Ask about this productRelated genes to: 40787 antibody
- Gene:
- TMEM45B NIH gene
- Name:
- transmembrane protein 45B
- Previous symbol:
- -
- Synonyms:
- BC016153, FLJ40787
- Chromosome:
- 11q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-04
- Date modifiied:
- 2019-03-19
Related products to: 40787 antibody
Related articles to: 40787 antibody
- Despite advancements in targeted therapies and immunotherapy, liver cancer (LC) remains a prominent contributor to cancer-related deaths globally, primarily attributable to its high recurrence and metastasis rates. Recent investigations have underscored the crucial function of transmembrane proteins in advancing cancer by regulating proliferation, invasion, and epithelial-mesenchymal transition (EMT). Transmembrane protein 45B (TMEM45B), a transmembrane protein implicated in tumor aggressiveness in various cancer types, requires further investigation to clarify its specific role in LC. This study investigates the expression patterns, biological functions, and underlying mechanisms of TMEM45B in LC. Bioinformatic analyses were conducted on publicly available datasets to evaluate TMEM45B expression in LC and its correlation with clinical outcomes. TMEM45B knockdown and overexpression models were established in LC cell lines through lentivirus-mediated shRNA and plasmid transfection. The CCK-8 assay evaluated the influence of TMEM45B on tumor cell proliferation. Cell migration and invasion were assessed by Transwell migration and Matrigel invasion assays, respectively. EMT-related changes were examined by immunofluorescence staining of vimentin and E-cadherin. MET signaling activity was assessed by Western Blotting. Tumor growth in vivo was evaluated using a subcutaneous xenograft model in nude mice. Elevated expression of TMEM45B was detected in LC cell lines and tissues, correlating with poor prognosis and advanced clinical stages. Cox regression analyses in a 66-patient cohort further indicated that TMEM45B was an independent prognostic factor for overall survival. Knockdown of TMEM45B in vitro significantly suppressed LC cell proliferation, invasion, migration, and EMT, while its overexpression exacerbated these malignant phenotypes. Mechanistically, TMEM45B promoted MET signaling activation, as reflected by increased MET protein levels and enhanced phosphorylation of downstream effectors AKT and ERK. Rescue experiments confirmed the crucial role of MET signaling in mediating TMEM45B-induced oncogenic effects. In vivo, TMEM45B knockdown notably hindered tumor growth and decreased EMT marker expression in a subcutaneous xenograft model. Our study suggests that TMEM45B may facilitate LC progression, at least in part, through MET signaling activation and EMT induction. These results underscore TMEM45B's significance as a prognostic indicator and therapeutic target in LC. Further research on developing TMEM45B-targeted therapy could improve the effectiveness of treating advanced LC patients. - Source: PubMed
Publication date: 2026/04/17
Shen HongzhuoZheng WenyingLi MeiqiPei LijunXie Jie - The Transmembrane protein 45 (TMEM45) family comprises multi-pass transmembrane proteins that harbor the ancient DUF716 domain and are predominantly localized to the endomembrane system (endoplasmic reticulum, Golgi apparatus). In mammals, TMEM45 members exhibit highly tissue-specific expression patterns and their functions are tightly linked to endomembrane activities. TMEM45A directly binds prolyl-4-hydroxylase (P4HA1) to modulate extracellular matrix (ECM) synthesis, thereby contributing to fibrosis and corneal disorders. TMEM45B participates in the Golgi processing and trafficking of nociceptive signaling molecules and also influences viral replication. Another paralog, TEDDM1, is implicated in sperm maturation. Expression of TMEM45 proteins is stringently regulated by upstream signaling cascades including TGF-β1/Smad, hypoxia/HIF-1α, calcium signaling, and JAK2/STAT3. In turn, these proteins serve as regulatory nodes that modulate downstream pathways such as Jagged1/Notch, Rho/ROCK, unfolded protein response (UPR), NF-κB, AKT/mTOR, Wnt/β-catenin, DNA-damage repair, and apoptosis. This review integrates current knowledge on the tissue distribution and upstream/downstream signaling networks of TMEM45 proteins to clarify endomembrane protein function and provide new perspectives on intracellular signal transduction mechanisms. - Source: PubMed
Publication date: 2026/03/25
Zhang XiaoqianZhang YanpingZhai ZhenguoWang Xietong - To evaluate changes in gene expression activity during preoperative testing for tumor hormone sensitivity to aromatase inhibitors and tamoxifen in postmenopausal women with ESR+/HER2- breast cancer. - Source: PubMed
Kometova V VBurmenskaya O VTrofimov D YuRodionova M VRodionov V VAshrafyan L AMikhaleva L M - This study aimed to investigate the role of Tmem45b, a gene expressed in itch-associated Dorsal root ganglion (DRG) neurons, in the regulation of itch sensation. - Source: PubMed
Publication date: 2025/12/10
Wang Sa-ShuangLiang ChenWang Ruo-LinSun Ze-LinRen Peng-YuWu BinSun Juan-JuanFu LiXiao Li-ZuSun Wu-PingLi Chang-Lin - PACT (encoded by the PRKRA gene) is a double-stranded RNA binding protein with defined antiviral defense and cytoplasmic RNA-induced silencing actions in mammals. We previously described a further role for PACT as a modulator of nuclear receptor (NR)-regulated gene expression. Here, we investigated the role of PACT in prostate cancer (PCa) using a loss-of-function approach. Depletion of PACT in multiple PCa cell lines resulted in a reduction in cell proliferation, but viability was maintained. RNA-sequencing analysis of LNCaP PCa cells ± PACT revealed a depletion of biological processes involved in cell cycle, mitochondrial function, and NR-response pathways in the PACT knockout (KO) cells. In the PACT KO cells, downregulated genes included the androgen-regulated KLK3 (prostate specific antigen, PSA), together with H2AFJ, PSMD5, AQP3, TMEM45B, and SLC22A3, and siRNA-mediated knockdown of these genes reduced cell growth and proliferation in LNCaP cells. Further, reducing PACT or PSA induced cell cycle arrest at G0/G1. Additionally, the hormone-mediated upregulation and AR antagonist-driven downregulation of PSA gene expression were respectively attenuated and enhanced in PACT KO cells. Taken together, these data support a pro-proliferative role for PACT in PCa, and siRNA therapeutic targeting of PACT, or downregulated genes with PACT KO, could represent a new therapeutic approach. - Source: PubMed
Publication date: 2025/10/21
Beveridge Dianne JWoo Andrew JRichardson Kirsty LBrown Rikki A MStuart Lisa MSingh ManjotRedfern Andrew DLeedman Peter J