Ask about this productRelated genes to: MKRN1 antibody
- Gene:
- MKRN1 NIH gene
- Name:
- makorin ring finger protein 1
- Previous symbol:
- -
- Synonyms:
- RNF61
- Chromosome:
- 7q34
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-19
- Date modifiied:
- 2014-11-19
Related products to: MKRN1 antibody
Related articles to: MKRN1 antibody
- Renal angiomyolipomas (AMLs) are clonal tumors formed by the abnormal differentiation of transformed renal progenitor cells. However, the cytogenetic and malignant transformations of renal AMLs require further investigation. Makorin ring finger protein 1 (MKRN1), a transcriptional co-regulator and E3 ubiquitin ligase, may act as a tumor regulator that mediates tumor biological processes. Although it is known as a prognostic marker of renal cell carcinoma, hepatocellular carcinoma, and pancreatic adenocarcinoma, its expression and function in renal AMLs remain unclear. Therefore, we aimed to investigate the expression and function of MKRN1 in AML cells. - Source: PubMed
Publication date: 2026/01/30
Chang Tzu-HsuanChang Ying-HsuLiu Chung-YiWang Tze-KaiPang Jacob See-TongChuang Cheng-Keng - An increased understanding of molecular alterations over the last decade has also impacted the landscape of sinonasal squamous cell carcinoma (SNSCC). In addition to traditional SCC risk factors (e.g. smoking) and high-risk HPV (HR- HPV), other drivers are emerging, such as DEK::AFF2 fusion in non-keratinizing and papillary SNSCC. Treatment of squamous cell carcinoma has been revolutionized with development of drugs that target key driver mutations and immune checkpoints. We describe a case report of nasal nonkeratinizing squamous cell carcinoma- HPV-high risk (HPV-HR) positive and harboring an MKRN1::BRAF fusion. We further discuss the significance of these findings, integrated in the context of current literature. - Source: PubMed
Publication date: 2026/03/13
Bell DianaWang Eric WChoby GarretSnyderman CarlArivarasan KarunamurthySeethala Raja R - BRAF, when mutated at V600E, is a well-known potent early oncogenic driver in papillary thyroid carcinoma (PTC), with potential prognostic and therapeutic implications. Non-V600E mutations are less common and without clear functional or therapeutic significance. One class of non-V600E mutations is BRAF gene fusions, which typically involve the C-terminal kinase domain of BRAF joined to a wide repertoire of potential N-terminal fusion partners. The aim of this study was to employ a sequential algorithmic approach to identify patients with BRAF fusions based on an integrated analysis of histologic, immunohistochemistry (IHC), and molecular (NGS) features of BRAF-rearranged PTCs. Nine patients with PTC previously scrutinized as BRAF V600E negative by IHC were analyzed by NGS. The studied 9 cases showed conventional PTC growth; 2 cases displayed a minor high-grade component (tall cell and hobnailing, < 20%), 1 case qualified as high-grade differentiated thyroid carcinoma (presence of necrosis and mitotic activity > 5 MF/ 2 mm; adjacent conventional PTC was present), and 1 case represented neck (lymph node) recurrence after 10 years. BRAF fusions were detected in all cases (10 different fusion partners: NRF1, MKRN1, MACF1, MTDH1, ARHGAP26, STRBF, FCHSDH2, POM121C, UBAP2L, SND1). To our knowledge, 7 of these fusions have not been reported so far in PTC (NRF1::BRAF, MTDH1::BRAF, ARHGAP26::BRAF, BRAF::STRBF, FCHSDH2::BRAF, BRAF::POM121C, UBAP2L::BRAF). In 3 PTCs, BRAF fusions were sole genomic events. Concurrent TERT (c.-124C > T) mutations were detected in 3 PTCs; pathogenic IGF2 amplification was present in another PTC, in addition to BRAF fusion. Two simultaneous fusions BRAF::STRBF and FCHSDH2::BRAF were found in one case of PTC; two BRAF fusions (BRAF::POM121C; UBAP2L::BRAF) co-existed with 2 FOXO1 fusions (FOXO1::TES, YWHAG::FOXO1) in one PTC. In summary, we report 7 new BRAF fusions in PTC BRAF V600E-WT. Additional clinical research is needed to elucidate the behavior of BRAF fusion-driven thyroid carcinomas and the therapeutic utility of MAPK pathway inhibitors. - Source: PubMed
