, pancreatic fibroblasts release chemokines and cytokines that regulate the recruitment of immune cells to the damaged organ. Furthermore, IL‐1α primes fibroblasts, resulting in increased tissue fibrosis during chronic pancreatitis.
Hala Mazloum, Shenja Buchholz, Hanna Schifter, Sabine Ameling, Leif Steil, Ben Lewin Becker, Elke Hammer, Georg Homuth, Uwe Völker, Barbara M. Bröker, Lukas Zierke, Frank Ulrich Weiss, Juliane Glaubitz, Matthias Sendler   +13 more
wiley   +1 more source

Leveraging Microphysiological Systems to Facilitate Neutrophil‐Based Cancer Immunotherapy

Advanced Science, EarlyView.
Microphysiological systems are emerging as powerful human‐relevant platforms for studying neutrophil biology in cancer. Current applications of spheroids, organoids, and organ‐on‐a‐chip models are reviewed, together with future opportunities in behaviorome profiling, multi‐omics integration, personalized medicine, immune crosstalk, and multi‐organ ...
Shuai Shao, Markus Isfeld Diehl, Caroline N. Jones   +2 more
wiley   +1 more source

Mitochondria‐Targeted Multimodal Nanotherapeutics Suppress Oxidized mtDNA‐Driven Inflammation at the Source

Advanced Science, EarlyView.
Ox‐mtDNA fragments escaping from mitochondria drive robust inflammatory responses. A targeted nanoplatform simultaneously inhibits mitochondrial FEN1‐mediated mtDNA cleavage and scavenges ROS, preventing the generation of immunogenic Ox‐mtDNA fragments. The released SeNPs further promote autophagic clearance of cytosolic mtDNA. Consequently, cGAS‐STING,
Wen‐Ling Li, Juan Cao, Yu‐Lin Wang, Yu‐Han Fan, Jia‐Qi Xu, Xian Wu Cheng, Lei Xing, Hu‐Lin Jiang   +7 more
wiley   +1 more source

Ultrasound‐Activated Nanoinhibitors Blocking the Chemo‐Immune Checkpoint to Overcome Chemotherapy‐Induced Immune Resistance

Advanced Science, EarlyView.
A sono‐responsive chemo‐immune checkpoint nanoinhibitor (Sono‐TT8) co‐delivering TPZ chemotherapy and siXkr8 simultaneously kills tumor cells and blocks PS externalization, reversing chemotherapy‐induced immunosuppression and enhancing antitumor immunity. ABSTRACT Breast cancer features an immunosuppressive tumor microenvironment following chemotherapy
Yunfan Liu, Chier Du, Leilei Zhu, Hongjin An, Shengzhe Hou, Yi Lan, Xuemei Tang, Min Xu, Peng Luo, Hua Teng, Hao Yang, Xun Guo, Jianli Ren, Zhiyi Zhou   +13 more
wiley   +1 more source

Glucocorticoid Receptor Signaling in Myeloid Cells Orchestrates Inflammation Resolution and Muscle Repair

Advanced Science, EarlyView.
Glucocorticoids (GC) are widely used to reduce inflammation. We show that the glucocorticoid receptor in myeloid cells regulates macrophage cell cycle and genome integrity during muscle regeneration. We demonstrate that dexamethasone administration during the early inflammatory phase delays muscle repair by increasing macrophage proliferation ...
Sirine Souali‐Crespo, Joe G. Rizk, Emilia Calvano, Rajesh Sahu, Emina Colovic, Imane Chabba, Valentine Gilbart, Erwan Grandgirard, Bastien Morlet, Qingshuang Cai, Daniel Metzger, Delphine Duteil   +11 more
wiley   +1 more source

Identification of a new caspase homologue: caspase-14 [PDF]

Cell Death and Differentiation, 1998
Caspases are cysteinyl aspartate-specific proteinases, many of which play a central role in apoptosis. Here, we report the identification of a new murine caspase homologue, viz. caspase-14. It is most related to human/murine caspase-2 and human caspase-9, possesses all the typical amino acid residues of the caspases involved in catalysis, including the
Peter Vandenabeele, Van Loo Geert, W Declercq   +2 more
exaly   +3 more sources

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Caspases and caspase inhibitors

Trends in Biochemical Sciences, 1997
Five years ago, little was known about mechanisms of apoptotic execution. Now, one class of cell-death gene, the cysteine and aspartases (caspases) has come under intensive study. This review discusses the two classes of caspases, the reasons why humans may have so many caspase genes, the growing list of caspase substrates, and viral and ...
P, Villa, S H, Kaufmann, W C, Earnshaw
openaire   +2 more sources

Caspases

Current Protocols in Protein Science, 2001
AbstractCaspases are a family of cysteine proteases with a strict specificity for aspartate residues involved in inflammatory process and programmed cell death. This overview unit provides basic information on their structure, enzymatic activity, substrate specificity, activation,inhibition and their implication in pathologies.
Jean-Bernard, Denault, Guy S, Salvesen
openaire   +2 more sources