GATA4 Pre-design Chimera RNAi
- Known as:
- GATA4 Pre-design Chimera RNAi
- Catalog number:
- H00002626-R01
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- GATA4 Pre-design Chimera RNAi
Related genes to: GATA4 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: GATA4 Pre-design Chimera RNAi
- Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, characterized by rapid and disorganized electrical activity in the atria. Although traditionally attributed to aging and structural remodeling secondary to cardiovascular comorbidities, AF has a well-recognized heritable component, with genetic factors contributing substantially to disease susceptibility. This review systematically evaluates the molecular landscape of AF, focusing on genetic mutations and their functional consequences in disease development. AF-associated genes are organized into four functional modules: (1) ion channelopathies (, , , ); (2) structural myopathies (, , , ); (3) transcriptional regulators ( ); and (4) calcium handling proteins (RYR2, CASQ2, JPH2, ANKB, PLN, TRDN). For each gene, population prevalence and penetrance of associated variants are discussed alongside the specific molecular and biophysical consequences of causative mutations. By elucidating how these protein alterations converge on shared electrophysiological and structural substrates, we provide a framework for transitioning from generalized therapeutic strategies to precision medicine approaches in cardiac electrophysiology. - Source: PubMed
Publication date: 2026/05/29
Hinge Dilip DShelke AbhijeetKawade RameshPatil Satish - In mammalian sex differentiation, Sox9 expression in undifferentiated gonads determines male development. Sox9 is regulated by multiple enhancers, of which Enh13/mXYSRa is the most critical. Disruption of the GATA4 binding site in Enh13/mXYSRa causes XY sex reversal in the C57BL/6J (B6J) strain, but not in the mixed genetic background of B6J × DBA/2. To clarify the cause of these differences, mice with the same mutation were generated in DBA/2. Homozygous mutants developed as XY males. We hypothesized that the phenotypic differences between strains were due to functional differences of another enhancer. Mice lacking TESCO and carrying a mutation in the GATA4 binding site were generated and analyzed. The mutants developed according to their chromosomal sex despite reduced Sox9 expression. These findings imply that the DBA/2 genetic background contains factors preventing Sox9 expression from falling below the threshold required for male development. Bulk RNA-seq analysis of fetal gonads during sex determination identified strain-dependent differences in intermediate mesoderm development and protease inhibition pathways; the study also revealed that the expression of Sox8 has a redundant role in Sertoli cell differentiation to that of Sox9 in male embryonic gonads. These differences may contribute to the phenotypic variation observed between strains. - Source: PubMed
Tsuchiya IkuTsuji-Hosokawa AtsumiFuruhashi SuzuneSugiyama KarinOgawa YuyaOishi AkiTerao MihoTakada Shuji - Somatic cell nuclear transfer (SCNT) holds great promise for regenerative medicine and agriculture, but its application is severely hampered by low efficiency, primarily attributable to aberrant epigenetic reprogramming. Although embryonic stem cells (ESCs) and trophoblast stem cells (TSCs) have been successfully derived from cloned embryos, an in vitro counterpart of the primitive endoderm (PrE) lineage has remained unavailable. To address this gap, this study reports the first successful establishment of extra-embryonic endoderm stem cell lines (XENs) from mouse SCNT-derived blastocysts (NT-XENs). Under conventional culture conditions, NT-XENs were generated from hybrid B6D2F1 blastocysts at a high efficiency of 55%, statistically comparable to that of fertilization-derived XEN lines (FD-XENs, 50%), whereas derivation from inbred C57BL/6J SCNT-derived blastocysts was markedly lower (12.5%). Immunofluorescence and NanoString multiplex gene expression profiling confirmed that NT-XENs robustly expressed specific marker genes for PrE/XENs (e.g., , , and ), while exhibiting negligible or absent expression of pluripotency and trophoblast markers. Based on NanoString assay data, NT-XENs and FD-XENs shared highly similar gene expression patterns, yet also exhibited some nonnegligible differences, exemplified by the differentially expressed genes (DEGs) , , , and . These differences raise a preliminary hypothesis that the NT-XENs might exhibit a slight transcriptional propensity toward a more differentiated state, and potentially reflect lingering traces of SCNT-associated epigenetic errors, such as localized dysregulation of imprinted genes and X-linked transcripts. In summary, this study successfully establishes NT-XEN cell lines, providing a valuable in vitro model for investigating the reprogramming scenarios of PrE lineage in SCNT and the mechanisms underlying developmental failure of cloned embryos. - Source: PubMed
