ENDOV

Last update 08 May 2025

Basic Info

Synonyms

endonuclease V, ENDOV, FLJ35220

+ [2]

Introduction

Endoribonuclease that specifically cleaves inosine-containing RNAs: cleaves RNA at the second phosphodiester bond 3' to inosine (PubMed:23912683, PubMed:23912718, PubMed:25195743, PubMed:27573237, PubMed:31703097). Active against both single-stranded and double-stranded RNAs (PubMed:25195743, PubMed:31703097). Has strong preference for single-stranded RNAs (ssRNAs) toward double-stranded RNAs (dsRNAs) (PubMed:23912718). Cleaves mRNAs and tRNAs containing inosine (PubMed:23912683, PubMed:31703097). Also able to cleave structure-specific dsRNA substrates containing the specific sites 5'-IIUI-3' and 5'-UIUU-3' (PubMed:23912718, PubMed:27573237). Inosine is present in a number of RNAs following editing; the function of inosine-specific endoribonuclease is still unclear: it could either play a regulatory role in edited RNAs, or be involved in antiviral response by removing the hyperedited long viral dsRNA genome that has undergone A-to-I editing (Probable). Binds branched DNA structures (PubMed:23139746). Endoribonuclease that specifically cleaves inosine-containing RNAs: cleaves RNA at the second phosphodiester bond 3' to inosine (PubMed:31703097). Active against both single-stranded and double-stranded RNAs (PubMed:31703097). Cleaves tRNAs containing inosine (PubMed:31703097). Endoribonuclease that specifically cleaves inosine-containing RNAs: cleaves RNA at the second phosphodiester bond 3' to inosine (PubMed:31703097). Active against both single-stranded and double-stranded RNAs (PubMed:31703097). Cleaves tRNAs containing inosine (PubMed:31703097).

100 Clinical Results associated with ENDOV

100 Translational Medicine associated with ENDOV

0 Patents (Medical) associated with ENDOV

198

Literatures (Medical) associated with ENDOV

01 Apr 2025·International Journal of Cancer

Search for germline gene variants in colorectal cancer families presenting with multiple primary colorectal cancers

Article

Author: Ambrozkiewicz, Filip ; Försti, Asta ; Hemminki, Kari ; Lubinski, Jan ; Marciniak, Magdalena

AbstractA double primary colorectal cancer (CRC) in a familial setting signals a high risk of CRC. In order to identify novel CRC susceptibility genes, we whole‐exome sequenced germline DNA from nine persons with a double primary CRC and a family history of CRC. The detected variants were processed by bioinformatics filtering and prioritization, including STRING protein–protein interaction and pathway analysis. A total of 150 missense, 19 stop‐gain, 22 frameshift and 13 canonical splice site variants fulfilled our filtering criteria. The STRING analysis identified 20 DNA repair/cell cycle proteins as the main cluster, related to genes CHEK2, EXO1, FAAP24, FANCI, MCPH1, POLL, PRC1, RECQL, RECQL5, RRM2, SHCBP1, SMC2, XRCC1, in addition to CDK18, ENDOV, ZW10 and the known mismatch repair genes. Another STRING network included extracellular matrix genes and TGFβ signaling genes. In the nine whole‐exome sequenced patients, eight harbored at least two candidate DNA repair/cell cycle/TGFβ signaling gene variants. The number of families is too small to provide evidence for individual variants but, considering the known role of DNA repair/cell cycle genes in CRC, the clustering of multiple deleterious variants in the present families suggests that these, perhaps jointly, contributed to CRC development in these families.

01 Mar 2025·Journal of Indian Association of Pediatric Surgeons

Genetic Markers of Spina Bifida: Enrichment of Pathogenic Variants and Variants of Uncertain Significance

Article

Author: Jain, Vishesh ; Dhua, Anjan Kumar ; Kumar, Sourabh ; Kaushik, Himani ; Goel, Prabudh ; Sharma, Mahima ; Sharma, Jyoti ; Agarwala, Sandeep ; Yadav, Devendra Kumar ; Pandey, Himani ; Lal, Devi

ABSTRACTIntroduction:The genetic diversity of the population in India, shaped by its unique history of migrations and varied ethnic landscape, suggests the possibility of genetic profiles distinct from the western populations.Objective:The objective is to investigate the genetic basis of spina bifida in the Indian cohort through whole-exome sequencing and pathway enrichment.Methods:The variants of uncertain significance (VUS) of spina bifida were identified through whole-exome sequencing in the study cohort (n = 3). The pathogenic, likely pathogenic, and VUS were analyzed for protein–protein interactions and functional associations with genes implicated in spina bifida using tools such as STRING and KEGG pathways, which were validated through a literature review. The study was focused on the Wnt/planar cell polarity signaling pathway, which is crucial for neural tube closure.Results:The study-cohort was collectively represented through 40 common VUS, including eight deleterious SNPs related to genes AP3D1, NLRP9, PCDHGA11, PRSS3, MTSS2, ENDOV, C9, and NSD3. These genes were functionally linked to neural development, immune response, and cellular processes critical for neural tube closure. Notably, interactions were observed between four genes (NLGN2, PKD1, PRSS3, and PLK1) and CTNNB1 (Wnt signaling pathway) crucial for embryonic neural tube formation.Conclusions:This study has identified novel genetic variants and pathways potentially contributing to the etiopathogenesis of spina bifida in the Indian population. Future research with larger cohorts and functional studies is necessary to validate these findings and explore their potential for clinical applications in spina bifida.

09 Jan 2025·The Journal of Physical Chemistry B

How Can One Metal Power Nucleic Acid Phosphodiester Bond Cleavage by a Nuclease? Multiscale Computational Studies Highlight a Diverse Mechanistic Landscape

Review

Author: Kaur, Rajwinder ; Wetmore, Stacey D. ; Nikkel, Dylan J.

Despite the remarkable resistance of the nucleic acid phosphodiester backbone to degradation affording genetic stability, the P-O bond must be broken during DNA repair and RNA metabolism, among many other critical cellular processes. Nucleases are powerful enzymes that can enhance the uncatalyzed rate of phosphodiester bond cleavage by up to ∼10¹⁷-fold. Despite the most well accepted hydrolysis mechanism involving two metals (M_A²⁺ to activate a water nucleophile and M_B²⁺ to stabilize the leaving group), experimental evidence suggests that some nucleases can use a single metal to facilitate the chemical step, a controversial concept in the literature. The present perspective uses the case studies of four nucleases (I-PpoI, APE1, and bacterial and human EndoV) to highlight how computational approaches ranging from quantum mechanical (QM) cluster models to molecular dynamics (MD) simulations and combined quantum mechanics-molecular mechanics (QM/MM) calculations can reveal the atomic level details necessary to understand how a nuclease can use a single metal to facilitate this difficult chemistry. The representative nucleases showcase how different amino acid residues (e.g., histidine, aspartate) can fulfill the role of the first metal (M_A²⁺) in the two-metal-mediated mechanisms. Nevertheless, differences in active site architectures afford diversity in the single-metal-mediated mechanism in terms of the metal-substrate coordination, the role of the metal, and the identities of the general acid and base. The greater understanding of the catalytic mechanisms of nucleases obtained from the body of work reviewed can be used to further explore the progression of diseases associated with nuclease (mis)activity and the development of novel nuclease applications such as disease diagnostics, gene engineering, and therapeutics.

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ENDOV

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