Tpm2 siRNA_Lentivectors
- Known as:
- Tpm2 siRNA_Lentivectors
- Catalog number:
- i064444b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Tpm2 siRNA_Lentivectors
Related genes to: Tpm2 siRNA_Lentivectors
- Gene:
- TPM2 NIH gene
- Name:
- tropomyosin 2
- Previous symbol:
- AMCD1
- Synonyms:
- DA1, NEM4
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-18
- Date modifiied:
- 2019-04-23
Related products to: Tpm2 siRNA_Lentivectors
Related articles to: Tpm2 siRNA_Lentivectors
- Lenvatinib is the primary targeted drug for hepatocellular carcinoma(HCC). However, the development of drug resistance significantly hinders its therapeutic efficacy. The present study aimed to identify new target molecules of lenvatinib-resistant HCC, and improve the treatment of liver cancer. A lenvatinib-resistant HCC cell line, Bel7404(named Bel7404-R), was established, and the protein expression profile of the Bel7404-R cell line and changes in functional enrichment were analyzed. The expression of the identified lenvatinib-resistant critical protein B4GALT4 was validated, and its correlation with immune infiltration and drug resistance was analyzed. Apoptosis and ferroptosis of HCC cell were observe by Calcein-AM/PI staining and transmission electron microscopy. The results indicated that Bel7404-R cells significantly enhanced colony formation and decreased apoptosis ratio compared with parental Bel7404 cells. 111 upregulated and 170 downregulated proteins in the Bel7404-R cells. Notably, upregulated proteins included B4GALT4, CD55, RFTN1, and SHROOM3, whereas downregulated proteins included GRHPR, CLU, TPM2, TMEM185B and TRPM2. B4GALT4 was significantly overexpressed in Bel7404-R cells and identified as a central protein in the molecular regulatory network of these cells. Knockdown of B4GALT4 expression inhibited the levels of PKM2, LDHA and PI3K/AKT signaling, while stimulating the expression of cleaved-Caspase-3. B4GALT4 could protect the integrity of mitochondria and inhibit ferroptosis. The protein expression profile of Bel7404-R cells were significantly different from those of the parental HCC cells. B4GALT4 was identified as a critical molecule for HCC resisting to lenvatinib, and B4GALT4 can be used as a new therapeutic target for lenvatinib-resistant liver cancer. - Source: PubMed
Publication date: 2026/05/07
Wu XueqinPan YinglianPu JianghanFeng SirenLiu KunWu GangLin BoYin QiushiZhu MingyueLi Mengsen - Idiopathic pulmonary arterial hypertension (IPAH) is characterized by irreversible pulmonary vascular remodeling. This pathological remodeling is mainly driven by the aberrant proliferation and migration of pulmonary artery smooth muscle cells (PASMCs). However, the molecular mechanisms underlying these dysfunctions remain incompletely understood. In this study, we integrated single-cell RNA sequencing (scRNA-seq) analysis with in vivo and in vitro validation to identify key driver genes implicated in IPAH. The GSE169471 dataset was acquired from the Gene Expression Omnibus and processed via quality control, clustering, and cell subtype annotation. Further analyses identified dominant cell subtypes, cell-cell communication networks, and differentially expressed genes (DEGs). Hub genes were then screened using multiple bioinformatic algorithms. The selected hub genes were validated in pulmonary arteries from a monocrotaline (MCT)-induced PAH rat model via qPCR and Western blotting. Furthermore, siRNA-mediated knockdown was conducted to investigate the effects of hub gene silencing on HMGB1-induced PASMC proliferation and migration. Our results revealed that SMCs were the dominant communicating cell subtype and were significantly increased in IPAH. A total of 63 upregulated DEGs were identified, primarily enriched in biological processes such as extracellular matrix organization and signaling pathways, including the focal adhesion pathway. Four hub genes (COL1A1, MYL9, COL1A2, and TPM2) were identified, with significantly increased expression observed in the pulmonary arteries of PAH rats. Subsequently, silencing these genes notably reduced HMGB1-induced PASMC proliferation and migration. These findings provide novel insights into the molecular mechanisms of IPAH and highlight these hub genes as potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/30
Li BinbinZhu EnpengWang YijieHu YatingZhang QiLi Fangwei - Non-alcoholic fatty liver disease (NAFLD) is associated with profound alterations in the hepatic immune microenvironment; however, a comprehensive understanding of immune cell dynamics across disease stages remains limited. - Source: PubMed
Publication date: 2026/04/10
Huang GuozhenXing SiyiLong ZhaojunGao WeiKuang ShaoleiLiu MingjiangZou YanZhuo ChenyiDong Xiaofeng - Prognostic biomarker panels identified through bulk sequencing approaches have shown utility in localized prostate cancer but are limited by underlying molecular heterogeneity. Spatial transcriptomics offers a complementary approach to investigate spatial gene expression patterns and the tissue- and cell-type-associated localization of their constituent biomarker genes. - Source: PubMed
Publication date: 2026/03/30
Taylor Kristofer GJohannessen BjarneMills Ian GRye Morten BAxcrona KarolSkotheim Rolf I - The heterogeneous etiology and limited therapeutic options of pediatric restrictive cardiomyopathy (RCM)underscore the urgent need to elucidate its molecular mechanisms and identify potential treatment targets. - Source: PubMed
Publication date: 2026/03/24
Fu XihangLiu JieGuo QingWang LinWu JingWu ZuboXing YanlinZhu PengDong NianguoShi JiaweiPeng Hua