Last update 01 Nov 2024

ABHD6

Last update 01 Nov 2024

Basic Info

Synonyms

2-arachidonoylglycerol hydrolase, ABHD6, abhydrolase domain containing 6

+ [3]

Introduction

Lipase that preferentially hydrolysis medium-chain saturated monoacylglycerols including 2-arachidonoylglycerol (PubMed:22969151). Through 2-arachidonoylglycerol degradation may regulate endocannabinoid signaling pathways (By similarity). Also has a lysophosphatidyl lipase activity with a preference for lysophosphatidylglycerol among other lysophospholipids (By similarity). Also able to degrade bis(monoacylglycero)phosphate (BMP) and constitutes the major enzyme for BMP catabolism (PubMed:26491015). BMP, also known as lysobisphosphatidic acid, is enriched in late endosomes and lysosomes and plays a key role in the formation of intraluminal vesicles and in lipid sorting (PubMed:26491015).

Drugs associated with ABHD6

ABHD6 inhibitor(Ono Pharmaceutical)

Target

ABHD6

Mechanism

ABHD6 inhibitors

Active Org.

Ono Pharmaceutical Co., Ltd.

Originator Org.

Ono Pharmaceutical Co., Ltd.

Active Indication

Autoimmune Diseases [+4]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

[18F]JZP-MA-11

Target

ABHD6

Mechanism

ABHD6 inhibitors

Active Org.

The University of Queensland

Originator Org.

The University of Queensland

Active Indication-

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ABHD6

100 Translational Medicine associated with ABHD6

0 Patents (Medical) associated with ABHD6

121

Literatures (Medical) associated with ABHD6

01 Aug 2024·NeuroImage

Elucidating genetic and molecular basis of altered higher-order brain structure-function coupling in major depressive disorder

Article

Author: Fang, Zhaolin ; Xu, Xinli ; Xiao, Jie ; Long, Haixia ; Lv, Mingqi ; Zhou, Qianwei ; Yang, Xu-Hua ; Fan, Ming ; Chen, Zihao ; Sun, Hui

Previous studies have shown that major depressive disorder (MDD) patients exhibit structural and functional impairments, but few studies have investigated changes in higher-order coupling between structure and function. Here, we systematically investigated the effect of MDD on higher-order coupling between structural connectivity (SC) and functional connectivity (FC). Each brain region was mapped into embedding vector by the node2vec algorithm. We used support vector machine (SVM) with the brain region embedding vector to distinguish MDD patients from health controls (HCs) and identify the most discriminative brain regions. Our study revealed that MDD patients had decreased higher-order coupling in connections between the most discriminative brain regions and local connections in rich-club organization and increased higher-order coupling in connections between the ventral attentional network and limbic network compared with HCs. Interestingly, transcriptome-neuroimaging association analysis demonstrated the correlations between regional rSC-FC coupling variations between MDD patients and HCs and α/β-hydrolase domain-containing 6 (ABHD6), β 1,3-N-acetylglucosaminyltransferase-9(β3GNT9), transmembrane protein 45B (TMEM45B), the correlation between regional dSC-FC coupling variations and retinoic acid early transcript 1E antisense RNA 1(RAET1E-AS1), and the correlations between regional iSC-FC coupling variations and ABHD6, β3GNT9, katanin-like 2 protein (KATNAL2). In addition, correlation analysis with neurotransmitter receptor/transporter maps found that the rSC-FC and iSC-FC coupling variations were both correlated with neuroendocrine transporter (NET) expression, and the dSC-FC coupling variations were correlated with metabotropic glutamate receptor 5 (mGluR5). Further mediation analysis explored the relationship between genes, neurotransmitter receptor/transporter and MDD related higher-order coupling variations. These findings indicate that specific genetic and molecular factors underpin the observed disparities in higher-order SC-FC coupling between MDD patients and HCs. Our study confirmed that higher-order coupling between SC and FC plays an important role in diagnosing MDD. The identification of new biological evidence for MDD etiology holds promise for the development of innovative antidepressant therapies.

19 Jul 2024·Alternative therapies in health and medicine

Identification and Validation of Prognostic Risk Model for Female-Specific Lung Adenocarcinoma.

