ACTL6A Recombinant Protein
- Known as:
- ACTL6A Recombinant Protein
- Catalog number:
- XW-RP3003
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ACTL6A Recombinant Protein
Related genes to: ACTL6A Recombinant Protein
- Gene:
- ACTL6A NIH gene
- Name:
- actin like 6A
- Previous symbol:
- -
- Synonyms:
- Actl6, BAF53A, Arp4, Baf53a, INO80K
- Chromosome:
- 3q26.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-12
- Date modifiied:
- 2015-11-17
Related products to: ACTL6A Recombinant Protein
Related articles to: ACTL6A Recombinant Protein
- - Source: PubMed
Publication date: 2026/01/05
Kwok AngiePapke David JOdintsov Igor - Lung cancer is one of the deadliest cancers in the world with non-small cell lung cancer (NSCLC) being the most common subtype. Although advanced NSCLC patients undergone comprehensive treatment, their prognosis remains poor. Recent studies have elucidated that actin-like 6 A (ACTL6A) is aberrantly elevated in various cancers and acts as a driver of tumor progression. However, the main effect and mechanism of ACTL6A on NSCLC remains obscure. - Source: PubMed
Publication date: 2025/11/11
Cui LuyunZhao ShunjinLu GuohuaZhang ShumengZhang RuhuiZhou JianyingYao Yinan - Cilia are vital subcellular organelles whose assembly is regulated by master transcription factors, such as Foxj1 and Rfx. However, the mechanisms of epigenetic regulation over cilia stability remain largely unclear. Here, we investigate epigenetic control by manipulating chromatin-remodeling genes in zebrafish. We demonstrate that the depletion of multiple components of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex induces ciliopathy-like phenotypes in zebrafish embryos. Specifically, the loss of Actl6a, an essential component of the SWI/SNF complex, leads to cilia disassembly and cystic kidney defects, without affecting ciliary motility. Our multi-omics analyses (RNA-seq, ATAC-seq, and FitCUT&RUN) consistently reveal that in Actl6a-depleted pronephros or embryos, a critical set of ciliary genes, including the master regulators foxj1a and rfx2, exhibit concordant downregulation across the transcriptional level, chromatin accessibility, and SWI/SNF binding. Consistently, the depletion of foxj1a or rfx2 causes cilia assembly defects and cystic kidney formation in zebrafish. Furthermore, overexpression of either foxj1a or rfx2 mRNA substantially rescues the cystic kidney and cilia disassembly defects observed in actl6a mutant embryos. Collectively, these findings reveal that the SWI/SNF complex maintains cilia stability and kidney homeostasis by directly modulating the expression of the key ciliogenesis transcription factors foxj1a and rfx2. - Source: PubMed
Publication date: 2025/11/08
Cheng XiaoyuZhu QianshuMa ShilinPeng XiaoyuHuang GuanliangLiu GuifenZhang WentaoZhang YongJiang CizhongQiu AndongCao Ying - Actin-like protein 6A (ACTL6A) is thought to be associated with the survival and prognosis of patients with a variety of human cancers. This study investigates the effect of ACTL6A knockdown on ESCC radiosensitivity and explores molecular mechanisms that may enhance radiotherapy efficacy. The ACTL6A expression level was increased in esophageal squamous carcinoma cells after radiation irradiation. The protein expression level of ACTL6A in tumor tissue samples of clinical esophageal squamous cell carcinoma patients was analyzed by immunohistochemistry, and it was found that the prognosis of the high expression group was worse than that of the low expression group. Further knocking down the ACTL6A gene in esophageal squamous cell carcinoma cells, it was found that ACTL6A could regulate the proliferation, migration, invasion, DNA damage repair, cell cycle, and apoptosis of esophageal squamous cell carcinoma cells, which further affected the radiosensitivity of esophageal squamous cell carcinoma cells. Through functional enrichment analysis of gene set enrichment and validation of the mechanism using the Wnt pathway inhibitor XAV939, it was shown that ACTL6A is involved in the regulation of the Wnt/β-catenin signaling pathway. Knockdown of ACTL6A can inhibit the activity of this pathway, thereby increasing the radiosensitivity of esophageal squamous cell carcinoma. ACTL6A may become an important therapeutic target for esophageal squamous cell carcinoma, providing a necessary theoretical basis for future treatment strategies. - Source: PubMed
Zhou ShuoSun TongyouLiu LikunGuo DongZhang XueyuanShen WenbinGao ShaolinZhu Shuchai - Chromatin factors, defined here as proteins that chemically modify the DNA and histones, remodel chromatin and regulate nucleosome occupancy, play central roles in the transcriptional regulation of genes and are implicated in cancer initiation and progression in multiple cancer types. To systematically investigate the genomic and expression alterations of chromatin factors in head and neck squamous cell carcinoma (HNSCC), we utilized the molecular profiles from 530 HNSCC tumor samples in the Cancer Genome Atlas (TCGA), and characterized the mutational, copy number and transcriptional alterations of 422 chromatin factors, as well as their correlation with the "cold" tumor phenotype in HPV-negative and HPV-positive HNSCC. Histone-lysine N-methyltransferase 2D (MLL2) was the most frequently mutated chromatin factor in both HPV-negative and HPV-positive HNSCC, with mutation frequencies of 12-17 %. Actin Like 6A (ACTL6A), a component of the SWI/SNF chromatin remodeling complex, was the most frequently copy-number amplified chromatin factor in both HPV-negative and HPV-positive HNSCC, with amplification frequencies of 19-24 %. Double PHD Fingers 1 (DPF1), a component of the chromatin remodeling complex, and Ubiquitin Like With PHD AndRing Finger Domains1 (UHRF1) were the most overexpressed chromatin factors in HPV-negative and HPV-positive HNSCC tumors respectively. Components of the chromatin remodeling complex, such as ACTL6A, SMARCA1 and MORF4L2, were correlated with the "cold" tumor phenotype in both HPV-negative and HPV-positive HNSCC. This brief study highlights epigenetic chromatin factors that may drive oncogenesis and immune evasion, thereby identifying novel targets for cancer therapy in clearly defined, epigenetically-driven subtypes of HPV-negative and HPV-positive HNSCC. - Source: PubMed
Publication date: 2025/09/19
Cheng HuiJiang MeiyeKim SohyoungMoshiri ArfaDar Mohd SaleemAkhtar JawadSaloura Vassiliki