SALL2 Mouse Monoclonal Antibody
- Known as:
- SALL2 Mouse Monoclonal Antibody
- Catalog number:
- CYT-006297-M10
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- SALL2 Mouse Monoclonal Antibody
Ask about this productRelated genes to: SALL2 Mouse Monoclonal Antibody
- Gene:
- SALL2 NIH gene
- Name:
- spalt like transcription factor 2
- Previous symbol:
- -
- Synonyms:
- KIAA0360, Hsal2, ZNF795
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-11
- Date modifiied:
- 2016-10-05
Related products to: SALL2 Mouse Monoclonal Antibody
Related articles to: SALL2 Mouse Monoclonal Antibody
- Aberrant alterations in transcription factors often disrupt key signalling pathways, contributing to oncogenesis in multiple cancers, including breast cancer. Spalt-like (SALL) transcription factors are a highly conserved family of proteins with distinctive zinc finger motifs that are emerging as crucial players in tumorigenesis. Despite their pivotal roles in oncogenesis, limited studies have been carried out to explore their roles specifically in breast cancer. - Source: PubMed
Publication date: 2026/03/25
Sisodiya SandeepSingh PayalJoshi TannuKhan AsiyaMishra NeetuKumar SandeepTanwar PranayAgrawal UshaHussain Showket - Colorectal cancer (CRC) remains the second leading cause of cancer-related mortality worldwide, with aberrant activation of the Wnt/β-catenin signaling pathway constituting a key driver of tumorigenesis. , a zinc finger transcription factor deregulated in various cancers, has been implicated in Wnt signaling regulation through its Xenopus ortholog; however, its role in human CRC remains unclear. In this study, we investigated the expression and function of in CRC. Immunohistochemical analysis revealed that is present in the epithelium and stroma of normal colon tissue but is significantly downregulated in adenomas, carcinomas, and CRC cell lines. Reduced expression was associated with elevated levels of active β-catenin and poorer overall patient survival. Functional assays demonstrated that transcriptionally activates , a key negative regulator of the Wnt/β-catenin pathway. Chromatin immunoprecipitation and promoter-reporter assays confirmed binding to the proximal promoter and enhanced promoter activity. Furthermore, expression potentiated the pro-apoptotic effects of the Wnt pathway inhibitor XAV939 in CRC cells, suggesting a role in sensitizing cells to Wnt-targeted therapies. Collectively, these findings identify as a negative regulator of Wnt/β-catenin signaling and support its potential as a prognostic biomarker and therapeutic target in colorectal cancer. - Source: PubMed
Publication date: 2025/08/15
Quiroz AracellyEscalona EmiliaFarkas CarlosBenítez-Riquelme DiegoSepúlveda PaulinaPalma MarioMedina PaulaDelgado CarolinaHepp Matías IVillarroel-Espindola FranzCastro Ariel FPincheira Roxana - Oral cancer is the common reason for the poor prognosis in head and neck carcinomas and the increase in morbidity and mortality rates. The biological behavior of cancer is a complex process. About 50-60% of solid tumors exhibit hypoxic areas within the tumor stroma, which was influenced by the transcriptional activity of hypoxia inducible factor (HIF). HIF promotes stemness and the proliferation of vessel-like structures in tumors, which leads to invasion and metastasis. - Source: PubMed
Publication date: 2025/06/07
Murugesan AmbikaRavi SaranyanEkambaram ManivannanBalakrishnan SekarIndrapriyadharshini Kumaresan - Chemotherapy continues to be the primary treatment for certain types of breast cancer. However, despite an initial positive response to chemotherapeutic agents, the development of resistance is inevitable. The exact molecular mechanisms underlying this phenomenon remain unclear. In this research, a significant downregulation of SALL2 expression was observed in chemo-resistant breast cancer, which was attributed to promoter methylation. Decreased SALL2 expression correlated significantly with poorer relapse-free survival in chemotherapy-treated patients with breast cancer. Functionally, SALL2 silencing induced a stem cell-like phenotype in breast cancer cells, fostering resistance to cisplatin both in vitro and in vivo. This resistance was mediated, at least in part, through the transcriptional regulation of BTG2, a negative regulator of stemness, achieved by direct binding to its promoter regions. These findings underscore the critical role of SALL2 in modulating cisplatin response and propose SALL2 as a potential prognostic biomarker for chemotherapy response in breast cancer. - Source: PubMed
Publication date: 2024/11/22
Li QijiLi ChenxinZhang YuhaoZheng ZihanWang YunYang YingqianZhu QingqingWang RuiXu WanhuiZhu ChengmingTian QinWang MengYe Liping - Cancer is a leading cause of death worldwide, posing a substantial threat to human well-being. Microplastics (MPs) exposure can harm human health and the carcinogenicity of MP remains uncertain. In this study, we investigated carcinogenesis by MPs exposure. We observed MP significantly exacerbated hepatic injury in infectious conditions. In addition, cancer-related p53 and p21 signals are activated by MPs. Analysis of the liver transcriptomic landscape uncovered a noteworthy intensification of the carcinogenesis pathway by MPs compared with pre-infection. The transcription factor SALL2 could act as an oncogenic promoter in the promotion of cancer regulated by MPs. Further, big data analysis presents the correlation between MPs pollution and human hepatocellular carcinoma. This work revealed a toxic amplification effect of the non-bioactive MPs on the bioactive pathogens. This finding provides new insight into understanding the potential toxicity of the MPs. - Source: PubMed
Publication date: 2024/10/22
Huang HaipengHou JiaqiYu ChengzeWei FangchaoXi Beidou