GATA4 siRNA_Lentivectors
- Known as:
- GATA4 siRNA_Lentivectors
- Catalog number:
- i008538b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GATA4 siRNA_Lentivectors
Related genes to: GATA4 siRNA_Lentivectors
- Gene:
- GATA4 NIH gene
- Name:
- GATA binding protein 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-30
- Date modifiied:
- 2016-10-05
Related products to: GATA4 siRNA_Lentivectors
Related articles to: GATA4 siRNA_Lentivectors
- Mandibular incisors are the most frequently congenitally absent teeth in Asian populations, affecting mastication, speech, aesthetics, and oral and maxillofacial functions over the long term. However, the genetic etiology of mandibular incisor agenesis (MIA) remains obscure. In this study, we conducted the first genome-wide association study on MIA in a Chinese population and identified an enhancer variant, rs71514987, associated with an increased risk of MIA (odds ratio, 2.18; 95% CI, 1.83 to 2.58; = 3.62 × 10). Functional characterization indicated that the rs71514987 C allele reduced the binding affinity of GATA4 to the promoter, leading to increased expression via remote regulation. Notably, elevated levels promoted cell proliferation but diminished cell differentiation, migration, and apoptosis capabilities in stem cells from human exfoliated deciduous teeth, as well as abnormal development of pharyngeal teeth in zebrafish models. Mechanistic experiments further revealed that OSR2 bound to the promoter region of , promoting its transcription level in the GPCR pathway, thereby influencing odontogenic differentiation during tooth development. Our findings provide novel insights into the molecular etiology of MIA. - Source: PubMed
Publication date: 2026/07/18
Fan LZhang XMao JVona BXu XDu MMa LPan Y - Sepsis triggers profound organism-wide disturbances, yet the cellular logic underlying its systemic impact remains poorly defined. By integrating single-cell transcriptomes from six septic tissues, we uncovered a conserved cross-tissue program characterized by inflammation-driven senescence, disrupted intercellular communication, and coordinated transcriptional reprogramming. Senescence signatures were broadly elevated across cell types and strongly coupled to altered communication networks, suggesting that septic stress induces both cell-intrinsic and network-level remodeling. We identified several key transcription factors, with activation of Atf4, Cebpb and Cebpd, alongside repression of Foxo1, Gata4, and Yy1, which might rewire inflammatory and stress-adaptive programs toward senescence-like states. Endothelial and neutrophil populations were inferred to act as the principal amplifiers of this response through predicted Cxcl1-Cxcr2 and Cxcl2-Ackr1 circuits, potentially establishing self-reinforcing inflammatory-senescent loops. Finally, the neutrophil-derived signature serves as a robust molecular adjunct to traditional clinical metrics, significantly improving risk stratification and enhancing the prognostic accuracy for sepsis patients. Together, our findings position sepsis as a potent driver of accelerated immunological aging and provide conserved regulatory mechanisms that may represent therapeutic targets for mitigating both acute injury and long-term sequelae. - Source: PubMed
Publication date: 2026/07/17
Zhou ChenBai Yunmeng - Chemical reprogramming holds transformative potential for regenerative medicine. However, the regulatory mechanisms governing cell fate transitions are not well understood. Here, we identify Interleukin-1 Receptor-Associated Kinase 4 (IRAK4) as a barrier to multi-lineage reprogramming. Pharmacological inhibition of IRAK4 enhances the reprogramming of mouse embryonic fibroblasts (MEFs) through a chemically activated multi-lineage priming (CaMP) state and extraembryonic endoderm (XEN)-like intermediates, increasing colony formation, and the expression of core XEN regulators (Sox17, Gata4, Sall4, and Foxa2). Genetic knockdown of Irak4 similarly accelerates reprogramming, whereas its overexpression blocks cell fate transitions. IRAK4 inhibition enhances chromatin accessibility and reshapes cell cycle dynamics, characterized by G0/G1 shortening and G2/M lengthening, potentially contributing to multi-lineage state establishment. Furthermore, IRAK4 suppression enhances the direct conversion of MEFs to neuron-like and hepatocyte-like cells, which exhibit enhanced functional maturity, including increased glycogen storage and improved detoxification capacity. Our findings establish IRAK4 as a regulator that constrains cellular plasticity potentially by coordinating chromatin accessibility and cell cycle dynamics. - Source: PubMed
Publication date: 2026/07/15
Huang ChuanshuHan XiaoyunWang TaoZhao YangLi Jun - Apolipoprotein A-IV (apoA-IV) plays key roles in lipid metabolism, reverse cholesterol transport, and kidney function, yet its genetic determinants remain poorly defined. We conduct a genome-wide association study (GWAS) meta-analysis of apoA-IV concentrations measured by ELISA in 25,181 individuals and combine these with proteomic data from 33,995 UK Biobank participants (Olink platform), yielding a total sample of 59,176. We perform genetic correlations and colocalization analyses to explore links with lipid, renal, and other complex traits. - Source: PubMed
Publication date: 2026/07/14
Koller AdrianaSchnitzer FlorianKollerits BarbaraLamina ClaudiaMoix SamuelClaringbould AnniqueMishra Binisha HLu HaojieSchachtl-Riess Johanna FForer LukasGieger ChristianKheirkhah AzinLehtimäki TerhoMarques-Vidal PedroSchönherr SebastianStark Klaus JWürzner ReinhardEckardt Kai-UweHeid Iris MKavousi MaryamKöttgen AnnaRaitakari OlliSijbrands Eric J GPeters AnnetteVollenweider PeterKronenberg Florian - 2,4,6-tris(2,4,6-tribromophenoxy)-1,3,5-triazine (TTBP-TAZ) is a widely used novel brominated flame retardant with environmental persistence, yet its developmental toxicity remains poorly characterized. In this study, we investigated the developmental and cardiotoxic effects of TTBP-TAZ in zebrafish embryos/larvae. Embryos (4 hpf) were exposed to 0-20 μM TTBP-TAZ for 120 hpf. Assessments included survival, hatching kinetics, burst activity (24 hpf), heart rate (48 hpf), caudal venous blood-flow velocity (72 hpf), locomotor behavior under alternating light/dark conditions (120 hpf), cardiac morphology in Tg(myl7:EGFP), and transcription of key cardiac genes. Results indicated low mortality of embryos/ larvae across all concentrations. However, TTBP-TAZ accelerated hatching rate in a concentration-dependent manner (significant by 60 hpf) and increased burst activity. Elevated heart rate (48 hpf) and enhanced tail-vein blood flow (72 hpf) suggested tachycardia and stimulated circulation. Transgenic larvae exhibited reduced ventricular/atrial fluorescence intensity, along with enlarged cardiac size and indistinct contours, indicating structural abnormalities. qPCR analysis revealed up-regulation of nkx2.5, tbx20, and vmhc, and down-regulation of gata4, mef2, and myh7, suggesting disruption of core cardiogenic transcription and chamber-specific contractile programming. Locomotor assays demonstrated hyperactivity at higher concentrations under both light and dark conditions. These findings indicate sub-lethal TTBP-TAZ exposure induces significant developmental and cardiotoxic disturbances in zebrafish, associated with altered cardiac gene expression and functional hyperactivation. This study supports the need for further mechanistic investigation and exposure-relevant risk assessment of TTBP-TAZ. - Source: PubMed
Publication date: 2026/07/13
Bi ZeyuLi JuanLiu JiaLu MiaoWang LingLiang Yong