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Last update 08 May 2025

MMEL1

Last update 08 May 2025

Basic Info

Synonyms

MELL1, Membrane metallo-endopeptidase-like 1, Membrane metallo-endopeptidase-like 1, soluble form

+ [14]

Introduction

Metalloprotease involved in sperm function, possibly by modulating the processes of fertilization and early embryonic development. Degrades a broad variety of small peptides with a preference for peptides shorter than 3 kDa containing neutral bulky aliphatic or aromatic amino acid residues. Shares the same substrate specificity with MME and cleaves peptides at the same amide bond (By similarity).

Drugs associated with MMEL1

HG-1287

Target

MMEL1

Mechanism

MMEL1 modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Cardiovascular Diseases [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

SCH 39370

Target

MMEL1

Mechanism

MMEL1 inhibitors

Active Org.-

Originator Org.

Schering-Plough Corp.

Active Indication-

Inactive Indication

Hypertension

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MMEL1

100 Translational Medicine associated with MMEL1

0 Patents (Medical) associated with MMEL1

245

Literatures (Medical) associated with MMEL1

01 Jul 2025·Experimental Neurology

Inhibition of mitoNEET ameliorates traumatic brain injury-induced ferroptosis and cognitive dysfunction by stabilizing dihydroorotate dehydrogenase

Article

Author: Zeng, Xiaofeng ; Li, Qianqian ; Luo, Chengliang ; Xu, Yejia ; Li, Jing ; Zhao, Yang ; Yang, Rui ; Su, Li ; Jia, Bowen ; Wang, Shangwen

BACKGROUNDDue to the complexity of the causes and mechanisms of traumatic brain injury (TBI), there is still a lack of effective clinical treatments. Ferroptosis is an iron-dependent mode of cell death characterized by lipid peroxidation, which is involved in the pathophysiology of TBI. The process of ferroptosis involves mitochondria, and mitochondrial alterations are important biomarkers for the detection of ferroptosis. As an iron‑sulfur [2Fe-2S] cluster protein, mitoNEET (gene: CISD1) is located on the outer surface of mitochondria, and plays a key role in regulating cellular energy use, lipid metabolism, and mitochondrial iron content. However, whether mitoNEET is involved in regulating ferroptosis and cognitive decline caused by TBI is unclear.RESULTSIn the present study, we observed that a mitoNEET ligand or inhibitor, NL-1 intervention significantly inhibited the occurrence of ferroptosis and alleviated neuronal injury after TBI. The gain and loss-function models of mitoNEET were then used to confirm the role of mitoNEET in ferroptosis and cognitive dysfunction after TBI. Knockdown of mitoNEET alleviated cognitive dysfunction and exhibited significant anti-ferroptosis effects in a mouse model of TBI, whereas mitoNEET overexpression exerted the opposite effects. Furthermore, silencing of DHODH blocked the anti-ferroptosis and neuroprotective effects of NL-1.CONCLUSIONSTaken together, these data demonstrated that NL-1 reversed TBI-induced ferroptosis and neurodegeneration, at least in part through the activation of mitoNEET/DHODH signaling axis. Pharmacological and gene inhibition of mitoNEET ameliorated TBI-induced ferroptosis and cognitive dysfunction. Mechanically, NL-1 may be through targeting mitoNEET to potentiate DHODH-mediated ferroptosis defense.

01 Apr 2025·International Dental Journal

Identification of Potential Biomarkers and Therapeutic Targets for Periodontitis

Article

Author: Li, Chunhui ; Zhu, Hanfang ; Xiong, Junkai ; Mou, Yunjie ; Yang, Bin ; Chen, Xinyu ; Hou, Shuhan ; Huoshen, Wuda ; Sun, Chen ; Yi, Sha ; He, Yahan ; Huang, Haonan

BACKGROUNDPeriodontitis is a chronic and multifactorial inflammatory disease. However, existing medications often lack sufficient therapeutic effects. The aim is to identify potential biomarkers and efficient therapeutic targets using Mendelian randomisation (MR) and single-cell analysis.METHODSMR analysis was conducted based on the cis-expression quantitative trait loci (cis-eQTLs) extracted from the eQTLGen Consortium and genome-wide association study (GWAS) data of periodontitis sourced from the Gene Lifestyle Interactions in Dental Endpoints (GLIDE) consortium (17,353 cases, 28,210 controls). Subsequently, colocalisation analysis was employed to detect whether genes and periodontitis shared the same casual variant. Finally, enrichment analysis, protein-protein interaction (PPI) networks, drug prediction, phenome-wide association study (PheWAS), molecular docking, and single-cell analysis were conducted to validate the significance of target genes.RESULTSFourteen drug targets were significant related with periodontitis in MR analysis. Following the colocalisation and summary-data-based MR (SMR) analysis, 3 targets (S100A12, S100A9, and S100A8) were classified into tier 1 with strong evidence, 6 therapeutic targets (ADAM12, ADHFE1, BLK, HEBP1, SERPINE2, and TEK) were classified into tier 2 with moderate evidence, and 5 therapeutic targets (LY86, MMEL1, S100B, SPP1, and TRIB3) were classified into tier 3 with convincing evidence. PheWAS analysis showed that only TEK and SPP1 in tier 2 may induce side effects, including cardiometabolic and oncological issues. Molecular docking demonstrated strong binding between drugs and their respective protein targets. In the single-cell analysis, 5 target genes (HEBP1, LY86, S100A8, S100A9, and S100A12) exhibited enrichment in monocytes, while BLK and LY86 were primarily enriched in B cells.CONCLUSIONThe study identified 14 potential therapeutic targets for periodontitis. Among these, 3 therapeutic targets (S100A12, S100A9, and S100A8) demonstrated robust and well-supported results. Drugs designed to target these genes have a higher possibility of success in clinical trials, which are hopeful for prioritising periodontitis drug development.

01 Mar 2025·Plant Biotechnology Journal

The OsNL1‐OsTOPLESS2‐OsMOC1/3 pathway regulates high‐order tiller outgrowth in rice

Article

Author: Lin, Qibing ; Wang, Jiachang ; Luo, Wenfan ; Jiang, Xiaokang ; Ren, Yulong ; Shao, Jiale ; Xun, Ziqi ; Zhang, Feng ; Wan, Jianmin ; Zhao, Huixian ; Cheng, Zhijun ; Liu, Xin ; Wang, Jian ; Li, Shuai

SummaryTiller is an important factor in determining rice yield. Currently, researches mainly focus on the outgrowth of low‐order tiller (LOT), while the regulation mechanism of high‐order tiller (HOT) outgrowth has remained unknown. In this study, we detected one OsNL1 mutant, nl1, exhibiting HOT numbers increase, and found that OsNL1 interacts with OsTOPLESS2, which was mediated by the core motif of nine amino acids VDCTLSLGT within the HAN domain of OsNL1. The topless2 mutant exhibits similar HOT number increase as in the nl1. Through ChIP‐seq analysis, we revealed that OsNL1 recruits OsTOPLESS2 to conduct histone deacetylation in the promoters of OsMOC1 and OsMOC3 to regulate HOT outgrowth. Moreover, we showed that the HAN domain is essential for OsNL1 function as a repressor. In summary, our study reveals partial mechanism of HOT outgrowth in rice and deciphers the molecular biology function of the HAN domain. This will contribute to the comprehensive understanding of tiller outgrowth and the role of HAN‐domain‐containing genes.

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MMEL1

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