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
- Inflammation is a pivotal driver of the progression from metabolic dysfunction-associated steatotic liver disease (MASLD) to metabolic dysfunction-associated steatohepatitis (MASH), an aggressive form associated with substantial liver-related mortality. However, the molecular mechanisms underlying the initiation and persistence of liver inflammation remain poorly defined. Here, we demonstrated a previously unrecognized role for hepatic acetyl-CoA synthetase short-chain family member 2 (ACSS2) in MASH, showing that ACSS2 upregulation in patients exacerbates MASH progression by functioning as an epigenetic regulator, independent of its canonical lipogenic role. Mechanistically, ACSS2, in complex with lysine acetyltransferase 5 (KAT5), upregulates allograft inflammatory factor-1 (AIF1) transcription via histone crotonylation, thereby inducing liver inflammation and subsequently resulting in the aberrant accumulation of senescent hepatocytes, which further enhances proinflammatory cytokine production. This ultimately initiates a vicious cycle of chronic inflammation, which directly promotes the progression from simple steatosis to MASH. Thus, our work reveals a mechanistically defined and pivotal role for ACSS2 in promoting the MASLD-to-MASH transition, highlighting its potential as a compelling therapeutic target. - Source: PubMed
Publication date: 2026/07/25
Wen XiaoWu KeyanWang MengyaoMa ZihanWang TaoZhang JingWang BeiChen SiyuanWang JingyiChen SiyueYang FanLiu ChuweiChen XianyangDeng LuCheng YafanMiao Qing RobertSun BaofaRuan XiongzhongLi KaiDuan YajunHu Wenquan - Thyroid cancer (THCA) is the most common endocrine malignancy worldwide, understanding the pathophysiological mechanism is vital for developing effective strategies for prevention, diagnosis, and treatment. In this study, paired tumor and adjacent noncancerous tissues were collected from THCA patients. Cell viability and proliferation were assessed using CCK-8 and EdU assays. Cell migration and invasion were evaluated by wound healing and Transwell assays. Co-immunoprecipitation was performed to examine RNF123-mediated KAT5 ubiquitination, and chromatin immunoprecipitation was used to assess KAT5 enrichment at the PSPC1 promoter. An experimental lung metastasis model was established to evaluate the effects of RNF123 overexpression on tumor growth and pulmonary metastasis. RNF123 was down-regulated in THCA tissues and cell lines, and its overexpression suppressed cell viability, proliferation, migration, and invasion. KAT5 and PSPC1 were up-regulated in THCA cells. KAT5 knockdown inhibited THCA malignant behaviors. Mechanistically, RNF123 promoted the ubiquitination and degradation of KAT5, thereby reducing KAT5-mediated histone acetylation at the PSPC1 promoter and subsequent IGF1R up-regulation. In conclusion, RNF123 inhibited THCA malignant phenotype by promoting KAT5 ubiquitination and degradation, which reduced KAT5-mediated histone acetylation at the PSPC1 promoter, thereby down-regulating PSPC1 and IGF1R expressions. - Source: PubMed
Publication date: 2026/08/23
Guo LinJiang SenheWang XuehanFeng YirenJin Gang - Polycystic ovary syndrome (PCOS) is characterized by oxidative stress (OS). This study reveals a novel epigenetic mechanism linking lysine acetyltransferase 5 (KAT5) and thrombospondin-1 (TSP-1) in PCOS pathogenesis. A meta-analysis of 50 clinical studies demonstrated elevated systemic oxidative markers (total oxidant status, nitric oxide, malondialdehyde) and reduced paraoxonase-1 levels in PCOS patients, alongside compromised total antioxidant capacity in follicular fluid. Bioinformatic analysis identified TSP-1 as a key downregulated gene in PCOS, and the hTFtarget database predicted KAT5 as an upstream regulator of TSP-1. In vitro, H₂O₂-induced oxidative stress in KGN granulosa cells suppressed TSP-1, KAT5, and H2AK5ac levels, which were restored by N-acetylcysteine (NAC). Mechanistically, KAT5 was found to regulate TSP-1 expression via H2AK5 