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From Immune Storm to Nerve Damage: Decoding the "Source of Multiple Diseases" Role of JAK Kinase
From Immune Storm to Nerve Damage: Decoding the "Source of Multiple Diseases" Role of JAK KinaseJAKs are a class of non receptor tyrosine kinases, including four members: JAK1, JAK2, JAK3, and TYK2. They participate in regulating various biological processes such as hematopoiesis, immune response, inflammation, and cell survival through interactions with cytokine receptors. In recent years, the role of JAKs in the occurrence and development of various diseases has gradually been revealed. In addition to malignant tumors, abnormal activation of the JAK signaling pathway is a key driving factor in inflammatory autoimmune diseases (such as rheumatoid arthritis, psoriasis), aller......
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JAK Family Decoding: Key Hubs and Potential Targets in Tumors
JAK Family Decoding: Key Hubs and Potential Targets in Tumors1. Introduction of the JAK FamilyJanus kinase (JAK) is an intracellular non-receptor tyrosine kinase that transduces cytokine-mediated signals through the JAK-signal transducer and activator of Transcription (JAK-STAT) pathway. The name "Janus" is derived from the Roman god Janus, who has two faces, because JAK has two similar phosphate transfer domains, one of which shows kinase enzyme activity, while the other motif negatively regulates the kinase activity of the former in the feedback loop.1.1 Structure of the JAK FamilyThe JAK family consists of four members: JAK1, JAK2, JAK3 and tyrosine kinase 2 (TYK2). And th......
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STAT family proteins: The "commander" of cell fate and the key driver of disease development
STAT family proteins: The "commander" of cell fate and the key driver of disease development1. 1. Introduction of the STAT FamilySignal transducer and activator of transcription (STAT) proteins are the key intracellular protein family that act as both cytoplasmic signal transducer and nuclear transcription factor. When signaling molecules such as cytokines, growth factors, or hormones bind to cell surface receptors, STATs are activated. Activated STATs form dimers, which are transported into the cell nucleus and directly bind to specific DNA sequences to regulate the expression of target genes, thereby mediating a variety of important cellular processes such as cell prolifera......
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Ferroptosis: A Rising Star in Cancer Treatment,Unveiling How Iron-Dependent Cell Death Mechanisms Are Becoming New Targets for Cancer Therapy
Ferroptosis, an iron-dependent form of lipid peroxidation that causes cell death, has come to the fore in cancer research in recent years. This cell death mode is different from traditional apoptosis, autophagy and other mechanisms, and its core lies in the accumulation of iron ions and reactive oxygen species in the cell, leading to lipid peroxidation of the cell membrane, and finally destroying the cell structure and causing cell death. Cancer cells are often more susceptible to ferroptosis due to their rapid proliferation and high demand for iron. Studies have shown that tumor cells have an "iron addiction", that is, their uptake and utilization of iron ions is much higher......
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Cuproptosis: New therapeutic targets for cardiovascular disease - from molecular mechanisms to clinical interventions
Copper (Cu) is a catalytic cofactor for various physiological processes such as energy metabolism, mitochondrial respiration, and antioxidation. Generally, the intracellular Cu concentration is relatively low. When Cu levels accumulate within cells, excessive Cu ions bind to mitochondrial proteins, leading to protein toxicity stress-mediated cell death. In cardiovascular diseases (CVD), cuproptosis can interfere with lipid metabolism and cause oxidative stress, mitochondrial damage, and endothelial cell dysfunction.Recent evidence suggests that cuproptosis plays a significant role in the occurrence and development of many CVD, such as myocardial ischemia/reperfusion (I/R) injury, heart......
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Cuproptosis: Mechanism Breakthrough and Clinical Dawn of a New Target for Cancer Treatment
In 2022, Tsvetkov and colleagues proposed a different form of regulated copper (Cu)-induced cell death and the term " cuproptosis". Cuproptosis is a form of cell death triggered by the accumulation of copper in mitochondria, which drives the aggregation of acylated dihydrolipoamide S-acetyltransferase (DLAT), which is associated with the mitochondrial tricarboxylic acid (TCA) cycle, leading to protein toxic stress and ultimately cell death.An increasing number of studies have shown that the copper levels in tumor tissues and serum of cancer patients are significantly higher than those of healthy people. Elevated copper levels exist in various cancers and are related to the et......