MORF4L1 Antibody - C-terminal region (ARP31510_P050)
- Known as:
- MORF4L1 Antibody - C-terminal region (ARP31510_P050)
- Catalog number:
- arp31510_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MORF4L1 Antibody - C-terminal region (ARP31510_P050)
Related genes to: MORF4L1 Antibody - C-terminal region (ARP31510_P050)
- Gene:
- MORF4L1 NIH gene
- Name:
- mortality factor 4 like 1
- Previous symbol:
- -
- Synonyms:
- MRG15, MORFRG15, HsT17725, Eaf3, MEAF3
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-10
- Date modifiied:
- 2014-11-18
Related products to: MORF4L1 Antibody - C-terminal region (ARP31510_P050)
Related articles to: MORF4L1 Antibody - C-terminal region (ARP31510_P050)
- Mortality factor 4-like 1 (MORF4L1) is a highly ubiquitinated protein, initially discovered for its role in reversing cellular immortalization. It functions as a component of multi-subunit complexes, including the NuA4 (nucleosome acetyltransferase of H4) histone acetyltransferase, SIN3B histone deacetylase complexes, and histone methyltransferase. It thereby directly influences histone acetylation, methylation, and gene expression. MORF4L1 has emerged as a key player in several biological processes, such as chromatin remodeling, DNA damage response, and cellular senescence. Recent research findings highlight its expanded role in lipid metabolism and metabolic diseases. Genome-wide association studies reveal single-nucleotide polymorphisms near the MORF4L1 locus correlating with lipid traits, type 2 diabetes, and coronary artery disease. This review provides a comprehensive overview of MORF4L1's regulation and its multifaceted roles, implicating its emerging importance in vascular homeostasis and cardiometabolic disease. We propose that MORF4L1's intricate mechanisms demand a deeper understanding. As a regulatory protein at the interface of chromatin biology, cellular senescence, and lipid metabolism, MORF4L1 holds promise as a potential therapeutic target for ameliorating vascular and metabolic dysfunction in cardiometabolic diseases. - Source: PubMed
Publication date: 2026/03/10
Tanni Fatema YeasminZoni Rachelle NelsonFaysal Md AtikSun Xinghui - Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapies and poor prognosis. Unc-51-like kinase 1 (ULK1), a central regulator of autophagy, has emerged as a potential therapeutic node in cancer but remains poorly understood in TNBC. Here, we investigated the proteomic consequences of pharmacological ULK1 modulation in MDA-MB-231 TNBC cells. Cells were treated with the ULK1 activator LYN-1604 or inhibitor MRT68921 at EC₅₀ concentrations. Autophagic activity, validated through LC3B immunoblotting and fluorescence microscopy, increased under both treatments. Quantitative label-free LC-MS/MS proteomics prioritized 182 and 196 candidate differentially abundant proteins in response to LYN-1604 and MRT68921, respectively. ULK1 activation primarily altered transcriptional regulation and suppressed translation, whereas inhibition was associated with enrichment of immune-related pathway and vesicle-mediated transport. Five proteins consistently downregulated across both treatments (PSIP1, AGO2, MORF4L1, HNRNPC, and SETD2) were prioritized as candidate hubs based on shared regulation across perturbations and network ranking using CytoHubba/MCC. These candidates mapped to autophagy-associated pathway modules/terms related to MET-FAK signaling, extracellular matrix-related processes, and mitochondrial Ca²⁺ handling/transport. These findings suggest that ULK1 modulation, regardless of direction, associated with proteomic changes in pathways linked to tumor-promoting networks. Our study provides a comprehensive proteomic framework linking ULK1 perturbation to transcriptional, immune, and epigenetic regulation, and highlights downstream effectors as candidate targets for future functional and translational validation in TNBC. - Source: PubMed
Publication date: 2026/03/03
Bal Albayrak Merve GulsenYanar SevincKorak TuğcanAkpinar GurlerKasap Murat - Colorectal cancer (CRC) liver metastasis (CRLM) represents a major clinical challenge, and acquired resistance to radiotherapy (RT) significantly limits therapeutic efficacy. A deep and comprehensive understanding of the cellular and molecular mechanisms driving RT resistance is urgently required to develop effective combination strategies. Here, we aimed to dissect the dynamic cellular landscape of the tumor microenvironment (TME) and identify key epigenetic regulators mediating radioresistance in CRLM by integrating cutting-edge single-cell and spatial omics technologies. We performed integrated single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) on matched pre- and post-radiotherapy tumor tissues collected from three distinct CRLM patients. Employing a robust machine-learning framework on the multi-omics data, we successfully identified (Mortality Factor 4 Like 1), an epigenetic reader, as a critical epigenetic mediator of acquired radioresistance. High-resolution scRNA-seq analysis