KAT5 Antibody Autophagy Antibody
- Known as:
- KAT5 Antibody Autophagy Antibody
- Catalog number:
- AUT-7339
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- KAT5 Antibody Autophagy
Related genes to: KAT5 Antibody Autophagy Antibody
- Gene:
- KAT5 NIH gene
- Name:
- lysine acetyltransferase 5
- Previous symbol:
- HTATIP
- Synonyms:
- TIP60, PLIP, cPLA2, HTATIP1, ESA1, ZC2HC5
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-04-13
- Date modifiied:
- 2016-10-05
Related products to: KAT5 Antibody Autophagy Antibody
Related articles to: KAT5 Antibody Autophagy Antibody
- Spinal stenosis is a common pathological condition characterized by the narrowing of the spinal canal, contributing to substantial morbidity and imposing a significant socioeconomic burden. Despite its clinical importance, the genetic drivers and cellular mechanisms driving its progression remain inadequately understood, necessitating integrative approaches to identify therapeutic targets. - Source: PubMed
Publication date: 2026/04/01
Xia DemengChen YongjieWu RuiTang YifanSun YanqingChen Xiongsheng - Sepsis induced myocardial injury (SIMI) remains a life threatening complication with mortality rates exceeding 40% to 50%, yet effective therapies are lacking. This study investigates the cardioprotective effects of eupatilin (EUP), a bioactive flavonoid derived from Artemisia argyi, and reveals a previously unrecognized mechanism involving selective modulation of KAT5 mediated histone H3K27 lactylation (H3K27la). Using an LPS induced murine model and TNF-α stimulated human AC16 cardiomyocytes, we evaluated cardiac function, inflammatory responses, and apoptotic pathways through dose response analyses. Multi omics approaches including RNA seq, metabolomics, ChIP seq, and molecular docking were integrated to dissect the pharmacodynamic profile of EUP. EUP conferred concentration dependent cardioprotection with optimal effects at 25 μM. Compared with conventional glucocorticoid therapy, EUP showed enhanced target selectivity, markedly reducing pro inflammatory cytokines such as TNF-α, IL-1β, and IL-6 while improving cardiac function parameters including ejection fraction and fractional shortening. Mechanistically, EUP bound KAT5 with high affinity, suppressed its lactylation activity, and reduced H3K27la enrichment at the promoters of inflammatory genes. Metabolic flux analysis further indicated that EUP inhibited glycolytic lactate production and restored oxidative phosphorylation. Together, these findings identify EUP as a natural modulator of the KAT5-H3K27la axis, addressing both metabolic dysregulation and epigenetic reprogramming in SIMI. With a favorable pharmacokinetic profile and superior target specificity relative to standard immunosuppressive regimens, EUP holds promise for clinical translation in sepsis associated cardiac dysfunction. - Source: PubMed
Du QianqianHou ShuwanLiu MinfuWu JiaqinYu HuimingFeng FanLiang HuapingWang ChunliXu KangChi Qingjia - Breast cancer (BC) remains the leading cause of global female cancer-related mortality, with poor survival in advanced stages driven largely by metastasis. Ubiquitination, a key post-translational modification, critically regulates the stability and function of various proteins, including oncoproteins and tumor suppressors, and deubiquitinases (DUBs) reversing this process are emerging therapeutic targets. In this study, we report that haploid germ cell-specific nuclear protein kinase (HASPIN) is highly expressed in BC and is closely associated with poor prognosis. We identify the DUB Otubain-2 (OTUB2) as a critical regulator of the oncogenic kinase HASPIN in BC. We demonstrate that OTUB2 binds to and deubiquitylates HASPIN, specifically counteracting its K48-linked polyubiquitination and subsequent proteasomal degradation. Acetylation of HASPIN at lysine 751 by acetyltransferase lysine acetyltransferase 5 (KAT5) enhances its affinity for OTUB2, promoting HASPIN stability. Functionally, OTUB2 depletion reduces HASPIN protein levels, while OTUB2 overexpression-induced HASPIN upregulation drives BC cell proliferation and invasion both in vivo and in vitro. These findings establish OTUB2 as a novel DUB for HASPIN and reveal a previously unknown regulatory axis involving KAT5, acetylation, OTUB2, ubiquitination, and HASPIN, which is crucial for BC progression. Consequently, HASPIN acts as an oncogene in BC and represents a promising new therapeutic target for intervention. - Source: PubMed
Publication date: 2026/03/27
Guo JianiKang KangWang ShiqiJi ZhuqingLi HaoxuanZhu YifanSong WeiHuang Mingde - Discovery of therapeutic targets for hepatocellular carcinoma (HCC) is urgently needed. As an important hepatitis B virus (HBV) oncoprotein, pre-S2 mutant activates multiple signalling pathways to induce HCC development. - Source: PubMed
Lin Yueh-TeJeng Long-BinShih Fu-YingTeng Chiao-Fang - Cases of idiopathic male infertility may be caused by as-yet unrecognized genetic factors. Here, we report that the testis-specific protein coiled-coil glutamate-rich protein 1 (CCER1) regulates male fertility through the formation of a dynamic membraneless organelle within the spermatid nucleus. Using a humanized CCER1 knock-in mouse line, we demonstrate that CCER1 function is conserved between mice and humans. Next, we generated Ccer1-Tag knock-in mice and analyzed CCER1-interacting proteins using immunoprecipitation-mass spectrometry. We found that CCER1 nuclear aggregates may provide a 'reaction compartment' for the mutual recruitment of TIP60 and/or EPC1 subunits to the acetyltransferase NuA4 complex. Conversely, disruption of CCER1 droplets impairs the recruitment and interaction of TIP60 and EPC1 subunits, leading to reduced histone H4 hyperacetylation in nucleosomes, defective DNA strand breakage and insufficient histone-to-protamine (HTP) replacement during spermiogenesis. In conclusion, our data indicate that the TIP60/EPC1/NuA4-CCER1 complex is involved in the epigenetic regulation of HTP replacement in the testis, providing new insights into the genetic and epigenetic etiology of male infertility. - Source: PubMed
Publication date: 2026/02/26
Wang ShuChen YuanTang JinyanZhang TaoQin DongdongXu WeiyaWu Xin