STAT3 (Phospho_Ser727) Antibody
- Known as:
- STAT3 (Phospho_Ser727) Antibody
- Catalog number:
- E011046-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT3 (Phospho_Ser727) Antibody
Related genes to: STAT3 (Phospho_Ser727) Antibody
- Gene:
- STAT3 NIH gene
- Name:
- signal transducer and activator of transcription 3
- Previous symbol:
- -
- Synonyms:
- APRF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT3 (Phospho_Ser727) Antibody
Related articles to: STAT3 (Phospho_Ser727) Antibody
- Pre-metastatic niches composed of mainly myeloid cells are recognized as critical for tumor metastasis. However, whether adaptive immune cells also play an important role in pre-metastatic niche formation remains to be explored. - Source: PubMed
Publication date: 2026/08/14
Kujawski MaciejMartincuks AntonsSong MihaeZhang ChunyanHuang RuiWang TianyiSenguttuvan RosemaryNakamura BradPalmer MichaelBacon Eliza RIhle KenaForman Stephen JShively John ERodriguez-Rodriguez LornaPriceman Saul JYu Hua - C-C motif chemokine ligand 2 (CCL2) contributes to post-traumatic neuroinflammation and blood-brain barrier (BBB) disruption, but its role in post-traumatic external cerebral herniation and endothelial JAK-STAT signaling remains unclear. - Source: PubMed
Publication date: 2026/08/14
Chen QizuanXia JinbiaoZhang ShangmingPei JiashengLi ZiqiLiu ZhengWei LiangfengWang Shousen - Sepsis-associated encephalopathy (SAE) is a multifactorial medical condition characterized by pronounced neuroinflammation and linked to increased mortality risk and long-term cognitive impairment. Microglial pyroptosis has emerged as a crucial pathogenic mechanism in SAE. CD300f, an immune receptor expressed in microglia, regulates inflammatory processes and neuronal survival, exerting a protective effect against brain injury. However, its specific role in SAE remains unexplored. Bioinformatic analyses revealed upregulated CD300f expression in the hippocampus of SAE mice as well as in the peripheral blood of septic patients. Western blot and qPCR further confirmed increased hippocampal CD300f expression in SAE mice subjected to cecal ligation and puncture (CLP). Knockdown of CD300f promoted Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) phosphorylation, exacerbated microglial pyroptosis, aggravated neuronal damage, and worsened cognitive dysfunction in SAE mice. Conversely, CD300f overexpression attenuated lipopolysaccharide (LPS)- and adenosine triphosphate (ATP)- induced JAK2/STAT3 phosphorylation, suppressed microglial pyroptosis and proinflammatory cytokine release in vitro. Collectively, these loss- and gain-of-function data indicate that the upregulation of CD300f during sepsis represents a compensatory protective response aimed at counteracting hyperactive JAK2/STAT3 signaling and limiting pyroptotic damage. Pharmacological inhibition of STAT3 with Stattic or JAK2 with AG490 similarly inhibited STAT3 phosphorylation and attenuated microglial pyroptosis in vitro. In summary, we demonstrate that CD300f negatively regulates JAK2/STAT3 phosphorylation, attenuates microglial pyroptosis, and alleviates cognitive dysfunction in SAE mice. These findings highlight an association between CD300f and neuroprotection in SAE and suggest its potential as a therapeutic target, warranting further investigation through in vivo gain-of-function studies. - Source: PubMed
Publication date: 2026/08/14
Chen XueSun YeJiang SainanCheng JianiLi HaoyiYin ShengmingXiao Zhaoyang - Cerebral ischemia-reperfusion (I/R) injury triggers a complex cycle of biochemical disturbances that accelerate neuronal death and functional deterioration. Among the various regulated cell death pathways involved, ferroptosis has recently emerged as a central mechanism linking iron imbalance, lipid peroxidation, and oxidative damage. Excessive generation of reactive oxygen species (ROS) during reperfusion overwhelms endogenous antioxidant defenses, disrupts mitochondrial function, and enhances lipid peroxidation, thereby initiating ferroptotic signaling. Iron overload-driven by increased transferrin receptor expression, ferritinophagy, and Fenton chemistry-further amplifies lipid peroxide accumulation and GPX4 inactivation, establishing a self-propagating cycle of oxidative injury. Several key signaling pathways modulate this interplay between oxidative stress and ferroptosis. Activation of Nrf2 promotes the transcription of antioxidant and iron-regulatory genes, offering substantial protection against ferroptotic damage. In contrast, HIF-1α exerts a dual role; although it supports metabolic adaptation and angiogenesis under hypoxia, its prolonged activation may promote lipid peroxidation and ferroptotic vulnerability. Casein kinase 2 (CK2) also contributes to the redox landscape by regulating the activity of NADPH oxidase, STAT3/SOD2, and HIF-1α, leading to context-dependent protective or detrimental outcomes. This review examines the molecular crosstalk between oxidative stress and ferroptosis in ischemia-reperfusion injury and summarizes key pharmacological and natural agents that target these pathways to achieve neuroprotection. In response to recent translational concerns, the review further emphasizes cell-type-specific ferroptotic vulnerability, GPX4-independent defense systems, blood-brain barrier and pharmacokinetic barriers, clinical readiness, safety limitations, and unresolved controversies that must be addressed before ferroptosis-targeted interventions can be advanced for stroke therapy. - Source: PubMed
Publication date: 2026/08/14
Akhtar WasimKhan Mohd MuazzamKumar SanjayTarique MohammedRaza Mohd KhalidMaurya SaritaAhmad Usama - Advances in genetic analysis techniques and strategies have enabled the identification of rare novel genetic entities in children's interstitial lung disease (chILD). - Source: PubMed
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