Article

Author: Xie, Siyu ; Zhai, Jianxue ; Feng, Siyang ; Guo, Yunhui ; Yang, Wei

BackgroundLung adenocarcinoma (LUAD) is a major pathological subtype of non-small cell lung cancer and occurs more commonly in females than other lung cancer subtypes. Studying female-specific oncogenes in LUAD may provide personalized medicine approaches for females with LUAD.ObjectiveWe aimed to identify the possible female-specific oncogenes of LUAD and understand their potential impact on treatment strategies for specific cancer subgroups.MethodsThe gene expression profiles of LUAD were downloaded from The Cancer Genome Atlas (TCGA) database and the GSE72094 dataset. TCGA database is currently the largest database of cancer genetic information. Female-specific differentially expressed genes (DEGs) were identified by R programming software. Functional annotation of DEGs was conducted based on KEGG pathway enrichment analysis. Univariate and multivariate Cox proportion analyses were applied to construct a prognostic risk score model with the DEGs. Kaplan‒Meier and ROC curves were plotted to validate the predictive effect of the prognostic DEGs signature. Gene set enrichment analysis (GSEA) was applied to identify the potential pathways in the high-risk groups in female LUAD. Finally, the immunohistochemical staining (IHC) was conducted to verify the expression of CABLES1 in human LUAD samples.ResultsWe constructed a prognostic signature that includes 12 female-specific DEGs (P < .05). Among them, ABHD6, CABLES1, CXCL5, DNAJB4, EFNB2, HLX, MEOX2, MTMR10, PPFIBP1, and RERG were down-regulated in LUAD, while MFSD6L and SOX9 were up-regulated in LUAD (P < .0001). The Kaplan-Meier, and receiver operator characteristic (ROC) curves revealed efficient and stable prediction of the prognostic signature in the female LUAD patients. It was showed the risk score model has a good predictive effect on the prognosis of female LUAD patients but is not effective for male patients (P < .0001). The ROC curve showed that the areas under the curve (AUC) of first-, third- and fifth-year survival were 0.70, 0.69, and 0.79, respectively, which indicated good sensitivity and specificity of the 12-gene risk score algorithm in predicting the prognosis of female LUAD. GSEA revealed that the high-risk group was significantly enriched in the EMT, E2F targets, Myc targets, G2/M checkpoint, glycolysis, hypoxia, and mTORC1 signaling pathways (P < .05). Immunohistochemical staining showed lower CABLES1 expression was associated with higher pTNM stage in female LUAD but not in male LUAD (P < .05).ConclusionOur study constructed and verified a prognostic signature based on 12 female-specific DEGs of LUAD, which could improve the understanding of sex-related risk factors involved in LUAD carcinogenesis and progression, and may provide personalized treatment strategies for female LUAD patients.

01 Apr 2024·Molecular Carcinogenesis

ABHD6 suppresses colorectal cancer progression via AKT signaling pathway

Article

Author: Gao, Zhidong ; Zhang, Rui ; Wang, Shuo ; Jin, Yiteng ; Bao, Yudi ; Gan, Lin ; Xiong, Xiaoyu ; Ye, Yingjiang ; Zeng, Zexian ; Hou, Sen ; Yang, Changjiang

AbstractColorectal cancer (CRC) continues to be a prevalent malignancy, posing a significant risk to human health. The involvement of alpha/beta hydrolase domain 6 (ABHD6), a serine hydrolase family member, in CRC development was suggested by our analysis of clinical data. However, the role of ABHD6 in CRC remains unclear. This study seeks to elucidate the clinical relevance, biological function, and potential molecular mechanisms of ABHD6 in CRC. We investigated the role of ABHD6 in clinical settings, conducting proliferation, migration, and cell cycle assays. To determine the influence of ABHD6 expression levels on Oxaliplatin sensitivity, we also performed apoptosis assays. RNA sequencing and KEGG analysis were utilized to uncover the potential molecular mechanisms of ABHD6. Furthermore, we validated its expression levels using Western blot and reactive oxygen species (ROS) detection assays. Our results demonstrated that ABHD6 expression in CRC tissues was notably lower compared to adjacent normal tissues. This low expression correlated with a poorer prognosis for CRC patients. Moreover, ABHD6 overexpression impeded CRC cell proliferation and migration while inducing G0/G1 cell cycle arrest. In vivo experiments revealed that downregulation of ABHD6 resulted in an increase in tumor weight and volume. Mechanistically, ABHD6 overexpression inhibited the activation of the AKT signaling pathway and decreased ROS levels in CRC cells, suggesting the role of ABHD6 in CRC progression via the AKT signaling pathway. Our findings demonstrate that ABHD6 functions as a tumor suppressor, primarily by inhibiting the AKT signaling pathway. This role establishes ABHD6 as a promising prognostic biomarker and a potential therapeutic target for CRC patients.

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ABHD6

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