Affinage

CERS2

Ceramide synthase 2 · UniProt Q96G23

Length
380 aa
Mass
44.9 kDa
Annotated
2026-04-28
61 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CERS2 is an endoplasmic reticulum-resident ceramide synthase that generates very-long-chain ceramides (C22–C24) essential for myelin sphingolipid maintenance, pancreatic β-cell insulin secretion, and hepatic lipid homeostasis. Its catalytic activity toward C22:0/C24:0-CoA substrates is positively regulated by CK2-mediated phosphorylation at C-terminal serine residues, and the common E115A variant (rs267738) is a partial loss-of-function allele that causes glucose intolerance and hepatic steatosis in knock-in mice (PMID:26887952, PMID:33705551, PMID:39792658). Beyond its enzymatic role, CERS2 functions as a tumor suppressor through multiple protein–protein interactions: its homeodomain binds the V-ATPase V0 c-subunit (ATP6V0C) to inhibit proton pump activity, suppress extracellular acidification, and reduce MMP-dependent invasion; it stabilizes p53 by disrupting MDM2/MDMX-mediated degradation; it promotes phospho-β-catenin accumulation by inhibiting PP2A and engaging STK38/SCYL2; and it interacts with IP3R1 to modulate ER-to-mitochondria calcium flux and apoptosis (PMID:22580606, PMID:22991218, PMID:37963859, PMID:38191448, PMID:42012500). CERS2 knockout mice exhibit loss of compacted myelin, cerebellar degeneration, hepatocarcinoma, and impaired liver regeneration, underscoring its non-redundant roles in neural, hepatic, and metabolic tissue homeostasis (PMID:19801672, PMID:28958935).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 2007 High

    Identifying where CERS2 is expressed established it as the myelinating-cell ceramide synthase, predicting a role in myelin sphingolipid production before any loss-of-function data existed.

    Evidence In situ hybridization and RT-PCR in mouse brain showing oligodendrocyte- and Schwann-cell-specific expression peaking during active myelination

    PMID:17901973

    Open questions at the time
    • No functional loss-of-function data at this point
    • Expression pattern alone does not prove requirement
  2. 2009 High

    Gene-trap knockout mice demonstrated that CERS2 is non-redundantly required for C24 ceramide synthesis, myelin compaction, and hepatic tumor suppression, converting expression data into a causal framework.

    Evidence CERS2 knockout mice with loss of C24:1 ceramide synthase activity, 50% myelin loss, MBP reduction, cerebellar degeneration, and hepatocarcinoma

    PMID:19801672

    Open questions at the time
    • Mechanism linking ceramide loss to hepatocarcinogenesis unknown
    • Whether myelin loss is cell-autonomous was not tested
  3. 2009 High

    CERS2 knockdown revealed a sphingolipid rheostat: loss of very-long-chain ceramides paradoxically elevates long-chain ceramides and triggers ER stress, showing that CERS2 depletion remodels the entire ceramide landscape.

    Evidence siRNA knockdown with mass spectrometry lipidomics and UPR marker western blots in cultured cells

    PMID:19728861

    Open questions at the time
    • Mechanism of compensatory C16 ceramide increase not resolved
    • In vivo ER stress consequence not tested
  4. 2010 Medium

    Overexpression studies in hepatocellular carcinoma cells first linked CERS2's tumor-suppressive action to V-ATPase-dependent intracellular acidification and mitochondrial apoptosis, opening a non-enzymatic interaction axis.

    Evidence pH-sensitive fluorescence probes and Annexin-V/PI flow cytometry after LASS2 overexpression in HCCLM3 cells

    PMID:20571735

    Open questions at the time
    • Direct physical interaction with V-ATPase not yet mapped
    • Ceramide-dependent vs. -independent contribution not delineated
  5. 2012 High

    Demonstrating that CERS2 directly binds and inhibits V-ATPase subunit ATP6V0C established a ceramide synthase-independent protein-interaction mechanism for tumor suppression via extracellular pH control and MMP-2 reduction.

    Evidence Co-IP, V-ATPase activity assays, pH measurements, invasion assays, and xenograft models in breast cancer cells

    PMID:22580606

    Open questions at the time
    • Whether ceramide synthesis is dispensable for V-ATPase regulation not formally separated
    • Structural basis of interaction unknown
  6. 2013 High

    Domain-deletion mapping pinpointed the CERS2 homeodomain as the required interface for ATP6V0C binding, linking a specific structural element to V-ATPase inhibition and apoptosis induction.

