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Last update 08 May 2025

CERS2

Last update 08 May 2025

Basic Info

Synonyms

Ceramide synthase 2, CERS2, FLJ10243

+ [10]

Introduction

Ceramide synthase that catalyzes the transfer of the acyl chain from acyl-CoA to a sphingoid base, with high selectivity toward very-long-chain fatty acyl-CoA (chain length C22-C27) (PubMed:17977534, PubMed:18165233, PubMed:18541923, PubMed:19728861, PubMed:20937905, PubMed:22144673, PubMed:22661289, PubMed:26887952, PubMed:29632068). N-acylates sphinganine and sphingosine bases to form dihydroceramides and ceramides in de novo synthesis and salvage pathways, respectively (By similarity) (PubMed:17977534, PubMed:18165233, PubMed:18541923, PubMed:19728861, PubMed:20937905, PubMed:22144673, PubMed:22661289, PubMed:26887952, PubMed:29632068). Plays a non-redundant role in the synthesis of ceramides with very-long-chain fatty acids in kidney, liver and brain. Regulates the abundance of myelin-specific sphingolipids galactosylceramide and sulfatide that affects myelin sheath architecture and motor neuron functions (By similarity).

Drugs associated with CERS2

DH-20931

Target

CERS2

Mechanism

CERS2 agonists

Active Org.

University of Florida

Originator Org.

University of Florida

Active Indication

Triple Negative Breast Cancer

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CERS2

100 Translational Medicine associated with CERS2

0 Patents (Medical) associated with CERS2

259

Literatures (Medical) associated with CERS2

01 Dec 2025·Molecular Biology Reports

Lysophosphatidylcholine induces ceramide synthase-2 expression in primary culture model of astrocytopathy: potential therapeutic target in multiple sclerosis

Article

Author: Pancholi, Bhaskaranand ; Garabadu, Debapriya ; Mohapatra, Abhipsa ; Amarjeet ; Abate, Selamu Kebamo ; Babu, Raja

BACKGROUNDMultiple sclerosis (MS) is a chronic autoimmune condition that damages the myelin sheath of neurons in the central nervous system, resulting in compromised nerve transmission and motor impairment. The astrocytopathy is considered one of the prominent etiological factor in the pathophysiology of demyelination in MS. The expression level of ceramide synthase-2 (CS-2) is yet to be established in the pathophysiology of astrocytopathy although the derailed ceramide biosynthetic pathways is well demonstrated in the pathophysiology of demyelination. Therefore, in the present study, the expression level of CS-2 has been evaluated in lysophosphatidylcholine (LPC)-challenged primary astrocytes in the presence of anti-demyelinating agents such as Fingolimod, a clinically approved anti-demyelinating drug, and Ursolic Acid (UA), an experimentally accepted anti-demyelinating agent, in MS.METHODS AND RESULTSLPC (150 µg/ml) caused astrocytopathy evident by decrease in percentage of viable astrocytes, increase in percentage of apoptotic astrocytes, increase in the level of reactive oxygen species (ROS), and increase in the level of activated astrocytes. Interestingly, LPC significantly increased the expression level of CS-2 in the primary culture of astrocytes where as fingolimod and UA (1, 10, and 100 µM) were able to attenuate the extent of LPC-induced astrocytopathy in the primary culture model of MS. Further, both the drugs drastically reduced the LPC-induced increase in the level of expression of CS-2 in the astrocytes.CONCLUSIONSThese observations indicate the fact that CS-2 could be a potential target in the management of astrocytopathy and astrocytopathy-related neurological disorders including MS. In conclusion, CS-2-targeted drugs could be potential therapeutic options in the management of MS.

10 Jan 2025·Science Advances

Reduced circulating sphingolipids and CERS2 activity are linked to T2D risk and impaired insulin secretion

Article

Author: Zhang, Xiangyu ; Rabiee, Yasmin ; Gunderson, Erica P. ; Rodricks, Kaitlyn L. ; Nicholson, Rebekah J. ; Singh, Ishnoor ; Ye, Wenyue W. ; Summers, Scott A. ; Khan, Saifur R. ; Futerman, Anthony H. ; Van, Julie A. D. ; Razani, Babak ; Wheeler, Michael B.

Gestational diabetes mellitus (GDM), a transient form of diabetes that resolves postpartum, is a major risk factor for type 2 diabetes (T2D) in women. While the progression from GDM to T2D is not fully understood, it involves both genetic and environmental components. By integrating clinical, metabolomic, and genome-wide association study (GWAS) data, we identified associations between decreased sphingolipid biosynthesis and future T2D, in part through the rs267738 allele of the CERS2 gene in Hispanic women shortly after a GDM pregnancy. To understand the impact of the CERS2 gene and risk allele on glucose regulation, we examined whole-body Cers2 knockout and rs267738 knock-in mice. Both models exhibited glucose intolerance and impaired insulin secretion in vivo. Islets isolated from these models also demonstrated reduced β cell function, as shown by decreased insulin secretion ex vivo. Overall, reduced circulating sphingolipids may indicate a high risk of GDM-to-T2D progression and reflect deficits in CERS2 activity that negatively affect glucose homeostasis and β cell function.

01 Jan 2025·Current Pharmaceutical Biotechnology

Expression of LASS2 Can be Regulated by Dihydroartemisinin to Regulate Cisplatin Chemosensitivity in Bladder Cancer Cells

Article

Author: Ji, Chundong ; Li, Jun ; Li, Shijie ; Xue, Rongbo ; Qiao, Xuhua

Introduction:The aim of this study was to investigate the potential of dihydroartemisinin to augment the efficacy of cisplatin chemotherapy through the modulation of LASS2 expression.Methods:TCMSP, CTR-DB, TCGA-BLC, and other databases were used to analyze the possibility of LASS2 as the target gene of dihydroartemisinin. Cell experiments revealed the synergistic effect of DDP and DHA. Animal experiments showed that DHA inhibited the growth of DDP-treated mice. In addition, WB, real-time PCR, and immunohistochemical analysis showed that DHA enhanced LASS2 (CERS2) expression in bladder cancer cells and DDP-treated mice.Results:LASS2 is associated with cisplatin chemosensitivity.LASS2 expression levels are different between BLC tissues and normal tissues. COX analysis showed that patients with high LASS2 expression had a higher cumulative overall survival rate than those with low LASS2 expression. The Sankey plot showed that LASS2 expression is lower in BLC tissues with more advanced stage and distant metastasis. The docking score of DHA and LASS2 reached the maximum value of -5.5259, indicating that DHA had a strong binding affinity with LASS2 targets. CCK8 assay showed that the most effective concentration ratio of DHA to DDP was 2.5 μg/ml + 10μg/ml. In vivo experiments showed that DHA inhibited tumor growth in cisplatin-treated mice. In addition, WB, RT-qPCR, and immunohistochemical analysis showed that DHA was able to enhance LASS2 expression in BLC cells and DDP-treated mice.Conclusion:The upregulation of LASS2 (CERS2) expression in bladder cancer cells by DHA has been found to enhance cisplatin chemosensitivity.

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CERS2

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