ATF7 antibody - N-terminal region (P100817_P050)
- Known as:
- ATF7 (anti-) - N-terminal region (P100817_P050)
- Catalog number:
- p100817_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ATF7 antibody - N-terminal region (P100817_P050)
Related genes to: ATF7 antibody - N-terminal region (P100817_P050)
- Gene:
- ATF7 NIH gene
- Name:
- activating transcription factor 7
- Previous symbol:
- -
- Synonyms:
- ATFA
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-13
- Date modifiied:
- 2016-01-15
Related products to: ATF7 antibody - N-terminal region (P100817_P050)
Related articles to: ATF7 antibody - N-terminal region (P100817_P050)
- The introduction of domestic cattle to the Philippines is often attributed to Spanish and Chinese sources, yet the origins and adaptive history of Philippine Visayan native cattle remain unclear. This study examined the ancestry, structure, and putative selection signals of the Visayan native cattle from Panay and Siquijor islands (VNC) in a global context. Using genome-wide SNP data, population structure was assessed by PCA, IBS/Nei/ trees, and ADMIXTURE; historical relationships were explored with migration, f-statistics, and an admixture graph; and positive selection was scanned using commonly used methods such as ROH, Tajima's , iHS/XP-EHH, and with cross-validation across methods and functional enrichment of the overlapping regions. VNC exhibited low-to-moderate genetic diversity (Ho and He ≈ 0.21; and FIS = 0.01 to 0.02) with Siquijor enriched for long ROH segments indicating recent inbreeding. Across multiple complementary analyses, VNC showed predominantly indicine ancestry and occupied an intermediate bridge-like position between indicine from mainland Southeast Asia and from Southeastern China, with additional components that were most similar to Iberian taurine cattle and South Asian indicine. Moreover, the current study identified putative selection signatures that would possibly provide insights to better understand the local adaptation of VNC under insular tropical conditions of the Philippines: (1) small stature ( cluster, , , , ), (2) heat tolerance and immune robustness (, , , , , ); (3) early reproductive and maturity reproductive performance (, , , ). Overall, the VNC in Panay and Siquijor showed a predominantly indicine ancestry with putatively island-adapted physiology, emphasizing the need for conservation and island-specific breeding that preserves local adaptation while managing inbreeding. - Source: PubMed
Publication date: 2026/02/09
Dominguez Jorge Michael DYebron Medino Gedeun NBanayo Joy BChen NingboSalces Agapita JKim Kwan Suk - Mitochondrial dysfunction plays a central role in epithelial damage and persistent inflammation in ulcerative colitis (UC), but the transcriptional mechanisms that govern mitochondrial quality control in the intestinal epithelium remain poorly defined. Here, we identify Activating Transcription Factor 7 (ATF7) as a key regulator of mitophagy in colonic epithelial cells. Integrative transcriptomic and epigenomic analyses of patient-derived mucosal samples revealed marked ATF7 downregulation and widespread activation of inflammatory pathways. Chromatin immunoprecipitation and luciferase reporter assays demonstrated that ATF7 directly binds to and activates the promoter of PINK1, a master regulator of mitophagy. Genetic ablation of ATF7 or PINK1 in human epithelial cells impaired mitophagy, disrupted mitochondrial membrane potential, and increased reactive oxygen species. In vivo, intestinal epithelial cell-specific knockout of ATF7 or PINK1 exacerbated dextran sulfate sodium-induced colitis, with greater epithelial injury, elevated cytokine production, and transcriptional activation of TNF, NF-kappaB, and inflammatory bowel disease signalling pathways. These results establish ATF7 as a critical transcriptional regulator linking mitochondrial homeostasis to epithelial resilience in the inflamed colon. - Source: PubMed
