Ask about this productRelated genes to: SAMD4A antibody
- Gene:
- SAMD4A NIH gene
- Name:
- sterile alpha motif domain containing 4A
- Previous symbol:
- SAMD4
- Synonyms:
- KIAA1053, DKFZP434H0350, Smaug, SMG, SMGA, hSmaug1
- Chromosome:
- 14q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-01
- Date modifiied:
- 2016-04-25
Related products to: SAMD4A antibody
Related articles to: SAMD4A antibody
- The transcriptional cofactors YAP1 and TAZ regulate target gene expression by binding to the transcription factor TEAD. Due to their roles in cancer initiation, progression, and drug resistance, YAP1 and TAZ are promising targets for cancer therapy. SAMD4A/B are RNA-binding proteins that are broadly expressed across human tissues, but few of their molecular targets and biological functions have been identified. In Drosophila, the SAMD4A/B homolog Smaug participates in early embryonic development by disrupting the stability and translation of maternal mRNA. To discover targets inhibiting the YAP1/TAZ-TEAD oncogenic transcription program, we screened a whole-genome siRNA library and identified siSAMD4B as potently suppressing TEAD activity in human cancer cells. We showed that SAMD4A/B increased TEAD activity by destabilizing and repressing the translation of VGLL4 mRNA, promoting cancer progression in vitro. Conversely, inhibiting either SAMD4A or SAMD4B elevated VGLL4 mRNA, which suppressed TEAD activity and inhibited cancer progression. Notably, transgenic mice expressing liver-specific SAMD4B exhibited accelerated development of intrahepatic cholangiocarcinomas in an Nf2-deficient background. These tumors appeared in the mutants at one week of age and caused death due to hepatic failure by 100 days. Thus, SAMD4A/B may be a promising target for anticancer drugs designed to inhibit TEAD activation. - Source: PubMed
Publication date: 2026/04/21
Otani JunjiNishio MikiTokita RikoHikasa HirokiNishimori MakotoDan ShingoNaguro IsaoIchijo HidenoriMiyanishi MasanoriSasaki TakehikoNishina HiroshiMak Tak WahMaehama TomohikoSuzuki Akira - Ischemia/reperfusion injury (IRI) is a major cause of acute kidney injury (AKI), primarily driven by the increased production of reactive oxygen species (ROS). Elevated ROS levels can lead to cell apoptosis. However, effective therapeutic targets for IRI remain limited. - Source: PubMed
Publication date: 2026/02/03
Sun ChongHu HaoYuan XinweiChen XingyuFang FangLiu YunlongChen ZhijunGuan Han - The Sterile alpha motif domain-containing protein 4 (SAMD4) family consists of two evolutionarily conserved and highly homologous RNA-binding proteins, SAMD4A and SAMD4B. Previous studies have established SAMD4A as a tumor suppressor that is downregulated in breast cancer, while the function of SAMD4B in tumorigenesis remains poorly defined. In this study, we observed that SAMD4B expression is upregulated in breast cancer. Functional assays demonstrated that SAMD4B facilitated breast cancer cell proliferation, migration, and invasion by inducing epithelial-mesenchymal transition (EMT). Furthermore, SAMD4B accelerated G1-to-S phase cell cycle progression by modulating p53 expression, collectively supporting an oncogenic function of SAMD4B in breast cancer. Mechanistically, we found that SAMD4B enhanced TCF/LEF transcriptional activity and upregulated the expression of β-catenin, Cyclin D1, c-Myc, and Axin2. Further investigations confirmed that SAMD4B activated the Wnt/β-catenin pathway by stabilizing mRNA and increasing β-catenin protein expression level. Importantly, treatment with XAV-939, a specific Wnt/β-catenin pathway inhibitor, abrogated the pro-oncogenic effects of SAMD4B overexpression, including Wnt/β-catenin pathway activation, enhanced proliferation, and increased metastatic capacity. These results confirm that SAMD4B promotes the malignant phenotypes of breast cancer cells in a manner dependent on the Wnt/β-catenin pathway. In summary, our findings clarify that SAMD4B exerts an oncogenic role in breast cancer progression by activating the Wnt/β-catenin pathway. These data identify SAMD4B as a potential therapeutic target in breast cancer, although further in vivo investigations are required to validate its clinical relevance. - Source: PubMed
Publication date: 2025/10/07
Li Jia-HuiWang Xin-YaSong Huan-XiNie Xiao-FeiZhang Li-Na - Like-Smith protein 12 (LSM12), an RNA-binding protein, is highly expressed in tumor tissues of patients with lung squamous cell carcinoma (LUSC). However, the role of LSM12 in LUSC is unclear. In this study, overexpression of LSM12 promotes the proliferation, migration, and invasion and prevents the apoptosis of LUSC cells. In vivo, LSM12 accelerates the tumor growth and metastasis of LUSC cells using male BALB/c nude mice. Furthermore, we find that the Sterile alpha motif domain containing 4A (SAMD4A) is directly bound to the mRNA of LSM12 and accelerates the mRNA degradation. High-throughput omics analysis is performed to identify the potential target genes of LSM12 in LUSC cells. LSM12 regulates alternative splicing events and increases exon 13 skipped splicing of ARRB1 and mRNA expression. Our findings may provide fundamental research for the investigation of the development of LUSC and the potential role of LSM12 in LUSC cells. - Source: PubMed
Publication date: 2025/05/27
Wu LinZhang FangyuanChen HuanhuanZhao Gang - RNA-binding proteins (RBPs) are essential in cardiac development. However, a large of them have not been characterized during the process. - Source: PubMed
Publication date: 2025/03/18
Yi NaWang Han-RuiZhu Yu-PingXiao TaoLin QinLiu HuanMeng Yi-LeiSun Yi-ZhuoLin FangHu Sang-YuCao Hua-MingZhang Jun-FangPeng Lu-YingLi Li