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Last update 08 May 2025

RMI2

Last update 08 May 2025

Basic Info

Synonyms

BLAP18, BLM-associated protein of 18 kDa, C16orf75

+ [5]

Introduction

Essential component of the RMI complex, a complex that plays an important role in the processing of homologous recombination intermediates. It is required to regulate sister chromatid segregation and to limit DNA crossover. Essential for the stability, localization, and function of BLM, TOP3A, and complexes containing BLM. In the RMI complex, it is required to target BLM to chromatin and stress-induced nuclear foci and mitotic phosphorylation of BLM.

Drugs associated with RMI2

PIP-199

Target

FANCM x RMI1 x RMI2

Mechanism

FANCM inhibitors [+2]

Active Org.

The University of Sydney

Originator Org.

The University of Sydney

Active Indication

Bloom Syndrome [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with RMI2

100 Translational Medicine associated with RMI2

0 Patents (Medical) associated with RMI2

Literatures (Medical) associated with RMI2

01 Feb 2025·Journal of Ethnopharmacology

Glabridin inhibits proliferation and migration in hepatocellular carcinoma by regulating multi-targets

Article

Author: Wang, Fei ; Lu, Yi ; Liu, Yifei ; Yang, Yanfang ; Wu, Mojiao ; Yuan, Chong ; Wu, Hezhen

ETHNOPHARMACOLOGICAL RELEVANCEGlycyrrhiza uralensis Fisch. (GC) is widely utilized in traditional Chinese medicine (TCM) for its properties in Qi tonification, heat clearing, and detoxification. Within TCM theory, Qi is also implicated in tumor development. Numerous TCM formulas containing GC are used for their anti-tumor effects, and contemporary pharmacological research has demonstrated that ethyl acetate extracts (EAe) of GC, along with potential bioactive compounds like glabridin (Gla), possess anti-tumor properties. Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and a major challenge to global healthcare, with high incidence and poor prognosis. Nevertheless, the effects and mechanisms of action of Gla in inhibiting HCC have not been extensively studied.AIM OF STUDYThis study aims to elucidate the effects and mechanisms of action of Gla against HCC by in vitro and in vivo experiments.METHODSThe inhibitory effects of ethyl acetate extract (EAe) of GC and its bioactive compounds on HCC were studied using a drug-cell interaction system equipped with UPLC-MS/MS and high-throughput screening methods in vitro. RNA sequencing (RNA-seq) and bioinformatics technologies were employed to detect the differentially expressed genes (DEGs) and pathways in HepG2 cells. The findings were further validated using quantitative real-time PCR (qPCR) and Western blot (WB) assays. Additionally, an in vivo tumor-bearing mouse model established with H22 cells was utilized to examine alterations in tumor tissues via hematoxylin-eosin (HE) staining. Immunohistochemistry was used to assess the protein expression levels of hub targets within each group.RESULTSBoth in vitro and in vivo experiments demonstrated the effects of EAe against HCC, identifying Gla was one of its main bioactive compounds. Integration of RNA-seq data with clinical databases revealed that Gla inhibited HCC by up-regulating the expression levels of DUSP5, ZFP36, KLF10, and NR4A1, while down-regulating RMI2 expression. These findings were further validated by Gene Expression Omnibus (GEO), qPCR, WB and immunohistochemistry assays.CONCLUSIONSGla regulates the expression levels of DUSP5, ZFP36, KLF10, NR4A1, and RMI2 to against HCC, providing valuable insights for the application of Gla in HCC treatment.

