Tmem33 antibody - middle region (ARP47398_P050)
- Known as:
- Tmem33 (anti-) - middle region (ARP47398_P050)
- Catalog number:
- arp47398_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Tmem33 antibody - middle region (ARP47398_P050)
Related genes to: Tmem33 antibody - middle region (ARP47398_P050)
- Gene:
- TMEM33 NIH gene
- Name:
- transmembrane protein 33
- Previous symbol:
- -
- Synonyms:
- FLJ10525, Pom33
- Chromosome:
- 4p13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-28
- Date modifiied:
- 2019-03-07
Related products to: Tmem33 antibody - middle region (ARP47398_P050)
Related articles to: Tmem33 antibody - middle region (ARP47398_P050)
- Colorectal cancer (CRC) remains one of the most lethal malignancies worldwide, with tumor metastasis representing the primary driver of treatment failure and poor prognosis. Transmembrane Protein 33 (TMEM33) has been implicated in tumor progression across several cancer types, yet its expression pattern, biological function, and upstream transcriptional regulation in CRC remain undefined. In this study, TMEM33 expression in CRC and matched adjacent normal tissues was assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemistry (IHC), with prognostic associations analyzed via Kaplan-Meier survival curves. TMEM33 was significantly upregulated in CRC tissues, and high TMEM33 expression correlated with advanced tumor stage, lymph node metastasis, and unfavorable overall survival. TMEM33 knockdown in HCT116 and LOVO CRC cell lines, achieved via lentiviral infection, significantly suppressed cell proliferation as demonstrated by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assays. TMEM33 silencing also reduced cell migration and invasion in Transwell assays, and reversed epithelial-mesenchymal transition (EMT). Mechanistically, bioinformatics screening and dual-luciferase reporter assays identified E2F transcription factor 1 (E2F1) as a transcriptional activator of TMEM33, binding its promoter to drive expression. Rescue experiments further demonstrated that E2F1 overexpression partially restored proliferation, migration, invasion, and EMT in TMEM33-knockdown cells. In vivo, TMEM33 suppression significantly inhibited subcutaneous tumor growth and reduced lung metastatic burden in nude mouse models. Collectively, these findings establish E2F1 as an upstream transcriptional regulator of TMEM33 and demonstrate that the E2F1/TMEM33 axis promotes CRC malignant progression by driving proliferation, metastasis, and EMT, highlighting this axis as a candidate therapeutic target for CRC. - Source: PubMed
Publication date: 2026/09/16
Li RuiZhao LiChai NannanZhu QinghuaLiang JingWu XiangnanWang WanYang Lihong - Lung adenocarcinoma is a common type of lung cancer with high incidence and mortality rates. TMEM33, a tumor-associated protein, has not been fully elucidated in lung adenocarcinoma. To explore the expression of TMEM33 in lung adenocarcinoma, its impact on tumor progression, and its role in the PI3K/AKT/mTOR signaling pathway. Key genes associated with lung adenocarcinoma were screened using the Gene Expression Omnibus (GEO) dataset GSE140797 in combination with a weighted correlation network analysis (WGCNA). Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed on these key genes. TMEM33 expression in Lung adenocarcinoma patients was validated using data from the TCGA database. The directly interactive molecules were screened through a bioinformatics method. Cellular assays (Western Blot, CCK8, colony formation, scratch assay, Trans well assay) and a nude mouse model were used to investigate the effects of TMEM33 on cell proliferation, migration, and tumor growth. TMEM33 is highly expressed in lung adenocarcinoma tissues (P < 0.05) and associated with poor prognosis. Overexpression of TMEM33 promotes cell proliferation and migration, and activates the PI3K/AKT/mTOR signaling pathway (P < 0.01). In the nude mouse model, TMEM33 overexpression increases tumor volume (P < 0.001), and PI3K/AKT pathway inhibition suppresses these effects (P < 0.05, P < 0.01). TMEM33 acts as an oncogene in lung adenocarcinoma by activating the PI3K/AKT/mTOR pathway, providing new therapeutic targets. - Source: PubMed
