GATA4 EMSA Kit
- Known as:
- GATA4 EMSA Kit
- Catalog number:
- AY1097
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GATA4 EMSA Kit
Ask about this productRelated genes to: GATA4 EMSA Kit
- 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
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- Atrial septal defect (ASD) is a type of congenital heart defect characterized by the absence of atrial septal tissue. Research has shown that genetic factors play a significant role in the development of ASD. Variants in genes such as GATA binding protein 4 (GATA4), NK2 homeobox 5, and T-box transcription factor 5 have been identified in patients with ASD. In this study, we enrolled a Chinese family affected by ASD and PS. Whole exome sequencing and Sanger sequencing were used to investigate the genetic basis of lesions in this family. The AC16 cell line was used to perform the functional study. After data filtering and co-segregation analysis, we identified a rare mutation (NM_001308093.3: c.790G > A, p.Ala264Thr) in the GATA4 gene in the affected family members that was absent in the unaffected individuals. Bioinformatic analysis revealed that the newly identified mutation was deleterious and altered the hydrophobicity, size and polar of the GATA4 protein. Functional studies revealed that this rare mutation disrupted the stability of GATA4 and reduced the ability of GATA4 to activate the downstream target genes. Our findings highlight the importance of the N-terminal zinc finger structure of GATA4 in cardiac development. Additionally, our study contributes to the genetic diagnosis and counseling of families with congenital heart disease. - Source: PubMed
Publication date: 2026/05/08
Zhang Ai-QianLong Jie-YiXue WeiYu RongZhu LeiFan Liang-Liang - We previously demonstrated that fibroblasts can be reprogrammed through a proliferative progenitor stage to drive both cardiomyogenesis and neovascularization. However, it remains to be determined whether cardiac fibroblasts (CFs), the primary mediators of post-injury remodeling, retain the plasticity to be concurrently redirected into cardiovascular lineages within the environment. - Source: PubMed
Publication date: 2026/04/22
Dutta SuchandrimaChen SophieAhmad WaqasHuang WeiWang YigangLiang Jialiang - Hodgkin Lymphoma (HL) is a heterogeneous malignant disorder in the human body's lymphatic system with distinct clinical and molecular features. The objective of this research was to assess the hematological and molecular status of HL patients in Palestine and explore potential prognostic indicators and potential targets requiring further evaluation. Certain hematological factors, i.e., anemia, increased levels of lactate dehydrogenase, and inflammatory markers, are included in the International Prognostic Score (IPS) for HL. This study highlights the clinical value of accessible hematological biomarkers in resource-limited healthcare settings. A retrospective cohort study was conducted on 557 HL lymph node biopsies (2017-2023) from Palestinian Health Information Center (PHIC) database and hospital medical records. Hematological parameters (hemoglobin, MCV) and biochemical markers (ESR, LDH) were analyzed. Claudin-6 (CLDN6) mRNA expression was quantified in lymph node tissues from HL patients (n = 25) and healthy donors (n = 25) via qRT-PCR, while protein levels were assessed by Western blot. Serum GATA-4 concentrations were measured by ELISA. Nodular Sclerosis was the most common form, which predominantly occurred in young patients with a relatively equal sex distribution. The highest frequency was found in Hebron. Hemoglobin levels differed between subtypes, with the lymphocyte-depleted subtype showing the lowest mean hemoglobin values; the Lymphocyte-Depleted (LD) subtype exhibited the lowest hemoglobin and MCV (74.77 fL), indicating microcytic anemia. ESR was elevated across subtypes, with the highest levels observed in the NOS (63.5 mm/h), reflecting aggressive disease. Male mortality was highest in Mixed Cellularity (87.5%) and NS (75%), while LD and Lymphocyte-Predominant subtypes showed no male deaths. Molecularly, CLDN6 mRNA and GATA-4 levels were significantly elevated in HL tissues (P < 0.001), though Claudin-6 protein expression remained unchanged, suggesting post-transcriptional regulation. This study represents the first combined hematological and molecular characterization of Hodgkin lymphoma in Palestine and provides preliminary evidence for CLDN6-GATA4 regulatory involvement in HL pathogenesis. The hematological changes in Palestinian HL patients are unique. The roles of CLDN6 and GATA-4 as potential markers remain preliminary and require further validation in the context of Hodgkin lymphoma. - Source: PubMed
Publication date: 2026/05/01
Asees MohammadAmer JohnnyRezeq AyoubSalhab AhmadAbdalhaq Toleen - Autophagy is a double-edged sword for maintaining neural system homeostasis during the development of cerebral ischemia. However, the potential molecular mechanisms behind this remain unclear. Changes in miR-429 and its target GATA4, along with autophagy mediators and apoptosis in ischemic stroke, were examined in this research. Additionally, the study investigated these factors in combination with chlorogenic acid (CGA). Male Wistar rats were separated into three categories. (n=8): sham, IR (ischemia-reperfusion, Induction of transient cerebral ischemia via occlusion and reperfusion of the common carotid artery.) and IR+CGA (30 mg/kg, ip; administered intraperitoneally, 10 minutes before the onset of ischemia and 10 minutes prior to reperfusion). Levels of miR-429, GATA4, c-Caspase-3 / p-Caspase-3 ratio, LC3-I, LC3-II, Beclin1 and p62 were assessed using Real- time PCR and Western blot assays. At the end of the experiment, increased miR-429 gene expression (P<0.05) and c-Caspase-3/p-Caspase-3 ratio (P<0.01), along with decreased GATA4 protein expression (P<0.001), were observed in IR group. In addition, the brains of CCAO rats displayed significantly increased autophagy activation, as evidenced by an increased LC3-II/I ratio and Beclin1 protein expression, and decreased p62 expression after 24 h of reperfusion (P<0.001). Immunohistochemistry studies has alsorevealed that the ratio of overall LC3 immunoreactivity in the cortex tissue of male rats was significantly increased by cerebral IR (P<0.001). Treatment with CGA significantly attenuated autophagic activity and apoptosis, reversing the aforementioned molecule levels. Taken together, these results suggested that ischemic insult can increase autophagic activities and apoptosis, possibly through miR‑429 and GATA4 alterations in the brain cortex following cerebral IR insult, which can be alleviated by CGA as a potential therapy for individuals affected by ischemia. - Source: PubMed
Publication date: 2025/08/30
Rahil SalimiAlireza ShirpoorRoya Naderi - Cardiac ischemia induces substantial metabolomic reprogramming, which dysregulates cardiomyocytes (CMs) and non-myocyte stromal cell populations. The stromal cells derived from epicardial adipose tissue (EAT) and ventricle are critical for extracellular matrix (ECM) remodeling, paracrine signaling, and myocardial homeostasis. However, the metabolomic content and responses of EAT-derived stromal cells (EATDS) and ventricular stromal cells (VSCs) remain unknown. - Source: PubMed
Publication date: 2026/04/29
Sun DongweiPostajian AlexRostomian EdgminChen YuPark Junyoung OHatamian VediVartanian Kevin BabakhanThankam Finosh G