    Evidence Co-IP with domain-deletion constructs, immuno-electron microscopy, and BCECF pH probes

    PMID:22991218

    Open questions at the time
    • No atomic-resolution structure of the homeodomain–ATP6V0C complex
    • Homeodomain contribution to ceramide synthase activity not assessed
  7. 2014 High

    Loss-of-function studies extended the V-ATPase axis to prostate cancer metastasis, showing CERS2 silencing activates MMP-2/9 and promotes lymph node metastasis in vivo, reinforcing generality across cancer types.

    Evidence shRNA stable knockdown, MMP zymography, and lymph node metastasis xenograft model in PC-3M-2B4 cells

    PMID:24453046

    Open questions at the time
    • Relative contribution of ceramide product changes vs. V-ATPase interaction to metastasis unclear
  8. 2014 Medium

    Lipidomic analysis of CERS2 knockout kidneys revealed that phytosphingosine-based cortical sulfatides are entirely CERS2-dependent and cannot be compensated by other CerS isoforms, defining a unique lipid niche.

    Evidence Imaging mass spectrometry and LC-MS/MS in CerS2 knockout mouse kidneys

    PMID:25267995

    Open questions at the time
    • Functional consequence of phytosphingosine sulfatide loss in kidney not characterized
    • Single lab study
  9. 2016 High

    Identification of CK2-mediated phosphorylation as a Vmax regulator of CERS2 catalytic activity established the first post-translational control mechanism for this enzyme.

    Evidence CK2 inhibitor CX-4945, in vitro ceramide synthase activity assays, and phosphorylation site mapping in mouse brain

    PMID:26887952

    Open questions at the time
    • Specific phosphorylated residues not fully resolved
    • In vivo phosphosite mutant mice not generated
  10. 2017 Medium

    Liver-specific CERS2 knockout showed impaired hepatocyte cell cycle progression after partial hepatectomy, demonstrating a non-tumor-suppressive proliferative role for CERS2 in regenerating tissue.

    Evidence Cre-LoxP liver-specific knockout, partial hepatectomy, Co-IP for CDK4/cyclin D1

    PMID:28958935

    Open questions at the time
    • Whether the effect is ceramide-dependent or interaction-dependent unknown
    • Single lab observation
  11. 2018 Medium

    Placing CERS2 upstream of ERK–Drp1 signaling showed it controls mitochondrial dynamics: depletion shifts the fission–fusion balance toward fission, increasing invasion and chemoresistance.

    Evidence Gain/loss-of-function with ERK and Drp1 inhibitors, MitoTracker and JC-1 staining in bladder cancer cells

    PMID:29581781

    Open questions at the time
    • Mechanism connecting CERS2 to ERK inhibition not identified
    • No direct binding partner for ERK regulation shown
  12. 2020 Medium

    Discovery of the CERS2–NDUFS2 interaction linked CERS2 to mitochondrial complex I ROS production and downstream AMPK-mediated lipogenesis inhibition, revealing a metabolic regulatory arm.

    Evidence Co-IP and LC-MS identification of NDUFS2, AMPK/ACC phosphorylation western blots, lipid content assays

    PMID:32279995

    Open questions at the time
    • Interaction validated in single lab only
    • Whether CERS2 catalytic product or physical interaction drives ROS is unresolved
  13. 2021 High

    CRISPR knock-in of the human E115A variant (rs267738) in mice confirmed it as a partial loss-of-function allele causing metabolic syndrome features, bridging a common human polymorphism to CERS2 enzymatic insufficiency.

    Evidence CRISPR knock-in mouse, in vitro ceramide synthase activity, lipidomics, glucose tolerance testing

    PMID:33705551

    Open questions at the time
    • Human clinical phenotype data for homozygous carriers still limited
    • Tissue-specific consequences beyond liver not characterized
  14. 2021 Medium

    Epistasis experiments positioned CERS2-derived VLC ceramides as effectors of oncogene-induced senescence downstream of sphingosine kinase 1, providing a defined sphingolipid-to-cell-fate signaling axis.

    Evidence siRNA epistasis of CerS2 and SK1, lipidomics, p21/SA-β-gal assays in K-Ras-transformed MCF10A cells

    PMID:33414460

    Open questions at the time
    • Direct ceramide species responsible for p21 induction not identified
    • In vivo validation lacking
  15. 2021 Medium

    Ser248 phosphorylation was shown to be required for CERS2's ability to promote β-catenin ubiquitin-proteasomal degradation via a STK38/SCYL2/ATP6V0C complex, connecting V-ATPase interactions to Wnt pathway suppression.