01 Mar 2024·Journal of Crohn's and Colitis

Human Leukocyte Antigen Signatures as Pathophysiological Discriminants of Microscopic Colitis Subtypes

Article

Author: Zheng, Tenghao ; Vigren, Lina ; Almer, Sven ; Guagnozzi, Danila ; Iglesias, Eva ; Mellander, Marie-Rose ; Colombel, Jean-Frederic ; Bresso, Francesca ; Marsal, Sara ; Ludvigsson, Jonas F ; Miehlke, Stephan ; Pierik, Marieke ; Piqueras, Marta ; Ferrer, Carmen ; Khalili, Hamed ; Ohlsson, Bodil ; Weersma, Rinse K ; Janczewska, Izabella ; Liu, Xingrong ; Halfvarson, Jonas ; Julià, Antonio ; Peter, Inga ; Madisch, Ahmed ; Busquets, David ; Bujanda, Luis ; Escudero-Hernández, Celia ; Chen, Ye ; Sjöberg, Klas ; Lieb, Wolfgang ; D’Amato, Mauro ; Franke, Andre ; Münch, Andreas ; Esteve, Maria ; Jonkers, Daisy ; Roda, Giulia ; Fernández-Bañares, Fernando ; Verhaegh, Bas ; Bonfiglio, Ferdinando ; Kupčinskas, Juozas ; Lucendo, Alfredo J ; Pardi, Darrell ; Zabana, Yamile ; Camargo Tavares, Leticia

AbstractBackground and AimsMicroscopic colitis [MC] is currently regarded as an inflammatory bowel disease that manifests as two subtypes: collagenous colitis [CC] and lymphocytic colitis [LC]. Whether these represent a clinical continuum or distinct entities is, however, an open question. Genetic investigations may contribute important insight into their respective pathophysiologies.MethodsWe conducted a genome-wide association study [GWAS] meta-analysis in 1498 CC, 373 LC patients, and 13 487 controls from Europe and the USA, combined with publicly available MC GWAS data from UK Biobank and FinnGen [2599 MC cases and 552 343 controls in total]. Human leukocyte antigen [HLA] alleles and polymorphic residues were imputed and tested for association, including conditional analyses for the identification of key causative variants and residues. Genetic correlations with other traits and diagnoses were also studied.ResultsWe detected strong HLA association with CC, and conditional analyses highlighted the DRB1*03:01 allele and its residues Y26, N77, and R74 as key to this association (best p = 1.4 × 10-23, odds ratio [OR] = 1.96). Nominally significant genetic correlations were detected between CC and pneumonia [rg = 0.77; p = 0.048] and oesophageal diseases [rg = 0.45, p = 0.023]. An additional locus was identified in MC GWAS analyses near the CLEC16A and RMI2 genes on chromosome 16 [rs35099084, p = 2.0 × 10-8, OR = 1.31]. No significant association was detected for LC.ConclusionOur results suggest CC and LC have distinct pathophysiological underpinnings, characterised by an HLA predisposing role only in CC. This challenges existing classifications, eventually calling for a re-evaluation of the utility of MC umbrella definitions.

01 Feb 2024·Molecular Cell

BLM and BRCA1-BARD1 coordinate complementary mechanisms of joint DNA molecule resolution

Article

Author: Vendrell, Iolanda ; Jones, Samuel E ; Tsukada, Kaima ; Fawkes, Matthew ; Blackford, Andrew N ; Kessler, Benedikt M ; Fischer, Roman ; Durin, Mary-Anne ; Chapman, J Ross ; Bannister, Julius

The Bloom syndrome helicase BLM interacts with topoisomerase IIIα (TOP3A), RMI1, and RMI2 to form the BTR complex, which dissolves double Holliday junctions and DNA replication intermediates to promote sister chromatid disjunction before cell division. In its absence, structure-specific nucleases like the SMX complex (comprising SLX1-SLX4, MUS81-EME1, and XPF-ERCC1) can cleave joint DNA molecules instead, but cells deficient in both BTR and SMX are not viable. Here, we identify a negative genetic interaction between BLM loss and deficiency in the BRCA1-BARD1 tumor suppressor complex. We show that this is due to a previously overlooked role for BARD1 in recruiting SLX4 to resolve DNA intermediates left unprocessed by BLM in the preceding interphase. Consequently, cells with defective BLM and BRCA1-BARD1 accumulate catastrophic levels of chromosome breakage and micronucleation, leading to cell death. Thus, we reveal mechanistic insights into SLX4 recruitment to DNA lesions, with potential clinical implications for treating BRCA1-deficient tumors.

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RMI2

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