Stat4 Monoclonal Antibody (clone 2A2)
- Known as:
- Stat4 Monoclonal Antibody (clonality 2A2)
- Catalog number:
- ASA905-825
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Stat4 Monoclonal Antibody (clone 2A2)
Related genes to: Stat4 Monoclonal Antibody (clone 2A2)
- Gene:
- FAM27B NIH gene
- Name:
- family with sequence similarity 27 member B
- Previous symbol:
- -
- Synonyms:
- bA12A20.3, FAM27A2
- Chromosome:
- 9q21.11
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2005-04-01
- Date modifiied:
- 2016-09-30
- Gene:
- FAM92A1P1 NIH gene
- Name:
- family with sequence similarity 92 member A1 pseudogene 1
- Previous symbol:
- FAM92A2
- Synonyms:
- -
- Chromosome:
- 15q15.1
- Locus Type:
- pseudogene
- Date approved:
- 2005-09-22
- Date modifiied:
- 2016-09-30
- Gene:
- FNDC1 NIH gene
- Name:
- fibronectin type III domain containing 1
- Previous symbol:
- FNDC2
- Synonyms:
- bA243O10.1, KIAA1866, dJ322A24.1
- Chromosome:
- 6q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-22
- Date modifiied:
- 2016-10-05
- Gene:
- H2AFY2 NIH gene
- Name:
- H2A histone family member Y2
- Previous symbol:
- -
- Synonyms:
- macroH2A2
- Chromosome:
- 10q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2015-11-18
- Gene:
- HNF4G NIH gene
- Name:
- hepatocyte nuclear factor 4 gamma
- Previous symbol:
- -
- Synonyms:
- NR2A2
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-20
- Date modifiied:
- 2016-10-05
Related products to: Stat4 Monoclonal Antibody (clone 2A2)
Related articles to: Stat4 Monoclonal Antibody (clone 2A2)
- The third-generation EGFR tyrosine kinase inhibitor (TKI) osimertinib (AZD9291) has significantly improved the survival in EGFR-mutant lung cancer patients. Our team developed limertinib (ASK120067), a novel third-generation EGFR inhibitor with remarkable antitumor effects, which has been launched in China. Despite initial therapeutic responses, EGFR TKIs-treated patients ultimately experience fatal metastatic recurrence and disease progression. However, the underlying mechanism of driving metastasis remains poorly understood. Here, we aim to investigate the pro-metastatic mechanism following treatment with third-generation EGFR TKIs. Transcriptomics analyses of EGFR TKI-resistant tumor models revealed an aberrant upregulation of S1PR3, which conferred enhanced metastatic potential to lung cancer. S1PR3 inhibition dramatically reduced metastasis in resistant cells, while its overexpression potentiated metastatic abilities in parental cells. Notably, S1PR3 was highly enriched in clinical samples with AZD9291 resistance and correlates with poor prognosis. Mechanistically, we found that S1PR3 upregulated RAC1-GTP expression to activate PAK1, thereby promoting epithelial-mesenchymal transition (EMT) and enhancing metastatic capacity of resistant cells. Further studies identified that the overexpression of fibroblast growth factor receptor 1 (FGFR1) increased S1PR3 expression through signal transducer and activator of transcription 4 (STAT4) to promote the emergence of metastatic-resistant cells. Importantly, targeting S1PR3 or FGFR1 blocks metastasis in EGFR TKI-resistant models. - Source: PubMed
Publication date: 2026/04/23
Lai MengzhenChen JiayingQin YeZhang HuiPan ZiluZhang TaoTong LinjiangTang HaotianBai GangLiu QiupeiLi YanFeng FangSong PeiranLiu YingqiangChen YiFang YanTang BencanGeng MeiyuYu KerChen HaoDing JianXie Hua - Systemic lupus erythematosus (SLE) and autoimmune hepatitis (AIH) are clinically distinct autoimmune disorders characterized by multisystem involvement and liver-restricted inflammation, respectively; nevertheless, they exhibit considerable overlap in their underlying immunopathogenic features. - Source: PubMed
Publication date: 2026/04/22
Yechen WuWang FengjiaoXiao LanlanChen YanfeiLi Lanjuan - Little is known about the causes of serum aquaporin 4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (AQP4-positive NMOSD) or how its pathophysiology differs from other demyelinating autoimmune diseases, which limits therapeutic and preventative opportunities despite available diagnostic biomarkers. By performing a pan-ancestry genome-wide association study (GWAS), we aimed to deepen our understanding of the genetic architecture of AQP4-positive NMOSD and to explore shared heritability with other autoimmune diseases. - Source: PubMed