Publication date: 2026/06/24
Li ShuaipengWei ShuLi GuomengHu MeiLin JiangweiBao Wandong - : As the most prevalent supraventricular arrhythmia, affecting around 1% of people worldwide, atrial fibrillation (AF) is implicated with a multitude of detrimental clinical sequelae, encompassing congestive failure, thromboembolic cerebral stroke, and premature death. Accumulating epidemiological evidence convincingly demonstrates genetic defects as a cornerstone in the pathogenesis of idiopathic AF. Despite significant genetic underpinnings responsible for AF, owing to substantial genetic heterogeneity, the predisposing genetic substrates for AF in most individuals remain to be ascertained. : A four-generation pedigree suffering from familial AF and a cohort of 238 subjects affected with idiopathic AF, together with 266 healthy people, were enrolled prospectively. Pan-exome sequencing analysis was implemented on the chosen AF pedigree members, and Sanger sequencing assay was performed on all research subjects. The functional effects of the detected variations were examined via an in vitro dual-reporter gene measurement. : Two novel heterozygous truncating variations, NM_021973.3: c.138G>A; p.(Trp46*) and NM_021973.3: c.337C>T; p.(Gln113*), were discovered in the AF pedigree and one of the 238 AF cases, respectively. The two variants co-segregated with the AF phenotype and were absent from the 532 control chromosomes of 266 healthy individuals. Quantitative reporter gene assays unveiled that both Trp46*- and Gln113*-mutant HAND2 failed to transcriptionally activate and , two AF-causative genes. Additionally, the two variations nullified the synergistic transcriptional activation of by HAND2 and GATA4, another recognized gene predisposing to AF. : These findings support as a strong candidate gene contributing to AF susceptibility, which unravels novel etiopathogenesis underpinning the occurrence and perpetuation of AF and offers a potential molecular target for individualized medicine. - Source: PubMed
Publication date: 2026/06/17
Zhang HongHu Xiao-QingLi NingZhang Dao-LiangQiu Xing-BiaoYang Chen-XiXu Ying-JiaYang Yi-QingWang Juan - Women with bipolar disorder (BIP) have a higher risk of developing polyendocrine metabolic ovarian syndrome (PMOS). Shared genetic architecture may underlie this comorbidity. Valproate, a mood-stabilizer commonly used to treat BIP, increases the risk of PMOS. Still, the mechanism underlying PMOS in BIP remains unknown. Here, we aimed to identify genetic variants shared between BIP and PMOS, as well as their interaction with valproate. We used the results of large-scale genome-wide association studies of BIP (41,510 cases and 354,340 controls), and PMOS (3609 cases and 229,788 controls). Using conditional false discovery rate, we discovered genetic variants jointly associated with BIP and PMOS. Gene mapping of identified variants was performed using the Open Targets platforms. We analyzed the tissue-specific expression, interaction with valproate, and involvement in biological pathways of the mapped genes. We identified two loci shared between BIP and PMOS. Among the 10 genes mapped to the locus on chromosome 8:11,444,837-11,463,015, GATA4, NEIL2, and FDFT1 showed expression profiles suggesting their role in the observed comorbidity. Mapped to the locus on chromosome 12:2499,849-2514,270, CACNA1C, FKBP4, DCP1B, and ITFG2 are expressed in both the ovaries and the brain. Valproate interacts with CACNA1C, and CACNA1C is part of biological pathways that also include other genes interacting with valproate. We identified shared genetic underpinnings of BIP and PMOS and highlighted genes that may potentially contribute to the biological mechanisms underlying their comorbidity and to a hypothesized role of valproate in these mechanisms. - Source: PubMed
Publication date: 2026/06/25
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