ACTL8 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- ACTL8 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00081569-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ACTL8 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: ACTL8 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- ACTL8 NIH gene
- Name:
- actin like 8
- Previous symbol:
- -
- Synonyms:
- CT57
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-19
- Date modifiied:
- 2019-03-22
Related products to: ACTL8 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: ACTL8 293T Cell Transient Overexpression Lysate(Denatured)
- Protein kinases are essential regulators of cellular signaling pathways and are deeply involved in breast cancer (BC) progression. This study aimed to identify BC molecular subtypes and construct a prognostic model based on kinase-related genes (KRGs). - Source: PubMed
Publication date: 2026/05/12
Ye ShuanglaiJi Shengwei - Endometrial cancer (EC) is a common gynecological tumor. Insulin resistance (IR) increases the risk of EC. However, the common molecular basis between the two remains unclear. This study aims to screen the common differential expression genes (DEGs) between the two diseases and construct a prognostic risk model. - Source: PubMed
Publication date: 2026/02/11
Lu SiyunXu JieSun XiaoXiaoYuan JieCheng JiajingQin Jinlong - Glutamine metabolism is a key driver of tumor progression, yet the molecular basis and prognostic relevance of glutamine metabolism-related genes in breast cancer (BC) remain incompletely defined. In this study, integrated analysis of public datasets identified Actin-like protein 8 (ACTL8) as a key prognostic gene significantly upregulated in BC tissue and associated with poor patient survival. In vitro, shRNA knockdown of ACTL8 reduced MYC expression and its downstream targets SLC1A5 and GLS1, suppressing cell proliferation, migration and invasion. This disruption led to impaired redox homeostasis as evidenced by reduced GSH/GSSG and NADPH/NADP ratios. Mechanistically, MYC overexpression restored metabolic enzymes and phenotypes but failed to rescue p-AKT levels, confirming ACTL8 acts upstream of the PI3K/AKT/mTOR axis. Virtual screening identified Momordin Ic as a small molecule that directly interacts with ACTL8. Surface plasmon resonance (SPR) and Thermal shift assay (TSA) confirmed this high-affinity binding, which destabilized ACTL8 and promoted its ubiquitin-proteasome degradation. Moreover, ACTL8 knockdown significantly attenuated the sensitivity of BC cells to Momordin Ic treatment, confirming ACTL8 as the specific therapeutic target. In vivo, suppression of ACTL8 markedly reduced tumor growth. Together, these findings establish ACTL8 as a key oncogenic driver of BC progression. Targeting ACTL8 offers a novel strategy to disrupt glutamine-dependent metabolic reprogramming, and Momordin Ic represents a promising lead agent to combat ACTL8-driven BC. - Source: PubMed
Publication date: 2026/01/30
Guo AoYang BijunHuang Aolin XiaoNi JieZhang YanhuiJiang QinlinYan YunwenLuo QichaoYang JingYuan Bin - Head and neck squamous cell carcinoma (HNSCC) is an aggressive malignant neoplasm with an increasing need for precision therapeutics. Cancer-testis antigens (CTAs) represent promising targets given their aberrant tumor expression and otherwise localized expression to immune-privileged tissues with no (testis-restricted) or minimal (testis-selective) expression in other human body sites. Despite their potential, limited studies rigorously evaluate CTAs as therapeutic targets in HNSCC. - Source: PubMed
Memon Abdullah AAwan Musaddiq JEspinosa Oscar VillarrealKuehn RachelFrei AnneFoeckler JamieBruening JenniferAkakpo KennethMassey BeckyStadler MichaelWong StuartHimburg Heather AZenga Joseph - Endometrial cancer (EC) is one of the few malignancies with increasing incidence and mortality rates. Targeted therapy and immunotherapy have become pivotal treatment strategies for EC patients. However, the current methods and biomarkers for predicting immunotherapy responses and prognosis are remain limited. Programmed cell death (PCD) pathways play a crucial role in cancer development and progression and may serve as prognostic markers and indicators of drug sensitivity in EC. In our study, we integrated multiple PCD pathways and comprehensive multi-omics datasets from TCGA-EC and GEO databases. By analyzing distinct PCD signatures, we discovered two major EC subgroups with distinctive prognoses, tumor microenvironment (TME) profiles, and responses to immunotherapy. To further investigate the cellular basis of these PCD patterns, single-cell RNA sequencing analysis was conducted to explore tumor heterogeneity in PCD characteristics across EC subpopulations. Further investigation revealed seven key PCD-associated genes (HIF3A, ACTL8, SIRPG, FBN3, ARHGAP30, CD6, and P2RY13) that formed the basis for a novel prognostic scoring system-risk score (RS). Our findings showed that patients with lower risk scores had better survival rates and improved immunotherapy outcomes. Conversely, patients with higher risk scores experienced poor clinical outcomes and reduced immunotherapy efficacy, although alternative therapies such as docetaxel and olaparib demonstrated potential therapeutic benefits. Overall, the RS provides a valuable tool for early prognosis prediction and for identifying patients who may benefit from immunotherapy. - Source: PubMed
Publication date: 2025/07/01
Lu ShanWei YiyunChen LiuyanCheng JinlianQin LiuyanLu XuemeiPang Lihong