ENDOG

Last update 08 May 2025

Basic Info

Synonyms

Endo G, ENDOG, endonuclease G

+ [1]

Introduction

Endonuclease that preferentially catalyzes the cleavage of double-stranded 5-hydroxymethylcytosine (5hmC)-modified DNA (PubMed:25355512). The 5hmC-modified nucleotide does not increase the binding affinity, but instead increases the efficiency of cutting and specifies the site of cleavage for the modified DNAs (By similarity). Shows significantly higher affinity for four-stranded Holliday junction over duplex and single-stranded DNAs (By similarity). Promotes conservative recombination when the DNA is 5hmC-modified (PubMed:25355512). Promotes autophagy through the suppression of mTOR by its phosphorylation-mediated interaction with YWHAG and its endonuclease activity-mediated DNA damage response (PubMed:33473107). GSK3-beta mediated phosphorylation of ENDOG enhances its interaction with YWHAG, leading to the release of TSC2 and PIK3C3 from YWHAG resulting in mTOR pathway suppression and autophagy initiation (PubMed:33473107). Promotes cleavage of mtDNA in response to oxidative and nitrosative stress, in turn inducing compensatory mtDNA replication (PubMed:29719607).

100 Clinical Results associated with ENDOG

100 Translational Medicine associated with ENDOG

0 Patents (Medical) associated with ENDOG

588

Literatures (Medical) associated with ENDOG

01 Jun 2025·Food Chemistry

Potential mechanism of dietary palm kernel meal effect on muscle tenderness in Tibetan sheep revealed by proteomics and phosphorylated proteomics

Article

Author: Yang, Chao ; Hou, Shengzhen ; Sun, Shengnan ; Ma, Ying ; Yuan, Zhenzhen ; Gui, Linsheng ; Wang, Zhiyou ; Han, Lijuan ; Yang, Baochun

The labe free proteomics technology and 4D labe free phosphorylation proteomics technology was used to systematically analyse the protein expression regulatory mechanisms of muscle tenderness. 59 differentially expressed proteins were screened by proteomic data analysis. Phosphorylated proteomic analysis showed 681 modified peptide levels were changed, of which 235 modified peptide levels corresponded to 132 proteins up-regulated and 446 modified peptide levels corresponded to 253 proteins down-regulated. Then, the two-omics analysis further predicted that the regulatory mechanism of tenderness was mainly based on glycolysis, regulating mitochondrial autophagy, apoptosis, AMPK and HIF-1 signaling pathway to regulate muscle tenderness, which was specifically manifested in the modulation of Ca²⁺ release to promote the degradation of myofibrillar fibrillar proteins by the relevant proteins, shortening of post-slaughter muscle glycolysis and reducing the degree of muscle glycolysis. Which was verified by WB, P53, ENO5, ALDOA, ENDOG and PINK1 were identified as potential factors for tenderness regulation.

01 May 2025·Journal of Biochemical and Molecular Toxicology

Newly Synthesized PW06 Induced Cell Apoptosis in Human Glioblastoma Multiforme GBM 8401 Cells Through Caspase‐ and Mitochondria‐Dependent Pathways

Article

Author: Lien, Jin‐Cherng ; Huang, Yi‐Ping ; Lai, Kuang‐Chi ; Ma, Yi‐Shih ; Chueh, Fu‐Shin ; Hsu, Sheng‐Yao ; Chou, Yu‐Cheng ; Chu, Yung‐Lin ; Wu, Rick Sai‐Chuen ; Chen, Jaw‐Chyun

ABSTRACTGlioblastoma multiforme (GBM) is the most common, aggressive, and dangerous lethal tumor in the brain, which develops in adults. Currently, the efficiency of chemotherapy treatment for GBM patients is still unsatisfactory. PW06 was synthesized by Dr. Lien's laboratory (China Medical University, Taichung, Taiwan), and it was demonstrated to induce cancer cell apoptosis in human pancreatic carcinoma MIA PaCa‐2 cells. However, the anti‐cancer activities of PW06 on human GBM cancer cells are not reported. Thus, herein, PW06 was investigated on the anticancer activity on human glioblastoma multiforme GBM 8401 cells. Both PI exclusion and Annexin V/PI double staining methods were conducted for investing cell viability and apoptosis in GBM 8401 cells, respectively; they were analyzed with flow cytometer assay. Results showed that PW06 decreased total viable cell number with the process of cell apoptosis in GBM 8401 cells. Both productions of reactive oxygen species (ROS) and Ca2+, affect mitochondria membrane potential (ΔΨm) levels, and activities of caspase‐3, ‐8, and ‐9 in GBM 8401 cells after exposure with PW06 were assayed by flow cytometer. Results showed that PW06 promoted ROS production and Ca2+ release from ER but lowered the levels of ΔΨm, and it also induced higher activities in caspase‐3, ‐8, and ‐9 in GBM 8401 cells. Evaluation of protein expressions associated with apoptosis in GBM 8401 cells after being incubated with PW06 were conducted by Western blot analysis. Results show that PW06 increased GADD153, BiP, ATF‐6α, ATF‐6β, eIF2α, eIF2αpSer51, CHOP, and caspase‐4, and they are associated with ER stress‐associated protein expression. However, it induced higher pro‐apoptotic proteins (Bax and Bad) expression and inhibited anti‐apoptotic proteins (Bcl‐2, Bcl‐xl, and Mcl‐1) expression, even promoting higher cleaved caspase‐8, ‐9, and ‐3 protein expression and increased EndoG and AIF in GBM 8401 cells. Collectively, it may suggest PW06 exits anti‐GBM activity to process cell apoptosis in the human GBM 8401 cells in vitro.

08 Apr 2025·Proceedings of the National Academy of Sciences

Design of a halogen bond catalyzed DNA endonuclease

Article

Author: Rappé, Anthony K. ; Ho, Pui Shing ; Ho, Alexander N. ; Mendez, Cesar Gustavo ; Czarny, Ryan S. ; Walker, Margaret G.

In this study, we expand the repertoire of biological catalysts by showing that a halogen bond (X-bond) can functionally replace the magnesium (Mg 2+ ) cofactor in mouse endonuclease G ( m EndoG). We mutated the metal coordinating glutamate E136 in m EndoG to a meta- halotyrosine ( mX Y, X = chlorine or iodine) to form a mX Y- m EndoG construct that is both acid and base catalyzed. Under basic conditions, the enzyme is inactivated by the metal chelator ethylene diamine tetraacetic acid (EDTA), indicating that the halogen substituent facilitates deprotonation of the tyrosyl hydroxyl group, allowing recruitment of Mg 2+ to restore the metal-dependent catalytic center. At low pHs, we observe that the mX Y- m EndoG is resistant to EDTA inactivation and that the iodinated constructed is significantly more active than the chlorinated analogue. These results implicate a hydrogen bond (H-bond) enhanced X-bond as the catalyst in the mX Y- m EndoG, with asparagine N103 serving as the H-bond donor that communicates the protonation state of histidine H104 to the halogen. This model is supported by mutation studies and electrostatic potential (ESP) calculations on models for the protonated and unprotonated mX Y···N103···H104 system compared to the Mg 2+ coordination complex of the wild type. Thus, we have designed and engineered an enzyme that utilizes an unnatural catalyst in its active site—a catalytic X-bonding enzyme, or cX- Zyme—by controverting what constitutes a metal catalyst in biochemistry.

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ENDOG

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