GATAD1 antibody - middle region (ARP33194_P050)
- Known as:
- GATAD1 (anti-) - middle region (ARP33194_P050)
- Catalog number:
- arp33194_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GATAD1 antibody - middle region (ARP33194_P050)
Related genes to: GATAD1 antibody - middle region (ARP33194_P050)
- Gene:
- GATAD1 NIH gene
- Name:
- GATA zinc finger domain containing 1
- Previous symbol:
- -
- Synonyms:
- ODAG, RG083M05.2, FLJ22489
- Chromosome:
- 7q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-31
- Date modifiied:
- 2019-04-23
Related products to: GATAD1 antibody - middle region (ARP33194_P050)
Related articles to: GATAD1 antibody - middle region (ARP33194_P050)
- Blood-brain barrier (BBB) dysfunction represents a critical pathological manifestation in exacerbating ischemic stroke, contributing to neuronal death, edema formation, and unfavorable clinical outcomes. GATA zinc finger domain-containing 1 (GATAD1) is recognized as a critical transcription factor in cardiac development and cardiovascular disease. However, the role of GATAD1 in regulating BBB function and ischemic stroke remains elusive. Here, we found that GATAD1 was upregulated in cerebral endothelial cells (ECs) following ischemic stroke in mice. EC-specific Gatad1 deficiency demonstrated remarkable neuroprotection, manifested by reduced infarct volumes, ameliorated BBB dysfunction, and improved neurological outcomes following experimental stroke. Mechanistic investigations revealed that GATAD1 was involved in regulating CD36 expression, thereby modulating caveolae-mediated transcytosis in cerebral ECs. These findings established GATAD1 as a novel regulator of BBB permeability and a potential therapeutic target for ischemic stroke intervention. - Source: PubMed
Publication date: 2025/09/18
Fan LizhenLiu HuiLi ShanshanLi LinglingZhang ZhiLiu PinyiYang HaiyanXia ShengnanCao XiangWang ChunXu Yun - Advancements in AI-powered systems medicine have revolutionized biomarker discovery through emergent and explainable features. By use of complex network dynamics and graph-based machine learning, we identified critical determinants of lineage-specific plasticity across the single-cell transcriptomics of pediatric high-grade glioma (pHGGs) subtypes: IDHWT glioblastoma and K27M-altered diffuse midline glioma. Our study identified network interactions regulating glioma morphogenesis via the tumor-immune microenvironment, including neurodevelopmental programs, calcium dynamics, iron metabolism, metabolic reprogramming, and feedback loops between MAPK/ERK and WNT signaling. These relationships highlight the emergence of a hybrid spectrum of cellular states navigating a disrupted neuro-differentiation hierarchy. We identified transition genes such as DKK3, NOTCH2, GATAD1, GFAP, and SEZ6L in IDHWT glioblastoma, and H3F3A, ANXA6, HES6/7, SIRT2, FXYD6, PTPRZ1, MEIS1, CXXC5, KDM4C, and NDUFAB1 in K27M subtypes. We also identified MTRNR2L1, GAPDH, IGF2, FKBP variants, and FXYD7 as transition genes (plasticity signatures) that influence cell fate decision-making across both subsystems. We also discovered hub genes such as ITM2C, NOP16, ACTB in IDHWT, and MTRNR2L1, EEF1A1, RPS3A, and H3F3A in K27M gliomas, which serve as central regulators of glioma plasticity and potential therapeutic targets. Our findings suggest pHGGs are developmentally trapped in states exhibiting maladaptive behaviors, and hybrid cellular identities. In effect, tumor heterogeneity (metastability) and plasticity emerge as stress-response patterns to immune-inflammatory microenvironments and oxidative stress. Furthermore, we show that pHGGs are steered by developmental trajectories from radial glia predominantly favoring neocortical cell fates, in telencephalon and prefrontal cortex (PFC) differentiation. By addressing underlying patterning processes and plasticity networks as therapeutic vulnerabilities, our findings provide precision medicine strategies aimed at modulating glioma cell fates and overcoming therapeutic resistance. We suggest transition therapy toward neuronal-like lineage differentiation as a potential precision therapy to help stabilize pHGG plasticity and aggressivity. - Source: PubMed
Publication date: 2025/08/22
