STAT6 Antibody (Ab_641), pAb, Rabbit
- Known as:
- STAT6 Antibody (Ab_641), pAb, Rabbit
- Catalog number:
- A00282
- Product Quantity:
- 40ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- STAT6 Antibody (Ab_641) pAb Rabbit
Related genes to: STAT6 Antibody (Ab_641), pAb, Rabbit
- Gene:
- STAT6 NIH gene
- Name:
- signal transducer and activator of transcription 6
- Previous symbol:
- -
- Synonyms:
- D12S1644, IL-4-STAT
- Chromosome:
- 12q13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-09
- Date modifiied:
- 2019-04-23
Related products to: STAT6 Antibody (Ab_641), pAb, Rabbit
Related articles to: STAT6 Antibody (Ab_641), pAb, Rabbit
- - Source: PubMed
- Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with increasing prevalence and high heritability. As a key epigenetic mechanism in brain development and function, the specific mechanisms of N-methyladenosine (mA) modification in ASD remain unknown. This study conducted bioinformatics analysis of mA-QTL data from Yoruba lymphoblastoid cell lines and the RMVar database to identify mA-QTL SNPs and modification genes associated with ASD. A two-stage population validation includes 1244 Chinese children with ASD and controls, followed by replication in a large European cohort consisting of 18,382 cases and 27,969 controls. The potential functions of candidate variants and target genes were examined through functional annotations. There were 2830 SNPs associated with the mA modification levels of target genes. We further identified 91 mA-QTL-associated ASD candidate SNPs in Chinese samples and validated 8 variants in the European cohort (P < 0.05), including three high-confidence variants: rs10242048 (P = 8.06 × 10), rs2304447 (P = 5.01 × 10), and rs4074309 (P = 1.59 × 10). Functional annotations revealed that rs4074309 might potentially regulate mA levels of STAT6 and modulate LRP1 expression in brain tissues, binding the transcription factor THAP1. Both STAT6 and LRP1 are implicated in crucial neurodevelopmental pathways, such as the JAK-STAT signaling and the tau-protein kinase regulation, respectively. Our study suggests that genetic variants in mA modification genes may contribute to ASD susceptibility. The findings highlight the importance of mA modification in neurodevelopmental disorders and provide insights into the epigenetic mechanisms involved in ASD. - Source: PubMed
Publication date: 2026/05/27
Wang HaoxueZhao ShuaiChen YanlinHou FangZhu KaihengLiu RundongXiang ZhenChen QianhuiFan HongHuang MengyuanWang ZhikeZhang JiaoWang TianchunLiang XiZeng XiaoxueGong ZhaohuiLi LiSong Ranran - : The STAT (Signal Transducer and Activator of Transcription) family of seven transcription factors mediates cytokine and growth-factor signaling, regulating proliferation, differentiation, and immunity. While STAT3/STAT5 are established oncogenes and STAT1/STAT2 are classically viewed as tumor suppressors, emerging evidence indicates context-dependent roles in tumorigenesis. This study aimed to integrate evolutionary analysis with bulk transcriptomic, regulon, single-cell, and exploratory chromatin-binding analyses of the STAT family in human solid tumors. : Orthologs and paralogs of human STAT genes (81 sequences total) were retrieved across vertebrates and invertebrates; a phylogenetic tree was constructed using MUSCLE alignment and Neighbor-Joining in MEGA12. Differential expression was assessed in TCGA solid tumors versus GTEx normal tissues. Master-regulator activity was inferred using the algorithm. Single-cell RNA-seq datasets were used to compare malignant and non-malignant cell populations. STAT1 chromatin binding was examined via ChIP-seq in interferon-stimulated HeLa and K562 cells. : Phylogeny resolved seven conserved vertebrate clades, with endocrine-responsive STAT3/STAT5 showing higher conservation and immune-associated STAT1/STAT2/STAT4/STAT6 exhibiting faster divergence. The majority of STAT genes were frequently upregulated across multiple solid tumors, with activated regulons confirming functional transcriptional engagement. Single-cell analysis demonstrated tumor-cell-autonomous upregulation of STAT1 and STAT2 in the HNSCC dataset. STAT1 ChIP-seq revealed asymmetric forward/reverse-strand read density around peak summits, supporting non-canonical DNA recognition. : The STAT family operates as an evolutionarily conserved, broadly activated transcriptional module in human solid cancers, combining quantitative upregulation with qualitative shifts in DNA-binding dynamics. These findings refine our understanding of JAK/STAT signaling in oncology and highlight opportunities for network-targeted therapies. - Source: PubMed
Publication date: 2026/05/03
Lukic DunjaGuzzi Pietro HiramGiorgi Federico Manuel - Signal transducers and activators of transcription (STAT) proteins, which operate via canonical and non-canonical mechanisms, are critically implicated in thyroid tumorigenesis. This review integrates their multifaceted roles in thyroid cancer. STAT3 acts as a "double-edged sword": hyperactive STAT3 drives metastasis and BRAF inhibitor resistance in advanced carcinomas, yet paradoxically acts as a tumor suppressor by restraining the Warburg effect via non-canonical mitochondrial localization. Clinically, preserved nuclear STAT3 independently predicts a favorable prognosis and is inversely correlated with promoter mutations, offering a biological modifier for clinical risk stratification. Furthermore, STAT1 regulates differentiation via the IGF2BP2- axis, STAT5 drives proliferation upon release from TRβ suppression, and STAT6 confers chemoresistance. While novel direct STAT3 inhibitors (e.g., TTI-101) and rational combinations with immune checkpoint inhibitors or STING agonists show promise in overcoming refractory disease, the intricate dual functionality of STAT family proteins demands rigorous biomarker-guided precision medicine approaches. - Source: PubMed
Publication date: 2026/05/12
Masaki ChieInoue NorihitoChiba Tomohiro - The increasing global burden of cancer, together with the need for more sustainable resource management, has stimulated growing interest in the valorization of agro-industrial plant residues as sources of bioactive compounds with therapeutic potential. This review highlights the potential of plant by-products-including citrus peels, olive leaves, date palm residues, and tea and coffee processing wastes-as sustainable reservoirs of polyphenols and other phytochemicals with significant anticancer activity. Key compounds such as hesperidin and naringenin from citrus peels, oleuropein and hydroxytyrosol from olive leaves, quercetin and syringic acid from date palm residues, and chlorogenic acid and epigallocatechin gallate from tea and coffee by-products have demonstrated promising antitumor effects in both in vitro and in vivo studies. These molecules exert their activity through multiple mechanisms, including the inhibition of cancer cell proliferation, induction of apoptosis, regulation of the cell cycle, and modulation of major oncogenic signaling pathways such as PI3K/AKT, MAPK, NF-κB, and EGFR. For instance, hydroxytyrosol induces apoptosis and cell cycle arrest while inhibiting the PI3K/AKT and MAPK pathways. Quercetin limits metastasis and glycolysis and suppresses VEGF, PKM2, and AKT signaling. Ferulic acid suppresses tumor growth by inhibiting the PI3K/AKT and JAK2/STAT6 pathways, thereby promoting apoptosis (in vitro and in vivo). In addition to their pharmacological potential, the recovery of these compounds from plant waste supports circular economy strategies by reducing environmental impact and promoting the development of value-added products. Future research should focus on optimizing extraction methods, improving bioavailability and stability, and validating safety and efficacy through well-designed preclinical and clinical studies. - Source: PubMed
Publication date: 2026/04/29
Yazdanpanah SorurSepe FabriziaRomano SilviaValentino AnnaPetillo OrsolinaPeluso GianfrancoConte RaffaeleCalarco Anna