Polyclonal Rabbit AATF Antibody
- Known as:
- Polyclonal Rabbit AATF Antibody
- Catalog number:
- KA0037
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit AATF Antibody
Related genes to: Polyclonal Rabbit AATF Antibody
- Gene:
- AATF NIH gene
- Name:
- apoptosis antagonizing transcription factor
- Previous symbol:
- -
- Synonyms:
- DED, CHE-1, CHE1, BFR2
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-13
- Date modifiied:
- 2015-01-29
Related products to: Polyclonal Rabbit AATF Antibody
Related articles to: Polyclonal Rabbit AATF Antibody
- 17q12 microdeletion syndrome is a rare genetic disorder distinguished by diabetes, urogenital abnormalities, pancreatic hypoplasia, and neuropsychiatric developmental anomalies, with hyperuricemia being an infrequent occurrence. We present a unique case of 17q12 microdeletion, encompassing 17 protein-coding genes such as HNF1B, AATF, and DDX52 (3A:0), marking the first documented instance globally. - Source: PubMed
Publication date: 2026/03/25
Yang YueShen ZiyanZhang LiGuo WeiGong ShaominCai JieruWang JiayiYuan ShuangxinDing XiaoqiangZhang Xiaoyan - The ability of cancer cells to promote cellular proliferation by preferentially using glycolysis as primary source of energy has long been considered a hallmark of tumour metabolism. However, emerging evidence suggests a more complex situation with many tumours exhibiting a pronounced dependence on mitochondrial respiration through oxidative phosphorylation (OXPHOS) for their development and maintenance. In line with this, numerous studies have reported an upregulation of mitochondrial genes and OXPHOS components across multiple cancer types. Glioblastoma (GBM) is the most frequent and malignant brain tumour in adults, characterised by rapid proliferation, resistance to therapy and ability to recur. In addition to a profound genetic and molecular heterogeneity, GBM also exhibits strong metabolic heterogeneity with different grades of dependence on mitochondrial activity. Notably, the transcription factor Nuclear Respiratory Factor 1 (NRF-1), a key regulator of OXPHOS gene expression and mitochondrial functions, has recently been linked to GBM progression and poor prognosis. Che-1/Apoptosis Antagonising Transcription Factor (AATF) is a transcriptional regulator with a crucial role in several cancer types, where it contributes to tumorigenesis by promoting cell cycle arrest and apoptosis, as well as resistance to therapy. Here, we show that AATF expression correlates with clinical outcome in GBM patients. Moreover, we demonstrate that its depletion leads to cell cycle arrest, impaired mitochondrial respiration and disrupted mitochondrial architecture in GBM cells. Additionally, AATF-depleted cells exhibit a reduced ability to form colonies in vitro and tumour in vivo. At the molecular level, we provide evidence that AATF interacts with NRF-1 and is essential for NRF-1-mediated transcription of the OXPHOS genes by affecting RNA polymerase II recruitment and chromatin structure. Overall, our findings highlight a previously unrecognised role of AATF in GBM proliferation and mitochondrial metabolism supporting its potential as a target for therapeutic intervention. - Source: PubMed
Publication date: 2026/03/24
Sorino CristinaDi Giovenale StefanoFalcone ItaliaAuciello Francesca RomanaPulito ClaudioLo Sardo FedericaScalera StefanoDe Nicola FrancescaCatena ValeriaCiuffreda LudovicaArteni Brindusa Ana MariaGiuliani StefanoAmadio BrunoBlandino GiovanniFanciulli MaurizioIezzi Simona - Metabolic dysfunction-associated steatohepatitis (MASH) is a multifactorial disease driven by complex molecular mechanisms. Identifying key regulators is critical for developing targeted therapies. Here, we demonstrate the impact of the loss of the apoptosis-antagonizing transcription factor (AATF) on hepatic lipid metabolism and MASH progression. - Source: PubMed
Publication date: 2026/01/13
Srinivas Akshatha NSuresh DiwakarAnirvan PrajnaMoorthy ManjuRamaswamy GopalkrishnaNataraj Suma MSanthekadur Prasanna KumarSuvarna DeepakSingh Shivaram PKumar Divya P - The study aimed to investigate the role of apoptosis-antagonizing transcription factor (AATF) in regulating endoplasmic reticulum (ER) stress-ferroptosis interaction and its neuroprotective mechanism in cerebral ischemia-reperfusion injury (CIRI). - Source: PubMed
Publication date: 2025/11/10
Lei BoLuo WenzhangLi QinjingWu HonggangChen LiChen ShuWu JiachuanZheng Niandong - Early-onset hippocampal sclerosis is a major cause of focal epilepsy, yet many genetic contributors remain unknown. We investigate a 12-year-old girl with recurrent focal seizures, progressive memory impairment, and MRI evidence of left hippocampal atrophy with ipsilateral parietal gliosis. Singleton exome sequencing revealed a novel homozygous NOL10 variant (NM_024894.4: c.682 A > C; p.Asn228His), absent from population and clinical databases; both parents were heterozygous carriers. The variant alters a highly conserved residue within the WD-repeat domain. Proband fibroblasts maintained normal NOL10 transcript levels but exhibited nucleoplasmic mislocalization and loss of interaction with AATF and NGDN, key partners in small ribosomal subunit biogenesis. Structural modeling and ΔΔG calculations predicted that N228H is strongly destabilizing. Functionally, proband cells showed specific impairment of 40S maturation with reduced 40S, 80S and polysome content, accompanied by G/G arrest and increased cell death. Network and expression analyses place NOL10 at the center of nucleolar rRNA processing and ribosome assembly, with substantial expression across hippocampal subfields, supporting selective vulnerability of hippocampal neurons. Collectively, our data implicate biallelic NOL10:c.682 A > C as a novel, likely pathogenic cause of neurodevelopmental disorder characterized by hippocampal sclerosis and gliosis, and highlight disrupted ribosome biogenesis as a plausible disease mechanism. - Source: PubMed
Publication date: 2025/10/16
Kumar AbhishekGaurav VishalMathuria Yogendra PratapJain Buddhi PrakashGupta Shailesh KumarGhosh Debasish Kumar