Ask about this productRelated genes to: MIER2 Blocking Peptide
- Gene:
- MIER2 NIH gene
- Name:
- MIER family member 2
- Previous symbol:
- KIAA1193
- Synonyms:
- -
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2018-11-16
Related products to: MIER2 Blocking Peptide
Related articles to: MIER2 Blocking Peptide
- Intrinsically disordered regions (IDRs) and intrinsically disordered proteins (IDPs) play pivotal roles in cellular signaling, molecular recognition, and the regulation of various biological processes. These flexible and conformationally dynamic protein segments are difficult to study using structural analysis methods and computational approaches including AlphaFold. Therefore a critical challenge arises when attempting to understand the structural basis of protein-protein interactions involving IDRs. Here we demonstrate that the poorly characterized C16orf87 protein, which we rename as MHAP1, forms a stable complex with HDAC2 and MIER1. These three proteins all contain IDRs whose structure is unknown. We implemented an integrative approach combining experimental crosslinking data with computational modeling techniques (I-TASSER, HADDOCK, AlphaFold) to probe the IDR-driven assembly of the HDAC1:MIER2:MHAP1 complex and build an integrative structural model of this complex. The C-terminal domain of HDAC2, a poorly characterized IDR, promotes interactions between the ELM2 domain of MIER1 as well as the N- and C-termini of MHAP1. These results contrast with most current literature, including the results from AlphaFold alone that are missing structural information on HDAC C-domain. The approach herein can be generalized to study other complexes, emphasizing the need for integrative approaches in determining the 3D structures of IDR/IDP-driven complexes. - Source: PubMed
Publication date: 2026/03/25
Nde JulesKempf Cassandra GZimmermann Rosalyn CCesare JosephZhang YingWorkman Jerry LFlorens LaurenceWashburn Michael P - Colon adenocarcinoma (COAD) is highly malignant tumor in the gastrointestinal tract, and reliable biomarkers for predicting its prognosis are remain lacking. MIER Family Member 2 (MIER2) has been implicated in tumor biology, yet its role in COAD remains unclear. MIER2 expression in COAD was analyzed using TCGA and UALCAN databases. Survival analysis, Cox regression, and nomogram construction were performed to evaluate its prognostic value. Functional enrichment analysis was conducted via LinkedOmics. Immune infiltration was assessed using ESTIMATE and CIBERSORT algorithms. Additionally, the effect of MIER2knockdown on the proliferation, and migration of SW480 cell was evaluated. The expression of MIER2 was significantly higher in COAD tissues and associated with a poorer OS, DSS and PFI. Multivariate analysis confirmed MIER2 as an independent prognostic factor. Co-expressed gene analysis revealed enrichment in immune-related pathways, including type I interferon signaling and macrophage activation. In addition, MIER2 expression was associated with altered immune infiltration. MIER2 knockdown suppressed SW480 cell proliferation and migration, and RNA-seq further indicated that this might be related to the intrinsic apoptotic signaling pathway. High expression of MIER2 is associated with poor prognosis and immune cell infiltration, and it serve as a novel prognostic biomarker and potential therapeutic target for COAD. - Source: PubMed
Publication date: 2025/10/25
Zhao ChenLi XueZhu SuminShi Lihong - Emerging evidence suggests that circular RNAs (circRNAs), a class of non-coding RNAs, play a critical role in the progression of several cancers, including osteosarcoma (OS). In this study, we focused on a specific circRNA, hsa_circ_0002005, derived from the mesoderm-induced early response 1 family member 2 (MIER2) gene. We determined the expression levels of hsa_circ_0002005 in OS samples through the use of real-time quantitative polymerase chain reaction (RT-qPCR). To assess the effect of hsa_circ_0002005, we used lentiviral analysis and performed several assays including transwell migration, cell invasion, 5-ethynyl-2'-deoxyuridine assay (EdU), cell counting kit-8 (CCK-8), proliferation, colony formation, and western blotting. In addition, we investigated the delivery mechanism of hsa_circ_0002005 in nude mice and predicted the interaction network involving hsa_circ_0002005, microRNA (miRNA), and mRNAs through bioinformatics analysis. The results showed that hsa_circ_0002005 is overexpressed in OS tissues and cells and is derived from exons 2 to 7 of the MIER2 gene. Knockdown of hsa_circ_0002005 markedly reduced the proliferation, migration, and invasive capabilities of cells, as well as their metastatic potential. We discovered miRNAs that may engage with hsa_circ_0002005. Further mechanistic studies indicated that the suppression of hsa_circ_0002005 influenced the expression levels of proteins associated with the epithelial-mesenchymal transition (EMT), suggesting its regulatory role in EMT progression through modulation of cell proliferation, migration, and invasion. - Source: PubMed
Publication date: 2025/01/04
Yang JunxuHu ZizhuRu XiaoHe MingweiHu ZiweiQin XiongXiao ShihuiLiu DachangHuang HanjiWei Qingjun - Renal cell carcinoma (RCC) is one of the most common malignant tumors of the urinary system and accounts for more than 90 % of all renal tumors. Resistance to targeted therapy has emerged as a pivotal factor that contributes to the progressive deterioration of patients with advanced RCC. Metabolic reprogramming is a hallmark of tumorigenesis and progression, with an increasing body of evidence indicating that abnormal lipid metabolism plays a crucial role in the advancement of renal clear cell carcinoma. - Source: PubMed
Publication date: 2024/05/01
Wei ZhihaoYe YuzhongLiu ChenchenWang QiZhang YunxuanChen KaileiCheng GongZhang Xiaoping - To chemically modulate the ubiquitin-proteasome system for the degradation of specific target proteins is currently emerging as an alternative therapeutic modality. Earlier, we discovered such properties of the stem cell-supporting small molecule UM171 and identified that members of the CoREST complex (RCOR1 and LSD1) are targeted for degradation. UM171 supports the in vitro propagation of hematopoietic stem cells by transiently perturbing the differentiation-promoting effects of CoREST. Here, we employed global proteomics to map the UM171-targeted proteome and identified the additional target proteins, namely RCOR3, RREB1, ZNF217, and MIER2. Further, we discovered that critical elements recognized by Cul3 ligase in the presence of UM171 are located within the EGL-27 and MTA1 homology 2 (ELM2) domain of the substrate proteins. Subsequent experiments identified conserved amino acid sites in the N-terminus of the ELM2 domain that are essential for UM171-mediated degradation. Overall, our findings provide a detailed account on the ELM2 degrome targeted by UM171 and identify critical sites required for UM171-mediated degradation of specific substrates. Given the target profile, our results are highly relevant in a clinical context and point towards new therapeutic applications for UM171. - Source: PubMed
Publication date: 2023/03/29
Žemaitis KristijonasGhosh SudipHansson JennySubramaniam Agatheeswaran