Results 91 to 100 of about 18,020 (210)
Targeting RIPK1 for the treatment of human diseases [PDF]
Proceedings of the National Academy of Sciences, 2019 Significance RIPK1 plays a critical role in mediating deleterious responses downstream of TNFR1. RIPK1 inhibitors have been progressed successfully past human phase I clinical studies. This paper discusses why RIPK1 inhibitors present an opportunity for developing oral drugs for a range of human degenerative and inflammatory diseases ...Alexei Degterev, Dimitry Ofengeim, Junying Yuan +2 moreopenaire +2 more sourcesA Combined Colon Organoid‐Sensory Neuron Model Reveals Epithelial Contribution to Moringin Efficacy Against Painful Inflammatory Bowel Disease
Phytotherapy Research, EarlyView.Experimental workflow and main findings of the study. ABSTRACT
Visceral pain is a major symptom of inflammatory bowel diseases (IBDs), requiring effective treatment strategies. Gut epithelium, beyond maintaining barrier integrity and microbiota homeostasis, modulates neurosensorial circuitries, influencing visceral sensitivity.Francesco Margiotta, Elena Lucarini, Alessandra Toti, Maria Giovanna Cataldi, Clara Ciampi, Gina Rosalinda De Nicola, Lorenzo Di Cesare Mannelli, Carla Ghelardini +7 morewiley +1 more sourceDeciphering diverse cell‐death patterns to predict the prognosis and potential therapy target of hepatocellular carcinoma patients
VIEW, EarlyView.Abstract
Ninety percent of all primary liver malignancies are hepatocellular carcinomas (HCC), making liver cancer the third most common cause of cancer‐associated mortality. Different patterns of programmed cell death (PCD) are crucial for the survival of tumors, and they might serve as a prognostic marker for HCC.Lin Ding, Qian Li, Wenjing Yang, Te Liu, Tongtong Tian, Yu Liu, Chunyan Zhang, Baishen Pan, Beili Wang, Fan Wu, Wei Guo +10 morewiley +1 more sourceRIPK1 protects hepatocytes from death in Fas-induced hepatitis
Scientific Reports, 2017 Hepatocyte death is a central event during liver disease progression, in which immune cells play key roles by activating members of the Tumor Necrosis Factor Receptor Superfamily (TNFRSF), including TNFR1 (TNFRSF1A), Fas (TNFRSF6) and TRAIL-R2 (TNFRSF10B)Aveline Filliol, Muhammad Farooq, Claire Piquet-Pellorce, Valentine Genet, Marie-Thérèse Dimanche-Boitrel, Peter Vandenabeele, Mathieu J. M. Bertrand, Michel Samson, Jacques Le Seyec +8 moredoaj +1 more sourceTRADD Mediates RIPK1-Independent Necroptosis Induced by Tumor Necrosis Factor
Frontiers in Cell and Developmental Biology, 2020 As a programmed necrotic cell death, necroptosis has the intrinsic initiators, including receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3 and mixed-lineage kinase domain-like protein (MLKL), which combine to form necroptotic ...Lili Wang, Xixi Chang, Jinli Feng, Jiyun Yu, Jiyun Yu, Guozhu Chen +5 moredoaj +1 more sourcePUMA amplifies necroptosis signaling by activating cytosolic DNA sensors. [PDF]
, 2018 Necroptosis, a form of regulated necrotic cell death, is governed by RIP1/RIP3-mediated activation of MLKL. However, the signaling process leading to necroptotic death remains to be elucidated.Chen, Dongshi, Stolz, Donna B., Tong, Jingshan, Wei, Liang, Yang, Liheng, Yu, Jian, Zhang, Jianke, Zhang, Lin +7 morecore +2 more sourcesDecreased RIPK1 expression in chondrocytes alleviates osteoarthritis via the TRIF/MyD88-RIPK1-TRAF2 negative feedback loop
