Ask about this productRelated genes to: TMED4 Blocking Peptide
- Gene:
- TMED4 NIH gene
- Name:
- transmembrane p24 trafficking protein 4
- Previous symbol:
- -
- Synonyms:
- HNLF, p24alpha3, p24a3
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-21
- Date modifiied:
- 2015-08-11
Related products to: TMED4 Blocking Peptide
Related articles to: TMED4 Blocking Peptide
- Endoplasmic reticulum stress (ERS) and autophagy regulate tumor-infiltrating T cell function and exhaustion, but the underlying mechanisms remain unclear. Here, we identified the ERS-related transmembrane protein TMED4 (transmembrane emp24 domain-containing 4) as a critical regulator of CD8 T cell antitumor immunity. deletion in T cells enhanced antitumor responses by promoting CD8 T proliferation, infiltration, and killing capacity, while reducing terminal exhaustion. Mechanistically, deficiency hyperactivated the inositol-requiring enzyme 1α (IRE1α)-X-box binding protein 1 (XBP1) axis and induced autophagy flux in an IRE1α-dependent manner. Genetic deletion of (IRE1α) or (Beclin1) impaired the antitumor effects of deficiency, underscoring the role of ERS and autophagy in CD8 T cell function. Moreover, -deficient chimeric antigen receptor T cells (CAR T cells) displayed improved antitumor immunity. Pharmacological inhibition of using antisense oligonucleotide also enhanced CD8 T cell-mediated tumor control. In summary, our study reveals that TMED4 governs CD8 T cell effector function and limits terminal exhaustion through IRE1α-driven autophagy, establishing TMED4 as a promising immunotherapeutic target for improving CAR T cell efficacy. - Source: PubMed
Publication date: 2026/06/12
Wang HuiziShi LicaiJiang KeWu ShuyaoJiang ZhenyanTao YuexiaoLi JiaLi XinLiu JiaminNi JunWu Emily JiatongWu Sophia JiaxinChen GuangQin MingXu LinLai Chu-HuAicher AlexandraYe YouqiongHeeschen ChristopherCao Yu JWu Xuefeng - Chemotherapy remains the primary treatment modality for patients with lung cancer; however, substantial inter-patient variability exists in responses to chemotherapeutic agents. Therefore, predicting individual responses is critical for optimizing treatment outcomes and improving patient prognosis. - Source: PubMed
Publication date: 2025/07/24
Chen JinghongYi YonglinYang ChunqianYing HaoxuanZhang JianLin AnqiWei TingLuo Peng - Endoplasmic reticulum stress (ERS) plays crucial roles in maintaining Treg stability and function, yet the underlying mechanism remains largely unexplored. Here, we demonstrate that (Tmed4ΔTreg) mice with Treg-specific KO of ERS-related protein transmembrane p24 trafficking protein 4 (TMED4) had more Tregs with impaired Foxp3 stability, Treg signatures, and suppressive activity, which led to T cell hyperactivation and an exacerbated inflammatory phenotype and boosted antitumor immunity in mice. Mechanistically, loss of Tmed4 caused defects in ERS and a nuclear factor erythroid 2-related factor 2-related (NRF2-related) antioxidant response, which resulted in excessive ROS that reduced the Foxp3 stability and suppressive function of Tregs in an IRE1α/XBP1 axis-dependent manner. The abnormalities could be effectively rescued by the ROS scavenger, NRF2 inducer, or by forcible expression of IRE1α. Moreover, TMED4 suppressed IRE1α proteosome degradation via the ER-associated degradation (ERAD) system including the ER chaperone binding immunoglobulin protein (BIP). Our study reveals that TMED4 maintained the stability of Tregs and their suppressive function through IRE1α-dependent ROS and the NRF2-related antioxidant response. - Source: PubMed
Publication date: 2024/10/31
Jiang ZhenyanWang HuiziWang XiaoxiaDuo HongruiTao YuexiaoLi JiaLi XinLiu JiaminNi JunWu Emily JiatongXiang HongruiGuan ChenyangWang XinyuZhang KunZhang PengHou ZhaoyuanLiu YongWang ZhengtingSu BingLi BoHao YoujinLi BinWu Xuefeng - Several TMED protein family members are overexpressed in malignant tumors and associated with tumor progression. TMED1 belongs to the TMED protein family and is involved in protein vesicular trafficking. However, the expression level and biological role of TMED1 in colorectal cancer (CRC) have yet to be fully elucidated. In this study, the integration of patient survival and multi-omics data (immunohistochemical staining, transcriptomics, and proteomics) revealed that the highly expressed TMED1 was related to the poor prognosis in CRC. Crystal violet staining indicated the cell growth was reduced after knocking down TMED1. Moreover, the flow cytometry results showed that TMED1 knockdown could increase cell apoptosis. The expression of TMED1 was positively correlated with other TMED family members (TMED2, TMED4, TMED9, and TMED10) in CRC, and the protein-protein interaction network suggested its potential impact on immune regulation. Furthermore, TMED1 expression was positively associated with the infiltration levels of regulatory T cells (Tregs), cancer-associated fibroblasts (CAFs), and endothelial cells and negatively correlated with the infiltration levels of CD4+ T cells, CD8+ T cells, and B cells. At last, the CTRP and GDSC datasets on the GSCA platform were used to analyze the relationship between TMED1 expression and drug sensitivity (IC). The result found that the elevation of TMED1 was positively correlated with IC and implied it could increase the drug resistance of cancer cells. This research revealed that TMED1 is a novel prognostic biomarker in CRC and provided a valuable strategy for analyzing potential therapeutic targets of malignant tumors. - Source: PubMed
Publication date: 2024/01/29
Guo XinZhou WeiJin JinmeiLin JiayiZhang WeidongZhang LijunLuan Xin - Major depressive disorder (MDD) negatively affects patients' behaviours and daily lives. Due to the high heterogeneity and complex pathological features of MDD, its diagnosis remains challenging. Evidence suggests that endoplasmic reticulum stress (ERS) is involved in the pathogenesis of MDD; however, relevant diagnostic markers have not been well studied. This study aimed to screen for ERS genes with potential diagnostic value in MDD. - Source: PubMed
Publication date: 2023/08/15
Huang ShuwenLi YongShen JianyingLiang WennaLi Candong