Publication date: 2026/02/16
McGrath NathanLiang LiBakkar RaniaGernon Thomas JMaghami EllieAfkhami MichelleBell Diana - Postpartum depression (PPD) is a significant global health concern affecting women, yet effective and innovative therapeutic targets remain limited. Although genome-wide association studies (GWAS) have identified genetic risk loci, their underlying mechanisms and translational potential remain poorly understood. Therefore, we integrated PPD GWAS data with protein quantitative trait loci from two independent datasets to identify risk genes through proteome-wide association studies (PWAS). Validation was performed using colocalization analysis and Mendelian randomization (MR). To assess the safety of genes as drug targets, phenome-wide MR (Phe-MR) was conducted using the UK Biobank disease data. Finally, we performed gene methylation analysis in PPD patients, alongside validation of expression in key brain regions including anterior cingulate gyrus (AnCg), dorsolateral prefrontal cortex, and nucleus accumbens, as well as in peripheral blood (whole blood and leukocytes), across depressive patients and chronic mild stress mice. Co-expression enrichment was used to identify biological pathways associated with risk genes. PWAS and colocalization analysis identified MKRN1 and CCDC92 as overlapping risk genes, with MKRN1 validated in MR. Phe-MR showed non-significant association between MKRN1 dysregulation and disease beyond depression and mood disorders, suggesting minimal off-target effects. Methylation analysis in PPD patients' blood revealed significant hypomethylation of MKRN1, consistent with expression analysis that confirmed its upregulation in AnCg and as a biomarker in blood. Enrichment analysis indicated MKRN1 involvement in immune-inflammatory pathways. Our study identified MKRN1 as a therapeutic target for PPD, integrating multi-omics evidence from genomics, proteomics, and druggable proteome profiling, and offering a promising path for targeted treatments. - Source: PubMed
Publication date: 2026/02/10
Jia TingtingYuan ChengsongHu ShiyiXie LiangyueLiu AndiQin FengqinHe YongjiZhang Chengcheng - The p53-murine double minute 2 (MDM2) feedback loop plays a central role in tumor suppression by optimizing p53-dependent DNA damage responses (DDRs), though it has been suggested that factors other than MDM2 are also involved in the regulation of the p53-MDM2 feedback loop. We identified makorin ring finger protein 1 (MKRN1) as a novel ubiquitin E3 ligase that ubiquitinates MDM2 and thereby promotes the p53 activation. As previously demonstrated, MKRN1 ubiquitinates and degrades p53 under steady-state conditions. However, when DNA damage occurs, MKRN1 switches its substrate to MDM2. Thereafter, MKRN1 promotes the stabilization and activation of p53 through proteasomal degradation of MDM2, which contributes to the elimination of DNA-damaged cells. Moreover, we found that the switch in the substrate of MKRN1 was determined by the NAD(+)-dependent protein deacetylase Sirtuin-1 (SIRT1). Thus, our results suggest that MKRN1 working in conjunction with SIRT1 is a master regulator of the p53-MDM2 feedback loop modulated by crosstalk between ubiquitination and acetylation. - Source: PubMed
Publication date: 2026/01/30
Shimada TatsuyaNoguchi TakuyaKomatsu RyutoOtani KoheiKomatsu TakayaSuzuki SaraMitsuya MakiOkubo TakumiIto RyoYamada MayukaHirata YusukeMatsuzawa Atsushi