acetylation at its promoter. Knockdown of KAT5 exacerbated oxidative stress, apoptosis, and senescence, while TSP-1 overexpression counteracted these effects. In a letrozole-induced PCOS rat model, ovarian tissues exhibited decreased H2AK5 acetylation, reduced KAT5 and TSP-1 expression, and impaired redox homeostasis. Interventions with N-acetylcysteine or TSP-1 ameliorated ovarian pathological changes, hormonal imbalances, oxidative stress, apoptosis, and cellular senescence. Collectively, these findings establish the KAT5-TSP-1 axis as a critical regulator of ovarian redox homeostasis, unveiling a novel epigenetic mechanism and proposing a dual-target therapeutic strategy for PCOS. - Source: PubMed
Publication date: 2026/07/21
Jin QiuYang WeiWang ChaoLiu YuWang RuijingLiu LiZhang XianghanYan JinLiu Meimei - A rapid DNA damage response (DDR) and efficient DNA repair are essential for maintaining genome integrity. As a central apical kinase, ATM phosphorylates multiple downstream substrates to initiate DDR signaling and coordinate DNA repair following double-strand breaks (DSBs). However, the precise molecular mechanisms underlying ATM activation remain incompletely understood. Here, we identify the RNA-binding protein RALY as a critical regulator of ATM activation. We show that RALY directly interacts with and stabilizes the acetyltransferase Tip60, a key activator of ATM. Mechanistically, RALY competes with Tip60 for binding to the E3 ubiquitin ligase Mdm2, thereby inhibiting Mdm2-mediated ubiquitination and degradation of Tip60. Functionally, inhibition of RALY impairs ATM activation, compromises DNA repair capacity, and enhances radiosensitivity of cancer cells in a Tip60-dependent manner. Our findings uncover a previously unrecognized role of RALY in regulating ATM activation and indicate RALY as a potential therapeutic target for enhancing radiosensitivity in cancer. - Source: PubMed
Publication date: 2026/07/21
Yao BoZhao KailiangYu NingWang NingChang YinianLuo LinzhuWang FangMei Yide - Cisplatin resistance is a major barrier to effective treatment of squamous cell carcinoma (SCC) including cutaneous SCC and Head and neck SCC, where resistance develops in more than half of advanced cases. Our previous work demonstrated that genetic knockdown or pharmacological inhibition of TIP60 (KAT5), a histone acetyl transferase, sensitizes cisplatin-resistant SCC cells, induces cell cycle arrest and promotes cell death, suggesting a key role for TIP60 in mediating resistance. Here, we use cisplatin-sensitive and -resistant SCC cell lines, together with siRNA-mediated gene silencing, stable overexpression, pharmacological inhibition, immunodot-blot assays, and ICP-MS to demonstrate that TIP60 promotes resistance through two complementary pathways: (1) upregulation of the efflux transporter ABCC1, which reduces intracellular cisplatin accumulation, and (2) increased expression of XPC, a key component of the nucleotide excision repair pathway, involved in recognition and removal of cisplatin-DNA adducts. Elevated TIP60 levels correlate with reduced cisplatin-DNA adduct levels, enhanced removal of cisplatin-DNA adducts and increased cell survival in resistant lines. TIP60 depletion reduces ABCC1 expression and increases cisplatin-DNA adduct levels, effects similarly observed with the ABCC1 inhibitor, MK-571. In parallel, TIP60 knockdown impairs removal of cisplatin-DNA adducts and reduces expression of multiple DNA damage response (DDR) genes, including XPC. Combined inhibition of TIP60 with spironolactone (targeting XPB/NER) or with MK-571 further reduces cell survival and increases cell death in resistant cells. These findings establish TIP60 as a regulator of cisplatin resistance that integrates drug efflux and DNA repair pathways, highlighting TIP60 inhibition as a promising therapeutic strategy to overcome platinum resistance in SCC. - Source: PubMed
Publication date: 2026/07/16
Hira AkshayCraig Michael PMcLaughlin CarolineZhang JinTurchi John JKemp Michael GNahhas Ramzi WKadakia Madhavi P