Attfield Kathrine EArmen Angelos PKuttikkatte Subita BalaramFarooq RedwanFrancis Anna GDendrou Calliope ALeite M IsabelWaters Patrick Weinshenker Brian GKarczewski Konrad JNeale Benjamin MJensen Lise TorpRossjohn JamieGold RalfKorn ThomasMcVean GilPalace JacquelineFugger Lars - Atherosclerosis is linked to an increased risk of cognitive decline, with chronic inflammation being a common feature of both pathologies. IL-12 activates STAT4 to regulate myeloid cell functions, and blockade of this pathway alleviates cognitive impairment in Alzheimer's models. However, the mechanisms connecting vascular pathology to neuroinflammation remain unclear. Here, we examine whether STAT4 functions as a common mediator of neuroinflammation in atherosclerosis. We demonstrate that LysM-specific STAT4 deficiency ameliorates deficits in long-term memory in low-density lipoprotein-deficient (Ldlr) mice fed a high-fat diet (HFD-C). STAT4 deficiency moderately reduces Ser199-phosphorylated Tau burden. Atherosclerosis alters brain immune composition, characterized by increased numbers of CD45 leukocytes, activated microglia, and activated T and B cells, whereas STAT4 deficiency attenuates these effects. Nanostring gene-expression pathway analysis further highlights the importance of STAT4 in regulating multiple neuroinflammatory pathways and the Rhodopsin-like receptor signaling, which is associated with synaptic plasticity. LysM-specific STAT4 deficiency supports microglial efferocytosis in atherosclerotic Ldlr mice and increases the number of efferocytotic macrophages. Accordingly, STAT4 deficiency also reduces neuronal death. Overall, our data reveal an important role for myeloid-driven STAT4 expression in the pathogenesis of cognitive decline associated with atherosclerosis, mediated through impaired efferocytosis and enhanced leukocyte activation, leading to increased brain neuroinflammation. - Source: PubMed
Stahr NatalieMoriarty Alina KMa Shelby DKeeter W ColesKim Woong-KiSanford Larry DGalkina Elena V - Atherosclerosis is linked to an increased risk of cognitive decline, with chronic inflammation being a common feature of both pathologies. IL-12 activates STAT4 to regulate myeloid cell functions, and blockade of this pathway alleviates cognitive impairment in Alzheimer's models. However, the mechanisms connecting vascular pathology to neuroinflammation remain unclear. Here, we examine whether STAT4 functions as a common mediator of neuroinflammation in atherosclerosis. We demonstrate that LysM-specific STAT4 deficiency ameliorates deficits in long-term memory in low-density lipoprotein-deficient ( ) mice fed a high-fat diet (HFD-C). STAT4 deficiency moderately reduces Ser199-phosphorylated Tau burden. Atherosclerosis alters brain immune composition, characterized by increased numbers of CD45 leukocytes, activated microglia, and activated T and B cells, whereas STAT4 deficiency attenuates these effects. Nanostring gene-expression pathway analysis further highlights the importance of STAT4 in regulating multiple neuroinflammatory pathways and the Rhodopsin-like receptor signaling, which is associated with synaptic plasticity. LysM-specific STAT4 deficiency supports microglial efferocytosis in atherosclerotic mice and increases the number of efferocytotic macrophages. Accordingly, STAT4 deficiency also reduced neuronal death. Overall, our data reveal an important role for myeloid-driven STAT4 expression in the pathogenesis of cognitive decline associated with atherosclerosis, mediated through impaired efferocytosis and enhanced leukocyte activation, leading to increased brain neuroinflammation. - Source: PubMed
Publication date: 2026/03/23
Stahr NatalieMoriarty Alina KMa Shelby DKeeter W ColesKim Woong-KiSanford Larry DGalkina Elena V