SOK1 (Dominant Negative) Recombinant Adenovirus
- Known as:
- SOK1 (Dominant Negative) Recombinant Adenovirus
- Catalog number:
- ADV-143
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- SOK1 (Dominant Negative) Recombinant Adenovirus
Related genes to: SOK1 (Dominant Negative) Recombinant Adenovirus
- Gene:
- STK25 NIH gene
- Name:
- serine/threonine kinase 25
- Previous symbol:
- -
- Synonyms:
- SOK1, YSK1
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-18
- Date modifiied:
- 2014-11-19
Related products to: SOK1 (Dominant Negative) Recombinant Adenovirus
Related articles to: SOK1 (Dominant Negative) Recombinant Adenovirus
- Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most prevalent chronic liver disorder worldwide and a leading cause of liver-related morbidity and mortality. Insulin resistance and dysregulated hepatic lipid metabolism are key pathological mechanisms for simple hepatic steatosis, yet no specific drug is currently approved. Antisense oligonucleotides (ASOs) are single-stranded nucleotide drugs with high target specificity and long-lasting activity, representing a promising therapeutic approach for chronic metabolic diseases. Here, we report a novel ASO candidate targeting serine/threonine kinase 25 (STK25), a lipid droplet-associated kinase implicated in MASLD pathogenesis. The ASO (S-10c) potently suppressed STK25 expression in multiple human cell lines. Liver-specific delivery was achieved through N-acetylgalactosamine (GalNAc) conjugation, generating GS-10c. In a high-fat diet-induced early MASLD mouse model, GS-10c significantly improved insulin sensitivity, reduced hepatic lipid accumulation, and lowered body weight, exhibiting efficacy similar to resmetirom, the only FDA-approved treatment for metabolic steatohepatitis. A single injection achieved >50% hepatic Stk25 knockdown for over 35 days, demonstrating durable activity. Importantly, GS-10c was designed to avoid all known SNPs, ensuring consistent efficacy across genetically diverse populations. Notably, an alternative ASO differing by only 4 nt showed inconsistent silencing and safety, suggesting the unique therapeutic precision and translational robustness of GS-10c. - Source: PubMed
Publication date: 2026/07/27
Dong AoLi NaLang XipingChen ShunkaiQin YifengWang YuhangWang HaishengGuo MiaomiaoYan AomeiSong KaiBi JingyiRen GuipingLai FanYang JuanDang Yunkun - The metastatic potential of colorectal cancer (CRC) is a pivotal determinant of patient prognosis. Serine/threonine protein kinase 25 (STK25) is critically involved in diverse biological processes, and the function of STK25 in tumorigenesis and metastasis remains debatable across distinct tumor types. Here we identified that low STK25 expression was associated with increased tumor metastasis and poor survival in CRC patients. Functional experiments revealed that STK25 knockdown promoted CRC cells' epithelial-mesenchymal transition (EMT) and metastasis in vitro and in vivo. Mechanistically, STK25 depletion promoted migration and EMT progression through the TGF-β signaling pathway, and the kinase activity of STK25 was required to inhibit TGF-β signaling activation. These findings establish STK25 as a promising therapeutic target for intervening in TGF-β/SMAD2-mediated metastasis in CRC. - Source: PubMed
Gao PinHao HaoChen JiangboHou YifanSong TongkunWu FanXu KaiSu Xiangqian - Colon adenocarcinoma (COAD) remains a leading cause of cancer-related mortality worldwide. Although programmed cell death (PCD) and RNA N6-methyladenosine (m6A) modification have each been shown to regulate tumor progression and therapeutic responses, their combined prognostic significance in COAD has not been fully elucidated. The present study aimed to develop an integrated m6A-PCD prognostic model and to identify potential therapeutic targets in COAD. In total, 1,379 genes across 14 PCD-related pathways were systematically analyzed and a 21-gene m6A-PCD signature (MCDI) was constructed following multivariate Cox regression analysis. Single-cell RNA sequencing