Publication date: 2026/06/24
Wudu MuliLou HaijunMa YuyuZhang ZhenyuAlimujiang SureyanDeng YanchaoJing XiaoliangMeng MenggenXu ZhipengHasim Ayshamgul - Diabetic erectile dysfunction (DMED) is a common complication among male patients with diabetes. Therapies primarily based on phosphodiesterase type 5 inhibitors (PDE5Is) often yield suboptimal results. Extracellular vesicles (EVs) have emerged as a promising therapeutic strategy; however, their clinical translation is hindered by rapid in vivo clearance and limited inherent bioactivity. Therefore, we developed an innovative combined therapeutic approach. First, we fabricated an injectable, thermosensitive hydrogel (ECMTA-Hydrogel) by combining a decellularized porcine corpus cavernosum extracellular matrix (ECM) with tannic acid, which exhibits excellent biocompatibility and rapid gelation at body temperature (37 °C), enabling prolonged local retention of EVs within the corpus cavernosum. Second, we pretreated mesenchymal stem cells (MSCs) with pioglitazone to generate engineered EVs (PGZ-EVs) with enhanced bioactivity. Experiments confirmed that the ECMTA-Hydrogel facilitates sustained release of PGZ-EVs, extending their duration of action. In a DMED rat model, the combined ECMTA-PGZ-EVs therapy demonstrated superior efficacy, markedly improving erectile function and effectively reversing pathological phenotypic switching and apoptosis in corpus cavernosum smooth muscle cells (CCSMCs). Mechanistically, we identified that miR-203a-3p, highly enriched in PGZ-EVs, directly targets and suppresses the endoplasmic reticulum transmembrane protein TMEM33, thereby mitigating diabetes-induced endoplasmic reticulum stress (ERS). This pathway represents the key mechanism underlying the cytoprotective effects of PGZ-EVs. In summary, this study not only establishes an efficient natural matrix hydrogel-based delivery system but also augments the therapeutic potential of EVs via engineered modification. Furthermore, we elucidate a novel mechanism involving the miR-203a-3p/TMEM33/ERS axis, offering a promising therapeutic strategy for the clinical management of DMED. - Source: PubMed
Publication date: 2026/04/14
Liu HaoZang ZhenjieZhao DanfengZhang JingWang ZhenqingFu QiangZhang Keqin - - Source: PubMed
Publication date: 2026/01/29
Li YingYu HuifangWang JianjianKang Kai - Improving responses to cancer immunotherapies requires deeper insight into the cellular mechanisms governing T cell-mediated anti-tumor immunity. TMEM33 is an endoplasmic reticulum-resident transmembrane protein enriched across multiple tumor types, with reported functions in anti-viral immunity as well as calcium and lipid homeostasis, yet its role in tumor immunosurveillance remains unknown. Using murine genetic models, we demonstrate that host TMEM33 constrains anti-tumor CD8 T cell responses. Constitutive mice exhibited delayed melanoma tumor growth and increased CD8 T cell infiltration. Antigen-specific CD8 compartments in tumors of mice showed TCF-1PD-1 progenitor-exhausted cell (Tpex) enrichment, elevated effector function and reduced exhaustion, alongside improved effector memory expansion and T-bet expression in draining lymph nodes. We highlight that TMEM33 functions intrinsically within the T cell compartment, as TMEM33 deletion (1) enhanced polyclonal activation of naive CD8 T cells , (2) promoted preferential Tpex accumulation among adoptively transferred naive OT-I cells in B16F10-OVA tumors and draining lymph nodes, and (3) improved the potency of -expanded OT-I cells in controlling tumor growth during adoptive cell therapy. Finally, in a large, prospectively recruited metastatic melanoma cohort, lower expression in patient CD8 T cells significantly correlated with improved survival and elevated (encoding TCF-1). Collectively, our findings define TMEM33 as a formerly unrecognized intrinsic determinant of tumor-directed CD8 T cell fate that limits Tpex maintenance, and restrains cell therapy responses, suggesting that its modulation may strengthen immunotherapeutic efficacy. - Source: PubMed
Publication date: 2026/01/02
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