of the tumor cell compartment revealed that the -high subpopulation exhibited significant enrichment in DNA damage repair (DDR) pathways, heightened activity of multiple pro-survival metabolic pathways, and robust signatures of immune evasion. Pseudotime trajectory analysis further confirmed that RT exposure drives tumor cells toward a highly resistant state, marked by a distinct increase in expression. Furthermore, cell-cell communication inference demonstrated a pronounced, systemic upregulation of various immunosuppressive signaling axes within the TME following RT. Crucially, high-resolution ST confirmed these molecular and cellular interactions in their native context, revealing a significant spatial co-localization of -expressing tumor foci with multiple immunosuppressive immune cell types, including regulatory T cells (Tregs) and tumor-associated macrophages (TAMs), thereby underscoring its role in TME-mediated resistance. Our comprehensive spatial and single-cell profiling establishes as a pivotal epigenetic regulator underlying acquired radioresistance in CRLM. These findings provide a compelling mechanistic rationale for combining radiotherapy with the targeted inhibition of , presenting a promising new therapeutic avenue to overcome treatment failure and improve patient outcomes in CRLM. - Source: PubMed
Publication date: 2026/01/26
Zhang YuanyuanWang XiaoliLiu HaitaoXiang YanYu Le - Although radiotherapy (RT) plays a crucial role in the local treatment of hepatocellular carcinoma, its therapeutic efficacy is often hindered by radiation resistance, the mechanisms of which remain poorly understood. Single-cell and bulk RNA sequencing analyses identified the DNA damage repair gene mortality factor 4-like 1 (MORF4L1) as a critical regulator of hepatocellular carcinoma progression and resistance to RT. This finding was further validated using clinical cohorts, patient-derived xenograft models, and in vitro experiments. Immunoprecipitation followed by mass spectrometry analysis revealed that partner and localiser of BRCA2 is an interaction partner of MORF4L1. Furthermore, MORF4L1 was demonstrated to acetylate partner and localiser of BRCA2 at lysine 628, inhibiting its ubiquitination and subsequent degradation. Additionally, MORF4L1 enhanced histone H3 acetylation at lysine 4, which facilitates DNA damage repair factor recruitment. Cross-priming assay and genetically engineered mouse model results indicated that MORF4L1 antagonist argatroban in combination with RT enhances anti-tumor immune responses by activating the cyclic GMP-AMP synthase-stimulator of interferon genes signaling pathway. This combination significantly improved the therapeutic efficacy of RT when used alongside immune checkpoint inhibitors. The study findings underscore the pivotal role of MORF4L1 in hepatocellular carcinoma progression and RT resistance, suggesting that combining argatroban with RT may overcome RT resistance and improve therapeutic outcomes. - Source: PubMed
Publication date: 2025/11/05
Wang Si-WeiHong Wei-FengHuang Yi-LanZheng Yi-MinZheng Qiu-YiCheng Jun-JieTang Bu-FuChen Gen-WenLiang Bu-GangLu Jia-ChengYuan LiHsu Shu-JungZhang YangZheng Xiao-BinZeng Zhao-ChongZhou JianFan JiaKe Ai-WuGao ChaoDu Shi-Suo - Colorectal cancer is a common malignant tumor worldwide. Ubiquitin-specific proteases 53 (USP53) is a deubiquitinase that plays tumor-suppressing roles in multiple cancers. The analysis from databank showed that USP53 was downregulated in colorectal cancer specimens, and patients with USP53 low expression displayed poorer survival. This study aims to investigate the role of USP53 in colorectal cancer. Our clinical data displayed the low expression of USP53, compared with paired para-carcinoma tissues. Gain- and loss-of-function experiments firstly demonstrated that the overexpression of USP53 suppressed growth of colorectal cancer cells in vivo and in vitro, and aggravated bleomycin-induced cell damage. The silencing of USP53 played opposite roles. Through immunoprecipitation-liquid chromatogram/mass spectrum (IP-LC/MS) and ubiquitylome analysis, mortality factor 4-like protein 1 (MORF4L1) was screened as the potential substrate of USP53. The USP53 and MORF4L1 protein levels were positively related in colorectal cancer samples. USP53 bound to MORF4L1 and intercepted its ubiquitination and degradation, and the K249 and K227 of MORF4L1 protein were identified as the key sites. MORF4L1 was decreased in colorectal cancer samples, and patients with low MORF4L1 expression also exhibited poorer survival. Enhanced expression of MORF4L1 alleviated proliferation of colorectal cancer cells, and the effects of shUSP53 on colorectal cancer cells were abrogated by MORF4L1. In conclusion, USP53 suppressed growth of colorectal cancer cells by catalyzing the deubiquitination of MORF4L1. These findings may provide novel diagnostic markers or therapeutic targets for colorectal cancer in clinic. - Source: PubMed
Publication date: 2025/10/06
Xin HeWang ChuanzhuoChi YuanLiu Zhaoyu