GlcCer (d18:1/18:0)  (Synonyms: C18 Glucosyl(β) ceramide (d18:1/18:0); D-glucosyl-β-1,1' N-stearoyl-D-erythro-sphingosine)

GlcCer (d18:1/18:0) (C18 Glucosyl(β) ceramide (d18:1/18:0)) is a glycosphingolipids that activates the Wnt/β-catenin pathway by targeting LRP6. GlcCer (d18:1/18:0) drives EMT, migration, invasion and GBA1-mediated liver cancer metastasis. GlcCer (d18:1/18:0) accumulates to impair lysosomal function and induce toxic α-synuclein aggregation. GlcCer (d18:1/18:0) supports growth, sporulation, germination and virulence in Penicillium digitatum. GlcCer (d18:1/18:0) is reduced in demyelinated mouse corpus callosum. GlcCer (d18:1/18:0) can be used for the research of liver cancer, synucleinopathies, fungal, Parkinson’s disease and Gaucher disease^{[1][2][3][4][5]}.

GlcCer (d18:1/18:0) levels are elevated in both whole cells and the plasma membrane of HepG2 cells with stable GBA1 knockdown, representing the most markedly increased GlcCer subspecies in the plasma membrane and forming an endogenous in situ interaction with the Wnt co-receptor LRP6^[1].
GlcCer (d18:1/18:0) (4 days) is produced by wild-type Penicillium digitatum, is absent in PdGcs1 deletion mutants, and is reconstituted in PdGcs1 complement mutants, confirming PdGcs1 encodes the glucosylceramide synthase responsible for its biosynthesis^[3].
GlcCer (d18:1/18:0) deficiency in PdGcs1-deleted Penicillium digitatum suppresses vegetative growth, sporulation, and conidial germination, and these defects are fully restored in complemented strains^[3].
GlcCer (d18:1/18:0) (4 days) is produced by wild-type Penicillium digitatum PdKH8, is absent in PdGcs1 deletion mutants, and is reconstituted in PdGcs1 complement mutants^[4].
GlcCer (d18:1/18:0) (5 days (radial growth and sporulation); 8, 12, 16, 24 hours (conidial germination)) is required for normal vegetative growth, sporulation, and conidial germination in Penicillium digitatum, as evidenced by impaired growth, reduced sporulation, and delayed germination in PdGcs1 deletion mutants (which cannot produce GlcCer (d18:1/18:0)) and restoration of these traits in complement mutants^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

GlcCer (d18:1/18:0) is significantly reduced in the corpus callosum of Cuprizone (HY-W115718)-induced demyelinated mice and shows excellent discriminatory ability (AUC_0-t = 0.990) for the demyelination model^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

728.09

C₄₂H₈₁NO₈

95119-86-1

Solid

White to off-white

CCCCCCCCCCCCC/C=C/[C@@H](O)[C@@H](NC(CCCCCCCCCCCCCCCCC)=O)CO[C@@H]1O[C@@H]([C@H]([C@@H]([C@H]1O)O)O)CO

Room temperature in continental US; may vary elsewhere.

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Qiu Z, et al. GBA1-dependent membrane glucosylceramide reprogramming promotes liver cancer metastasis via activation of the Wnt/β-catenin signalling pathway. Cell Death Dis. 2022;13(5):508. Published 2022 May 30.

  [2]. Lerche S, et al. CSF d18:1 sphingolipid species in Parkinson disease and dementia with Lewy bodies with and without GBA1 variants. NPJ Parkinsons Dis. 2024;10(1):198. Published 2024 Oct 24.  [Content Brief]

  [3]. Zhu C, et al. Glucosylceramides are required for mycelial growth and full virulence in Penicillium digitatum. Biochem Biophys Res Commun. 2014;455(3-4):165-171.

  [4]. Zhao Z, et al. Untargeted Metabolomic Profiling of Cuprizone-Induced Demyelination in Mouse Corpus Callosum by UPLC-Orbitrap/MS Reveals Potential Metabolic Biomarkers of CNS Demyelination Disorders. Oxid Med Cell Longev. 2021;2021:7093844. Published 2021 Sep 14.