Liu FangChen YidongLi JiaminLi JunrongYu QiZhang XiaopengZhu Liangru - Ulcerative colitis (UC), a chronic inflammatory bowel disease, is marked by sustained inflammation and excessive apoptosis of intestinal epithelial cells (IECs). Despite progress in understanding UC pathogenesis, the role of activating transcription factors (ATFs) in disease progression remains elusive. Here, we profile the expression of ATF family members (ATF1-ATF7) in the colonic mucosa of UC patients and identify ATF7 as a critical regulator of mitophagy through its control of PTEN-induced kinase 1 (PINK1). Expression levels of ATF1-ATF7 were quantified in colonic mucosal samples from UC patients (n = 219) and healthy controls (n = 105) via quantitative PCR. Using IEC-specific ATF7 knockout mouse models and human CCD 841 CoN colonic epithelial cells, we employed ChIP-seq, dual-luciferase assays, transmission electron microscopy, and immunofluorescence to elucidate their roles in mitophagy and disease progression. Clinical correlation between ATF7 expression and disease severity was assessed using the Mayo score. ATF7 expression was significantly reduced in UC patients and inversely correlated with disease severity. Mechanistically, ATF7 was identified as a direct transcriptional activator of PINK1, a key mitophagy regulator. Loss of ATF7 or PINK1 disrupted mitophagy, exacerbating mitochondrial dysfunction, IEC apoptosis, and colonic inflammation in vivo and in vitro. Our findings uncover a pivotal ATF7-PINK1 axis that governs mitophagy and limits UC progression. The inverse correlation between ATF7 expression and UC severity highlights its potential as a therapeutic target, offering new avenues for intervention in this debilitating disease. - Source: PubMed
Chen YidongZhang XiaopengLi JunrongLiu FangYu QiLi JiaminZhu Liangru - -(1,3-Dimethylbutyl)-'-phenyl--phenylenediamine quinone (6-PPDQ) is widely distributed in the environment and bioavailable to organisms. Exposure to 6-PPDQ can impair the mitochondrial function. However, the underlying mechanisms for 6-PPDQ-induced mitochondrial dysfunction remain largely unclear. Mitophagy is important for organisms to maintain normal mitochondrial function. In the current study, was employed as model to determine the role of mitophagy suppression in 6-PPDQ-induced toxicity. After exposure to 6-PPDQ, it was found that, although mitophagy was increased by 0.1-1 μg L 6-PPDQ, 10 μg L 6-PPDQ downregulated the expression of genes involved in PINK1/Parkin-dependent mitophagy (-1, -1, and -1) and receptor-mediated mitophagy (-1 and -1). RNAi of these mitophagy-related genes enhanced the 6-PPDQ toxicity on mitochondrial function and lifespan. Moreover, after 6-PPDQ (10 μg L) exposure, 6-PPDQ could be accumulated in the nucleus and affected the expressions of some transcription factor (TF) genes (-5, -2, -7, -16, -1, and -1) thereby inducing the inhibition of these two types of mitophagy. Inhibition in both mitophagy and the mitochondrial unfolded protein response (mt UPR) caused more severe 6-PPDQ toxicity on the mitochondrial function and lifespan. Our results demonstrate the crucial role of mitophagy suppression in mediating the toxicity of 6-PPDQ, which is useful for predicting the environmental exposure risk of 6-PPDQ on organisms. - Source: PubMed
Publication date: 2025/07/16
Hua XinWang Dayong - SARS-CoV-2 can encode circular RNAs (circRNAs); however, the potential effects of exogenous SARS-CoV-2 circRNAs on cardiovascular sequelae remain unknown. Three circRNAs derived from the nucleocapsid (N) gene of SARS-CoV-2, namely, circSARS-CV2-Ns, were identified for functional studies. In particular, circSARS-CV2-N1368 was shown to enhance platelet adhesiveness to endothelial cells (ECs) and inhibit EC-dependent vascular relaxation. Moreover, exogenous expression of circSARS-CV2-N1368 suppressed EC proliferation and migration and decreased angiogenesis and cardiac organoid beating. Mechanistically, we elucidated that circSARS-CV2-N1368 sponged the microRNA miR-103a-3p, which could reverse circSARS-CV2-N1368-induced EC damage. Additionally, activating transcription factor 7 (ATF7) was identified as a target gene of miR-103a-3p, and Toll-like receptor 4 (TLR4) was verified as a downstream gene of ATF7 that mediates circARS-CV2-N1368-induced activation of nuclear factor kappa B (NF-κB) signaling and ROS production in ECs. Importantly, the reactive oxygen species (ROS) scavenger NAC mitigated the circSARS-CV2-N1368-promoted EC impairment. Our findings reveal that the TLR4/NF-κB/ROS signal pathway is critical for mediating circSARS-CV2-N1368-promoted oxidative damage in ECs, providing insights into the endothelial impairment caused by circSARS-CV2-Ns. - Source: PubMed
Publication date: 2025/03/11
Wen Yi-HongZhao Heng-LiWu Shao-YuJiang Jia-XueGao YuanWang Zi-FanLiu Xiao-YaoYu FeiOu TaoZhao An-ZhiChen Li-WenFang Jin-HuaWu Hua-YanZhu Jie-NingMa NingSun Jiu-FengFang Xian-HongShan Zhi-Xin