from publicly available datasets (GSE132465 and GSE205506), together with reverse transcription-quantitative PCR (qPCR) validation using clinical samples, were employed to identify genes with tumor-specific expression patterns. The functional role of serine/threonine kinase 25 (STK25) was further investigated through knockdown experiments, flow cytometry, m6A methylated RNA immunoprecipitation (MeRIP)-qPCR and RIP assays. In addition, small interfering RNAs targeting methyltransferase-like 3 (METTL3) and YTH domain-containing protein 1 (YTHDC1) were used to evaluate the involvement of m6A modification in STK25 mRNA stability and apoptosis regulation. The resulting MCDI signature demonstrated robust and independent prognostic value and effectively predicted differential responses to programmed death-ligand 1 immunotherapy. In total, 5 core genes [microRNA 210, STK25, TGFB2, tripartite motif containing (TRIM)6 and TRIM68] were identified as key prognostic markers. STK25 was specifically upregulated in tumor epithelial cells, and its knockdown significantly promoted apoptosis in COAD cells. Correlation analyses revealed positive associations between STK25 expression and multiple m6A regulators, with METTL3 and YTHDC1 showing the highest targeting credibility. Knockdown of METTL3 or YTHDC1 reduced STK25 mRNA levels. RIP assays confirmed their direct binding to STK25 mRNA, while MeRIP-qPCR demonstrated that METTL3 knockdown decreased the m6A modification level of STK25 mRNA. In conclusion, the reconstructed MCDI was established as a novel m6A-PCD-based prognostic model for patient stratification and the prediction of immunotherapy response in patients with COAD. STK25 was also identified as a potential therapeutic target linking m6A modification to the regulation of apoptosis in COAD. - Source: PubMed
Publication date: 2026/04/22
Yu HezhiLi TihuiHuang XiaoyunChen ZihanLin ZixiangChen Fenglin - Cancer-associated fibroblasts (CAFs) within the tumour microenvironment play a pivotal role in colorectal cancer (CRC) progression and therapeutic resistance. Serine/threonine protein kinase 25 (STK25) exerts multiple roles in tumourigenesis; however, its role in mediating tumour-stroma crosstalk remains largely unexplored. - Source: PubMed
Hou YifanChen JiangboHao HaoSong TongkunSong LinXing PuWeng KaiRan YumengYang XinyingQiao XiaowenChen JieYao RuibinYang HongChen LeiDi JiaboXu KaiSu XiangqianJiang Beihai - Atherosclerosis represents a chronic inflammatory disease of the arterial wall and remains a principal cause of cardiovascular morbidity and mortality. Macrophages critically govern lesion initiation, progression, and destabilization, and accumulating evidence indicates that protein kinases are key regulators of their phenotype and function.This systematic review synthesizes data from 162 publications encompassing 76 kinases to delineate the contribution of macrophage-associated kinase signaling to atherogenesis. The identified kinases span major families, including AGC, CaMK, CMGC, Ste20, and tyrosine kinases, each exerting distinct regulatory effects on macrophage survival, polarization, lipid handling, efferocytosis, and inflammatory activation. Several kinases, such as CaMK2γ, CaMK4, DCLK1, Trib1, and STK25, exhibit pro-atherogenic activity by promoting foam cell formation, expanding the necrotic core, and propagating inflammatory pathways. Conversely, kinases, including STK11 and the context-dependent mediator Akt1, exhibit protective or dual functions that contribute to metabolic homeostasis and reparative macrophage states. Despite substantial mechanistic insights and the established therapeutic utility of kinase inhibitors in oncology, clinical translation in the context of atherosclerosis remains limited.This review consolidates current knowledge, identifies critical gaps, and outlines prospective avenues to target macrophage-specific kinase pathways as novel therapeutic strategies for atherosclerosis. - Source: PubMed
Publication date: 2026/03/27
Müller Jana Svan der Vorst Emiel P C