Aging, 2019 Osteoarthritis (OA) is the most common degenerative joint disease and involves the loss of articular cartilage integrity, formation of articular osteophytes, remodeling of subchondral bone, and synovitis. Knockdown of receptor interacting serine/threonine kinase (RIPK) 1 leads to anti-inflammatory and anti-apoptotic effects. However, the involvement of Liang, Shuang, Wang, Zheng-Gang, Zhang, Zhen-Zhen, Chen, Kun, Lv, Zheng-Tao, Wang, Yu-Ting, Cheng, Peng, Sun, Kai, Yang, Qing, Chen, An-Min +9 moreopenaire +2 more sourcesAllergic Sensitization to Inhalant Allergens in the Upper Respiratory Tract—the B Cell Side
Allergy, EarlyView.ABSTRACT
Allergic diseases are on the rise worldwide, driven by respiratory epithelial barrier dysfunction that promotes sensitization to inhalant allergens such as pollen, dust mites, pet dander, and fungal spores. These antigens trigger IgE‐mediated immune responses that lead to diseases such as allergic rhinitis (AR) and asthma.Ola Grimsholm, Mohammed Zghaebi, Bita Hambrecht, Tanja Kalic, Christopher C. Udoye, Rudolf Manz, Barbara Bohle, Katarzyna M. Sitnik, Julia Eckl‐Dorna, Heimo Breiteneder +9 morewiley +1 more sourceMolecular mechanisms of cell death:recommendations of the Nomenclature Committee on Cell Death 2018 [PDF]
, 2018 Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.Aaronson, Stuart A., Abrams, John M., Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V., Arama, Eli, Baehrecke, Eric H., Barlev, Nickolai A., Bazan, Nicolas G., Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Katiuscia, Blagosklonny, Mikhail V., Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K. -M., Chandel, Navdeep S., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Cohen, Gerald M., Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D'Angiolella, Vincenzo, Dawson, Ted M., Dawson, Valina L., De laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M., Dixon, Scott J., Duckett, Colin S., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Fimia, Gian Maria, Fulda, Simone, Galluzzi, Lorenzo, Garcia-Saez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. Marie, Harris, Isaac S., Heiden, Matthew G. Vander, Hengartner, Michael O., Hetz, Claudio, Ichijo, Hidenori, Jaattela, Marja, Joseph, Bertrand, Jost, Philipp J., Juin, Philippe P., Kaiser, William J., Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Knight, Richard A., Kroemer, Guido, Kumar, Sharad, Lee, Sam W., Lemasters, John J., Levine, Beth, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., Lopez-Otin, Carlos, Lowe, Scott W., Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Molkentin, Jeffery D., Moll, Ute M., Munoz-Pinedo, Cristina, Nagata, Shigekazu, Nunez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Piacentini, Mauro, Pinton, Paolo, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rehm, Markus, Rizzuto, Rosario, Rodrigues, Cecilia M. P., Rubinsztein, David C., Rudel, Thomas, Ryan, Kevin M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, Brent R., Strasser, Andreas, Szabadkai, Gyorgy, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Boris, Vanden Berghe, Tom, Vandenabeele, Peter, Villunger, Andreas, Virgin, Herbert W., Vitale, Ilio, Vousden, Karen H., Vucic, Domagoj, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, James A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Boris, Zitvogel, Laurence +168 morecore +25 more sourcesRole of RIPK1/RIPK3/MLKL signalling pathway in sepsis‐associated acute kidney injury
Experimental Physiology, EarlyView.Abstract
Sepsis‐associated acute kidney injury (SA‐AKI) is a common clinical syndrome in critically ill patients, and its high mortality rate is closely related to complex pathological mechanisms. Existing studies have shown that the pathophysiological process of SA‐AKI involves complex multi‐mechanism interactions, including an uncontrolled systemic ...Huijun Yin, Jingyi Wang, Huirong Hanwiley +1 more source