GATA4
- Known as:
- GATA4
- Catalog number:
- 000595A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GATA4
Related genes to: GATA4
- 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
Related articles to: GATA4
- Human germ cell tumors (GCTs) occur in infants, children, and adults, and present as germinomatous and/or non-germinomatous (embryonal carcinoma (EC), teratoma, yolk sac tumor (YST), and choriocarcinoma) histologies at gonadal or extragonadal locations. Accurate subtyping is crucial for prognosis and treatment, but current clinical biomarkers lack sensitivity and specificity (serum proteins), or require a tissue biopsy (for histological and immunohistochemical characterization). Hence, less-invasive and improved subtype-specific biomarkers have significant potential for clinical utility. - Source: PubMed
Publication date: 2026/04/17
Janssen Ferdinand WGillis Ad J MGouswaart Puck BKester Lennart ATakami HirokazuIchimura KoichiEleveld Thomas FLooijenga Leendert H J - Ménière's disease (MD), a chronic inflammatory disorder with age-related increased incidence, exhibits poorly understood pathogenesis and limited therapeutic options. Here, we demonstrate that cellular senescence, marked by mitochondrial damage, reactive oxygen species accumulation, and senescence-associated secretory phenotype (SASP), is prevalent in the vestibular tissue of MD patients and an endolymphatic hydrops mouse model. The transcription factor GATA4 is upregulated in MD and mice, and its genetic deletion in hair cells alleviates LPS-induced audio-vestibular dysfunction and cellular senescence in mice and HEI-OC1 cells. Mechanistically, HDAC6 interacts with GATA4 and restrains its nuclear transport, while RNA-seq and ChIP-seq identify HtrA1, a serine protease, as a direct transcriptional target of GATA4. Inhibition of HDAC6 or AAV-mediated HtrA1 overexpression exacerbates MD-like symptoms, whereas inhibition of HtrA1 by Galegenimab ameliorates these phenotypes in mice. In aged mice, GATA4 deletion reduces age-related audio-vestibular deficits and senescence markers. Collectively, our findings establish GATA4 as a critical regulator of cellular senescence and inflammaging in inner ear pathologies, providing promising therapeutic targets for MD and age-related audio-vestibular disorders. - Source: PubMed
Publication date: 2026/04/14
Zhang NaLi NaWang YanZhang JingLiu JiahuiChen LeiSong YongdongMu YurongHan YuechenLyu YafengLi XiaofeiWang HanyueWang JingLu YaoFan ZhaominZhang DaogongWang Haibo - Mammalian sex determination is governed by two mutually antagonistic genetic programs that must be precisely balanced. Activation of Sox9 initiates testis development, while its repression is essential for ovarian fate. The distal enhancer, Enh13, is essential for testicular Sox9 expression, with its deletion or inactivation resulting in complete XY sex reversal. Here, we show that subtle mutations within Enh13, including a single-nucleotide insertion, produce the reciprocal phenotype: complete XX female-to-male sex reversal. Pro-female factors can strongly repress Enh13, suggesting they mediate Sox9 silencing in ovaries. The small enhancer alterations facilitate inappropriate Sox9 upregulation in the absence of Sry, triggering the testicular transcriptome and repressing ovarian gene expression. Mechanistically, these mutations disrupt the repressive effect of RUNX1, NR5A1 and GATA4, thereby reprogramming enhancer activity. Our findings identify Enh13 as a central regulatory hub, integrating opposing sex-specific cues, hence acting as a binary switch for gonadal fate. - Source: PubMed
Publication date: 2026/04/09
Abberbock ElishevaRidnik MeshiStévant IsabelleWeiss RoniBamberger CarmelZiv Lhermann ShellyLubman MaorYao Yumi MinyiAfek ArielPoulat FrancisGonen Nitzan - Resumption of proliferation by quiescent hepatocytes in response to liver injury is a hallmark event in live regeneration. We have previously reported that the zinc finger transcription factor GATA4 contributes live regeneration by promoting hepatocyte proliferation. In the present study we investigated the underlying mechanism. - Source: PubMed
Publication date: 2026/04/07
Zhou JiawenBao ZeqingWu MengGong ShanwenMiao XiulianDong WenhuiWang Bin - The objective of this work is to assess the effects and potential process of paternal acute sleep deprivation on cardiac function in their offspring. Male and female C57BL/6N mice aged 8-9 weeks (n = 4-5 mice/group) were used. Male mice were selected to construct an acute sleep deprivation model using the modified multiple platform method (MMPM) and mated with normal female mice. After gestation, the weight change of offspring mice was observed and recorded. At the time of 10 weeks, the changes of cardiac function were evaluated by blood pressure, heart rate and echocardiography; cardiac histology and cytopathological changes were observed by haematoxylin-eosin staining; and the molecular mechanism induced by acute paternal sleep deprivation were further elucidated by molecular biological techniques. In the acute sleep deprivation group, male offspring showed significant cardiac hypertrophy, whereas female offspring did not. mRNA levels of GATA binding protein 4 (GATA4) (P < 0.01) and mRNA levels of classic hypertrophic genes, such as atrial natriuretic peptide (ANP) (P < 0.05) and brain natriuretic peptide (BNP) (P < 0.05), increased significantly in the hearts of the acute sleep deprivation group. Paternal acute sleep deprivation may lead to cardiac dysfunction in offspring through cardiac hypertrophy. - Source: PubMed
Publication date: 2026/04/09
Zhang YingyingWang LeyaoWang JiePan YunSun WenZou ZhiweiBai WenlinFang RuilingZhang YueZhang PingZhang YuanbaoLei LijianZhang Wenping