Ask about this productRelated genes to: MYST2 antibody
- Gene:
- KAT7 NIH gene
- Name:
- lysine acetyltransferase 7
- Previous symbol:
- MYST2
- Synonyms:
- HBOA, HBO1, ZC2HC7
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-03
- Date modifiied:
- 2016-10-05
Related products to: MYST2 antibody
Related articles to: MYST2 antibody
- Mosquitoes, especially Aedes aegypti, transmit major human diseases such as dengue, Zika, and chikungunya. Epigenetic regulation, including histone acetylation, plays a key role in controlling Ae. aegypti development. However, the specific roles of histone acetyltransferases (HATs) and N-terminal acetyltransferases (NATs) in mosquito development remain poorly understood. In this study, we investigated 25 HAT/NAT genes functions by knocking them down via feeding Ae. aegypti larvae with dsRNA nanoformulations. Gene expression analysis confirmed that target gene expression was reduced by more than 50% in dsRNA-treated larvae. Knocking down 18 of these HATs/NATs resulted in over 50% mortality. Silencing KAT7, NATSCAN, NAT9, ATAT1, and TADA3 caused larval death, whereas knockdown of NAA80, NAA-Eco, GNPNAT1, HAT-B, and MCM3AP led to pupal mortality. Knockdown of NATSCAN, NF, TFIID, GNPNAT1, and NAA16 resulted in molting and metamorphic defects, characterized by untanned cuticles and failure to complete successful larval-pupal metamorphosis. Phylogenetic analysis of conserved domains of HATs and NATs revealed that evolutionarily conserved members cluster into distinct clades associated with larval- or pupal-specific functions. Developmental expression analysis showed stage-specific expression of these genes. Further, stage-specific expression analysis revealed that dynamic expression patterns of KAT7, RNACAT, NAT9, and NF are linked to larval growth and pupal metamorphosis. Treatment with 20-hydroxyecdysone (20E) or an ecdysone agonist increased mRNA levels of NAA30,NAA40,NAT9, and GNAT8, indicating hormonal control of histone acetylation. Ecdysone-induced HATs/NATs regulated the expression of primary ecdysone response genes: E75A and E93. These results demonstrate that HATs/NATs play key roles in Ae. aegypti development and therefore could serve as potential targets for mosquito control. - Source: PubMed
Publication date: 2026/04/27
Gaddelapati Sharath ChandraPalli Subba Reddy - Mutations in SETBP1 are associated with adverse prognosis in myeloid malignancies. These mutations stabilize SETBP1 protein, driving increased expression of a progenitor-associated gene expression program through incompletely described mechanisms. A proteomic screen revealed interactions between SETBP1 and MYST acetyltransferase complexes, including the catalytic subunits-KAT6A and KAT7. In cell line and primary hematopoietic models, mutant SETBP1 increased the localization of MYST complexes at known SETBP1 target genes, including the HOXA cluster, where they were shown to drive increased histone acetylation and gene expression. Treatment of SETBP1D868N-expressing myeloid progenitors with MYST inhibitors reduced target gene expression. To establish the efficacy of MYST inhibition in vivo, we treated mice harboring a syngeneic SETBP1-mutant leukemia with the clinical-grade MYST inhibitor-PF-9363. This resulted in hematologic control and increased survival. MYST inhibition was also highly effective against a SETBP1-mutant PDX model. These studies identify MYST acetyltransferases as promising therapeutic targets in SETBP1-mutant malignancies. - Source: PubMed
Publication date: 2026/04/19
Carlson Hanqian LNguyen Thai TTauchmann SamanthaCarratt Sarah AKruer Traci LDankyi Nana AdjoaBalasis Maria EKim HyeyoonTsai Chia-FengLiu TaoShrestha Shawn BFischer Jared MPadron EricBraun Theodore PMaxson Julia E - EGFR amplification frequently occurs within extrachromosomal DNAs (ecDNAs) and is the most prevalent mutation in glioblastoma (GBM). However, targeting EGFR for GBM treatments has been unsuccessful. Here we show a long non-coding RNA (lncRNA) that is co-amplified with EGFR, which we name hidden EGFR long non-coding downstream RNA (HELDR). HELDR is a GBM-selective lncRNA that promotes tumorigenicity independent of EGFR signalling. HELDR exhibits widespread chromatin association and recruits the transcription co-activator p300 to the KAT7 promoter. p300-induced H3K27ac at the KAT7 promoter enlists other co-transcription factors, activating KAT7 transcription. KAT7 induces H3K14ac and H4K12ac that activate KAT7-driven gene programmes that are critical for GBM malignancy. Targeting KAT7 or HELDR markedly enhances therapeutic effects of anti-EGFR treatments for GBM. These results not only reveal the role of HELDR in EGFR-amplified GBM but also provide a strong rationale to characterize the role of lncRNAs co-amplified with driver oncogenes in human cancers. - Source: PubMed
Publication date: 2026/03/27
Yu XiaozhouSong XiaoSchäfer Richard AMeng QingshuTiek DeannaWu RunxinHe QiuWalker MayaCao QiYang RendongHu BoCheng Shi-Yuan - Mitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer's disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5×FAD mice and human AD brains. Integrative transcriptomic and epigenomic analyses reveal that KAT7 activates transcription of , a mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces expression, impairs mtDNA replication and release, and consequently suppresses cGAS-STING and NLRP3 signaling. Importantly, both microglia-specific deletion and pharmacological inhibition of KAT7 mitigate cytosolic mtDNA-induced neuroinflammation, decrease amyloid-β burden, restore synaptic plasticity, and improve cognitive function in 5×FAD mice. Together, these findings uncover an epigenetic-mitochondrial axis sustaining microglial pathogenicity and establish KAT7 as a promising therapeutic target for AD. - Source: PubMed
Publication date: 2026/02/20
Liu YongqingFan MinghuaYe YingzhiCheng Henry YiSun ShuyingQiu Zhaozhu - Zinc is an indispensable micronutrient for optimal physiological functions, and zinc deficiency has been implicated in the pathogenesis of various human diseases. One potential mechanism underlying such pathogenic effects is the alteration of gene expression caused by zinc deficiency; however, the details of this process remain largely unexplored. Here, we show that during zinc deficiency, the histone acetyltransferase KAT7 loses its enzymatic activity, leading to the attenuated acetylation of histone H3 at Lys14 (H3K14ac) at enhancer regions. Physiologically, the decrease in H3K14ac leads to the upregulation of the expression of ZIP10, a plasma membrane-localized zinc transporter, thereby facilitating the import of extracellular zinc to maintain cellular zinc homeostasis. Moreover, prolonged zinc deficiency in mice induced by a zinc-deficient diet or high-fat diet, accompanied by decreased H3K14ac levels in the liver, upregulated the expression of genes associated with intracellular lipid droplet formation, leading to the accumulation of lipids within liver tissue. Our findings demonstrate that cells respond to zinc deficiency by converting it into an epigenetic signal that drives physiological or pathophysiological biological processes. - Source: PubMed
Publication date: 2026/02/17
Fujisawa TakaoTakenaka SatoshiMaekawa LilaOgawa MotoyukiKowada ToshiyukiMatsui ToshitakaMizukami ShinKato YugoSuzuki MichioNoma HisashiNaguro IsaoIchijo Hidenori