Results 101 to 110 of about 15,125 (218)

Ir(III) Complexes Convert Cold to Hot Tumors via Ferroptosis/Necroptosis‐Driven Immunogenic Cell Death and Photosensitized CD47 Downregulation

Advanced Science, Volume 13, Issue 8, 9 February 2026.
Red‐light‐activated Ir1 overcomes hypoxia tolerance and adapts to the immunosuppressive tumor microenvironment, converting immunologically cold tumors into inflamed hot microenvironments. This conversion is driven by synergistic induction of immunogenic cell death through coordinated ferroptosis‐necroptosis pathways and spatiotemporally controlled ...
Long‐Bo Yu, Peng Wang, Qing‐Hua Shen, Qi‐Xin Guan, Zhi‐Yuan Li, Ying‐Ying Han, Xin‐Yi Zhang, Qing‐Yuan Hu, Cai‐Ping Tan   +8 more
wiley   +1 more source

MLKL ubiquitylation: more than a makeover [PDF]

Cell Death & Differentiation, 2022
Weihong Wang, Yi-Nan Gong
openaire   +2 more sources

MLKL is a potential prognostic marker in gastric cancer

Oncology Letters, 2019
The mixed lineage kinase domain-like protein (MLKL), which is a major mediator of the necroptosis pathway, is involved in a certain cancers. The present study aimed to explore the expression patterns and exact role of MLKL in gastric cancer (GC) tumorigenesis and progression. In Cancer Cell Line Encyclopedia analysis, the MLKL mRNA expression levels in
Wei, Sun, Wenyan, Yu, Lili, Shen, Tieao, Huang   +3 more
openaire   +3 more sources

NLK facilitates Caspase‐8 activation to drive macrophage PANoptosis in sepsis

Clinical and Translational Medicine, Volume 16, Issue 2, February 2026.
By promoting Caspase‐8 activation within the PANoptosome, NLK modulates pyroptotic, apoptotic, and necroptotic programs in macrophages, thereby driving inflammatory injury and multiorgan damage during sepsis. Abstract Mounting evidence indicates that macrophage PANoptosis—an integrated inflammatory cell‐death program comprising pyroptosis, apoptosis ...
Yun Xia, Ren‐qi Yao, Hui‐fan Liu, Guo‐qing Jing, Delida Aidebaike, Jing Zuo, Shi‐qi Wan, Die Wu, Peng‐yue Zhao, Hai‐long Gong, Xing Wang, Hui‐min Zhou, Ning Dong, Yao Wu, Shi Liu, Xiao‐jing Wu, Yong‐ming Yao, Xue‐min Song   +17 more
wiley   +1 more source

MLKL limits inflammatory responses through negatively regulating Toll-like receptor signaling pathway [PDF]

, 2015
炎症是机体清除有害刺激时做出的保护性反应，同时也是修复受损组织的一个过程。先天性免疫对微生物感染、组织损伤等造成的炎症起到了重要作用。但是，先天性免疫信号必须经过严格的调控，才能避免过于强烈的炎症反应对机体造成的不必要的伤害。Toll样受体在宿主识别病原体的入侵、激活炎症反应的过程中发挥了关键作用，因此，关于Toll样受体信号通路的负调控的研究显得尤为重要。本论文的研究发现，混合系蛋白激酶样结构域蛋白（mixedlineagekinasedomain-likeprotein，MLKL ...
庄秋宇
core  

Is Ferroptosis the Mechanistic Bridge Connecting Iron Dysregulation to Muscle Wasting and Functional Decline in Aging?

Aging Cell, Volume 25, Issue 2, February 2026.
This work proposes ferroptosis as a mechanistic driver of age‐related muscle dysfunction, whereby iron dyshomeostasis and impaired antioxidant capacity promote lipid peroxidation, and eventually trigger ferroptosis, leading to muscle wasting, and ultimately contributing to weakness and functional decline with aging.
Rola S. Zeidan, Simon Reinhard, Anna Picca, Emanuele Marzetti, Christiaan Leeuwenburgh, James F. Collins, Stephen D. Anton   +6 more
wiley   +1 more source

Molecular 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 more
core   +25 more sources

Liquid–Liquid Phase Separation in Major Hallmarks of Cancer

Cell Proliferation, Volume 59, Issue 2, February 2026.
Aberrant condensates formed through phase separation are involved in the dysregulation of various critical cellular processes, including genome stability, transcriptional regulation and signal transduction, thereby promoting malignant transformation and the acquisition of multiple cancer hallmarks.
Chen‐chen Xie, Ting Wang, Xin‐ran Liu, Yan Wang, Qin Dang, Tian Ding, Jia‐qi Xu, Xian‐jun Yu, Hai Lin, Xiao‐wu Xu, Yi Qin   +10 more
wiley   +1 more source

Inactivation of necroptosis-promoting protein MLKL creates a therapeutic vulnerability in colorectal cancer cells

Cell Death and Disease
Mortality from colorectal cancer (CRC) is significant, and novel CRC therapies are needed. A pseudokinase MLKL typically executes necroptotic cell death, and MLKL inactivation protects cells from such death.
Peijia Jiang, Sandhya Chipurupalli, Byong Hoon Yoo, Xiaoyang Liu, Kirill V. Rosen   +4 more
doaj   +1 more source

RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome [PDF]

, 2017
韩家淮教授课题组的这项研究揭示了活性氧簇（ROS）通过直接特异地氧化受体相互作用丝氨酸/苏氨酸激酶1（RIP1）上的三个关键的半胱氨酸，进而特异地增强RIP1在S161上的自磷酸化，从而促进坏死小体的形成和程序性细胞坏死的发生。证实了RIP1的激酶活性在程序性细胞坏死中的主要功能是自磷酸化S161，且S161就是人们长期寻找的RIP1上与坏死相关的功能性磷酸化位点。坏死小体的形成是程序性细胞坏死发生的必要复合物，而S161的磷酸化是RIP1有效募集RIP3形成有功能的坏死小体所必需的 ...
Chuan-Qi Zhong, Deli Huang, Jiahuai Han, Qixu Cai, Rui Wu, Sheng Sean Su, Shubo Zhao, Xin Chen, Yingying Zhang, Zhang-Hua Yang, Zhentao Yang, 张荧荧, 苏晟, 韩家淮   +13 more
core   +1 more source