Uthamacumaran Abicumaran - Vascular injury is a common complication of type 2 diabetes mellitus (T2DM). Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a vascular regulator. This study is to explore the possible pathological mechanism of PECAM-1 in vascular injury in T2DM. Plasma PECAM-1 was detected using ELISA in plasma samples of T2DMs and normal subjects. NetworkAnalyst was used to analyze the PECAM-1 transcript genes. PECAM-1 transcriptional gene variation in T2DM was analyzed from GSE26168 data from the GEO database. STRING line network database was used to obtain the proteins related to PECAM-1, and the ClusterProfiler package in R language was applied to perform PPI, GO and KEGG enrichment analysis. PECAM-1targeted drugs prediction was performed by Drugbank. Compared with 66 healthy controls, the plasma PECAM-1 levels in 66 patients with T2DM were significantly decreased (p < 0.001). Moreover, multivariate regression analysis indicated that PECAM-1 was an independent risk factor for vascular injury in T2DM patients. GSE26168 data of T2DM blood mRNA showed that the levels of the PECAM-1 gene transcription factors CREB3, GATAD1 and TEAD3 were significantly reduced, while CUX1 and RELA were significantly increased in T2DM patients. Functional enrichment analysis of PPI, GO and KEGG suggested that PECAM-1 was involved in regulation of vascular stability, endothelial function, and angiogenesis. DrugBank search revealed that fostamatinib is a targeted drug closely matching the PECAM-1 molecule. In patients with T2DM, the decrease in PECAM-1 is an independent risk factor for vascular injury. Abnormalities in PECAM-1 transcriptional factors are likely associated with the reduction in plasma PECAM-1 levels, which may be involved in the mechanism of vascular injury in T2DM. Fostamatinib may be a candidate drug for vascular injury in T2DMs. - Source: PubMed
Publication date: 2025/07/01
Xu Jun-JunCai Han-ZhenSun HanChen XiangCai Xia-Ming - GATA zinc finger domain containing 1 (GATAD1) is an as-yet uncharacterized zinc finger domain protein, which was initially identified as a histone 3 trimethylated at lysine 4 (H3K4me3) interactor. A recessive mutation in GATAD1 is associated with adult-onset dilated cardiomyopathy and heart failure, suggesting that GATAD1 is critical for maintaining normal cardiac structure and function. However, little is known as to the specific role of GATAD1 in cardiomyocytes. A mammalian Gatad1 knockout model has yet to be generated for investigating its specific role in the heart. To address this, we generated a Gatad1 cardiomyocyte-specific knockout (cKO) mouse model. Gatad1 cKO mutants exhibited normal cardiac function during the aging process up to 18 months of age. Unlike the abnormal nuclei shape observed in patients carrying GATAD1 mutations, the nuclei shape of cardiomyocytes remained unaffected by the loss of Gatad1. Furthermore, Gatad1 cKO mice responded normally to pressure overload induced by transverse aortic constriction (TAC) surgery. Together, these observations suggest that deletion of Gatad1 in cardiomyocytes does not induce cardiomyopathy during aging or affect the response to pressure overload stress in mice. - Source: PubMed
Publication date: 2024/12/06
Pang JingZhu SitingShyy MelodyDuong JanelleTran TianaSanchez-Garcia EmilyChen ChaoGu YusuFang Xi - Modulating the equilibrium between glucose metabolism and fatty acid metabolism represents highly promising novel strategies for therapy of myocardial ischemia/reperfusion (I/R) injury. Sphingosylphosphorylcholine (SPC), an intermediate metabolite of sphingolipids, has shown cardioprotective roles during myocardial infarction by regulating the activities of various transcript factors. Gene microarray revealed that SPC significantly upregulated the expression of GATA zinc finger domain protein 1 (GATAD1), which is a vital transcript factor affecting heart development and various heart diseases. However, it remains unclear whether SPC is involved in the regulation of cardiac fatty acid and glucose metabolism via GATAD1. In this study, we found that myocardium-specific Gatad1 knockout (Gatad1 CKO) significantly increased the myocardial infarct size, impaired cardiac function in I/R mice, and disrupted the protective effect of SPC on the hearts of I/R mice. Immunofluorescence experiment and Western blot evaluation of the nuclear-cytoplasmic fractionation sample showed that GATAD1 acted as a transcription factor and was regulated by SPC. Double fluorescence reporting experiment and quantitative polymerase chain reaction (qPCR) revealed that GATAD1 could inhibit the expression of genes involved in fatty acid oxidation (FAO), i.e., acetyl-coenzyme A acyltransferase 2 (Acaa2) and medium-chain acyl-CoA dehydrogenase (Acadm), and promoted the expression of genes involved in glucose oxidation, i.e., pyruvate dehydrogenase E1 α subunit (Pdha1). Small interfering RNA (SiRNA) or overexpression strategies confirmed the pro-apoptotic roles of Acaa2 and Acadm and anti-apoptotic role of Pdha1 in cardiac myocytes challenged with I/R treatment. In summary, our findings suggest that SPC can be used as a candidate to prevent I/R injury by reshaping fatty acid and glucose metabolism. Transcription factor GATAD1 plays a crucial role in regulating fatty acid oxidation and glucose oxidation homeostasis and is involved in SPC-mediated cardioprotection during I/R of the heart. Our study identifies GATAD1 as a new therapeutic target for clinical treatment of myocardial I/R injury. - Source: PubMed
Publication date: 2024/12/01
Cai YuqingYu YifanZhang TianliangQian BaoshuoWang BenlongYan WenxiuZhao Jing