ATF7 Antibody
- Known as:
- ATF7 Antibody
- Catalog number:
- AF1124a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ATF7 Antibody
Related genes to: ATF7 Antibody
- 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
Related articles to: ATF7 Antibody
- We report a case of a 28-year-old man who presented with a slowly enlarging intramuscular mass in left posterior neck. Imaging demonstrated a relatively well-circumscribed mass with focal scattered calcifications. Histologic examination revealed a lobulated neoplasm composed of monotonous round to ovoid to spindle shaped tumor cells arranged in large nodules, loose fascicles, and solid nests within a sclerotic fibrous stromal background. Focal metaplastic bone formation and rare calcification were identified. No significant cytologic atypia, increased mitotic activity or necrosis was identified. The tumor showed immunophenotypic evidence of rhabdomyoblastic differentiation. Molecular studies identified a novel EWSR1::ATF7 fusion and methylation profiling yielded no matching classes. Overall, the findings favor classification as a fusion-associated spindle cell rhabdomyosarcoma. However, additional studies involving a larger number of cases will be required to confirm its classification as such and to better define its biologic behavior. - Source: PubMed
Publication date: 2026/09/01
Neyaz AzfarGestrich Catherine KBerning AricElmoryah Mohamed MZeitlinger LaurenJohn Ivy - Chronic, non-healing wounds are a severe diabetic complication. The underlying mechanisms are not fully understood, and the role of ATF7 in this context has not been well characterized. In our study, we utilized db/db diabetic mice and AAV-mediated keratinocyte-specific Atf7 overexpression in vivo. HaCaT keratinocyte/THP-1 macrophage cocultures under high glucose were used in vitro. Our results showed that ATF7 was upregulated in diabetic wounds. Keratinocyte-specific Atf7 overexpression accelerated diabetic wound closure, enhanced re-epithelialization, granulation tissue formation, and keratinocyte proliferation, while suppressing macrophage M1 polarization and inflammation. Multiomics screening identified NOTCH1 as a key ATF7 target. ATF7 transcriptionally repressed NOTCH1 by recruiting Suv39h1, increasing H3K9me3 at the NOTCH1 promoter. This reduced NOTCH1 protein and its active intracellular domain (N1ICD) within keratinocyte-derived exosomes. ATF7-overexpressing keratinocyte exosomes carried less N1ICD, leading to decreased N1ICD transfer to macrophages and subsequent inhibition of M1 polarization. Notably, local injection of exosomes from ATF7-overexpressing keratinocytes accelerated wound healing in db/db mice. In summary, ATF7 promotes diabetic wound healing by repressing NOTCH1 transcription via H3K9me3, thereby reducing exosomal N1ICD secretion from keratinocytes and inhibiting macrophage M1 polarization. This identifies the ATF7/NOTCH1/exosome axis as a therapeutic target. - Source: PubMed
Publication date: 2026/08/24
Xu PengchengXue YuanFeng LinlinKuang JingwenHu XiaochenTang HuiyiCheng BiaoWei Limin - 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