Last update 01 Nov 2024

ACSL6

Last update 01 Nov 2024

Basic Info

Synonyms

ACS2, ACSL6, acyl-CoA synthetase long chain family member 6

+ [8]

Introduction

Catalyzes the conversion of long-chain fatty acids to their active form acyl-CoA for both synthesis of cellular lipids, and degradation via beta-oxidation (PubMed:22633490, PubMed:24269233). Plays an important role in fatty acid metabolism in brain and the acyl-CoAs produced may be utilized exclusively for the synthesis of the brain lipid.

Drugs associated with ACSL6

CN118403167

Patent Mining

Target

ACSL6

Mechanism-

Active Org.

the First Affiliated Hospital of Sun Yat-Sen University

Originator Org.

the First Affiliated Hospital of Sun Yat-Sen University

Active Indication

Liver Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ACSL6

100 Translational Medicine associated with ACSL6

0 Patents (Medical) associated with ACSL6

110

Literatures (Medical) associated with ACSL6

01 Oct 2024·Cell Biochemistry and Function

Acyl‐CoA Synthetase Long‐Chain Isoenzymes in Kidney Diseases: Mechanistic Insights and Therapeutic Implications

Review

Author: Shelke, Vishwadeep ; Gaikwad, Anil Bhanudas ; Mishra, Swati

ABSTRACTLong‐chain acyl‐CoA synthetases (ACSLs) are pivotal enzymes in fatty acid metabolism, essential for maintaining cellular homeostasis and energy production. Recent research has uncovered their significant involvement in the pathophysiology of various kidney diseases, including acute kidney injury (AKI), chronic kidney disease (CKD), diabetic kidney disease (DKD), and renal cell carcinoma (RCC). While ACSL1, ACSL3, ACSL4, and ACSL5 have been extensively studied for their roles in processes such as ferroptosis, lipid peroxidation, renal fibrosis, epithelial‐mesenchymal transition, and tumor progression, the role of ACSL6 in kidney diseases remain largely unexplored. Notably, these isoenzymes exhibit distinct functions in different kidney diseases. Therefore, to provide a comprehensive understanding of their involvement, this review highlights the molecular pathways influenced by ACSLs and their roles in modulating cell death, inflammation, and fibrosis during kidney disease progression. By examining these mechanisms in detail, this review underscores the potential of ACSLs as biomarkers and therapeutic targets, advocating for further research to elucidate the precise roles of individual ACSL isoenzymes in kidney disease progression. Understanding these mechanisms opens new avenues for developing targeted interventions and improving therapeutic outcomes for patients with kidney diseases.

01 Oct 2024·Advanced Science

Blocking ACSL6 Compromises Autophagy via FLI1‐Mediated Downregulation of COLs to Radiosensitize Lung Cancer

Article

Author: Zhang, Kun ; Jin, Hai ; Bao, Shijun ; Xiao, Yanlan ; Yao, Liuhuan ; Xu, Xinyi ; Ding, Wen ; Zhao, Zhemeng ; Guo, Jiaming ; Lin, Xiaoting ; Fang, Kai ; Yang, Xiwen ; Hao, Wei ; Zhao, Qingwei ; Cui, Xinyue

AbstractLung cancer (LC) is the leading cause of cancer‐related mortality worldwide. Radiotherapy is the main component of LC treatment; however, its efficacy is often limited by radioresistance development, resulting in unsatisfactory clinical outcomes. Here, we found that LC radiosensitivity is up‐regulated by decreased expression of long‐chain acyl‐CoA synthase 6 (ACSL6) after irradiation. Deletion of ACSL6 results in significant elevation of Friend leukemia integration 1 transcription factor (FLI1) and a marked decline of collagens (COLs). Blocking of ACSL6 impairs the tumor growth and upregulates FLI1, which reduces the levels of COLs and compromises irradiation‐induced autophagy, leading to considerable therapeutic benefits during radiotherapy. Moreover, the direct interaction between ACSL6 and FLI1 and engagement between FLI1 and COLs indicates the involvement of the ACSL6‐FLI1‐COL axis. Finally, the potently adjusted autophagy flux reduces its otherwise contributive capability in surviving irradiation stress and leads to satisfactory radiosensitization for LC radiotherapy. These results demonstrate that enhanced ACSL6 expression promotes the aggressive performance of irradiated LC through increased FLI1‐COL‐mediated autophagy flux. Thus, the ACSL6‐FLI1‐Col‐autophagy axis may be targeted to enhance the radiosensitivity of LC and improve the management of LC in radiotherapy.

20 Sep 2024·Science Advances

ACSL6-activated IL-18R1–NF-κB promotes IL-18–mediated tumor immune evasion and tumor progression

Article

Author: Ye, Lvlan ; Wang, Ziyang ; Qin, Jiale ; Di, Yuqin ; Wang, Xiongjun ; Wen, Xiangqiong ; Zhang, Xiang ; Lu, Ligong ; Xiao, Jing ; He, Weiling

Aberrant activation of IL-18 signaling regulates tumor immune evasion and progression. However, the underlying mechanism remains unclear. Here, we report that long-chain acyl-CoA synthase 6 (ACSL6) is highly expressed in liver cancer and correlated with poor prognosis. ACSL6 promotes tumor growth, metastasis, and immune evasion mediated by IL-18, independent of its metabolic enzyme activity. Mechanistically, upon IL-18 stimulation, ACSL6 is phosphorylated by ERK2 at S674 and recruits IL-18RAP to interact with IL-18R1, thereby reinforcing the IL-18R1–IL-18RAP heterodimer and triggering NF-κB–dependent gene expression to facilitate tumor development. Furthermore, the up-regulation of CXCL1 and CXCL5 by ACSL6 promotes tumor-associated neutrophil and tumor-associated macrophage recruitment, thereby inhibiting cytotoxic CD8 + T cell infiltration. Ablation or S674A mutation of ACSL6 potentiated anti–PD-1 therapeutic efficacy by increasing the effector activity of intertumoral CD8 + T cells. We revealed that ACSL6 is a potential adaptor that activates IL-18–NF-κB axis–mediated tumor immune evasion and provides valuable insights for developing effective immunotherapy strategies for cancer.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

ACSL6

Basic Info

Related

Analysis