    Evidence Co-IP, S248A mutagenesis, ubiquitin-proteasome assays, and xenograft models in prostate cancer

    PMID:33852174

    Open questions at the time
    • Kinase responsible for Ser248 phosphorylation not identified
    • Single lab, not independently replicated
  16. 2021 Medium

    Identification of Nrf2 as a direct transcriptional activator of the CERS2 promoter via ARE elements established the first defined transcription factor–CERS2 regulatory relationship.

    Evidence Luciferase reporter assays with ARE-containing CERS2 promoter, siRNA knockdown in endometrial cancer cells

    PMID:33841656

    Open questions at the time
    • Other transcription factors regulating CERS2 not surveyed
    • Functional impact on ceramide levels not measured
  17. 2023 Medium

    Demonstrating that CERS2 binds MDM2 and MDMX to stabilize p53 (promoting Ser15 phosphorylation and Lys373 acetylation) added a p53-dependent tumor-suppressive mechanism independent of the V-ATPase axis.

    Evidence Co-IP for MDM2/MDMX, western blots for p53 modifications, overexpression/knockdown in liver cancer cells

    PMID:37963859

    Open questions at the time
    • Not independently replicated
    • Whether ceramide synthase activity is required for MDM2 binding unknown
    • Structural basis of CERS2–MDM2 interaction not resolved
  18. 2024 Medium

    Discovery of the CERS2–TFRC interaction linked CERS2 to iron homeostasis and ferroptosis regulation, opening a new functional axis beyond sphingolipid metabolism and V-ATPase.

    Evidence Co-IP LC-MS, proximity ligation assay, multi-omics, ferroptosis assays across thyroid, breast, and liver cancer lines

    PMID:38419028

    Open questions at the time
    • Mechanism by which CERS2 alters TFRC function not defined
    • Single lab
    • Ceramide dependence not tested
  19. 2024 Medium

    Showing that CERS2 inhibits PP2A to maintain phospho-β-catenin and reduce stemness markers (CD44, ABCC2) provided a mechanistic basis for cisplatin resensitization in bladder cancer stem cells.

    Evidence Co-IP, LC-MS, ChIP, luciferase reporters, patient-derived xenografts in bladder cancer

    PMID:38191448

    Open questions at the time
    • PP2A subunit specificity not determined
    • Independent replication needed
  20. 2025 High

    Ex vivo islet studies from both CERS2 knockout and E115A knock-in mice established that CERS2-derived VLC sphingolipids are required for glucose-stimulated insulin secretion, translating whole-body metabolic phenotypes to a defined β-cell mechanism.

    Evidence Two genetic mouse models with ex vivo islet glucose-stimulated insulin secretion assays and metabolomics

    PMID:39792658

    Open questions at the time
    • Specific sphingolipid species mediating β-cell exocytosis not identified
    • Human islet validation not performed
  21. 2025 Medium

    Identification of CERS2–IP3R1 interaction and pharmacological activation by DH20931 demonstrated that CERS2 modulates ER-mitochondrial calcium transfer and apoptosis, providing both a novel interactor and a tool compound.

    Evidence Co-IP, calcium flux measurements, ER-mitochondria proximity assays, DH20931 agonist treatment, xenograft models

    PMID:42012500

    Open questions at the time
    • DH20931 selectivity for CERS2 vs. other CerS not fully characterized
    • Whether IP3R1 interaction is ceramide-dependent unclear
  22. 2025 Medium

    Phospho-site mapping identified Ser348 as required for V-ATPase suppression and anti-invasive function, adding a second regulatory phosphosite (alongside Ser248) to the growing picture of CERS2 post-translational control.

    Evidence Mass spectrometry phosphosite mapping, S348A mutagenesis, V-ATPase and MMP-2 assays in prostate cancer cells

    PMID:41399074

    Open questions at the time
    • Kinase phosphorylating Ser348 not identified
    • Relationship between Ser348 and CK2-regulated C-terminal sites not clarified

Open questions

Synthesis pass · forward-looking unresolved questions
  • A central unresolved question is whether CERS2's numerous protein–protein interactions (ATP6V0C, MDM2, TFRC, IP3R1, NDUFS2, PP2A) operate independently of its ceramide synthase catalytic activity, and how its multiple phosphosites are coordinately regulated to direct these distinct functions.
  • No catalytic-dead separation-of-function mutant tested across interaction partners
  • No structural model of full-length CERS2
  • Interplay between CK2 phosphorylation and Ser248/Ser348 phosphorylation unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0098772 molecular function regulator activity 5 GO:0008289 lipid binding 3
Localization
GO:0005739 mitochondrion 3 GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-1430728 Metabolism 5 R-HSA-1643685 Disease 4 R-HSA-162582 Signal Transduction 3 R-HSA-5357801 Programmed Cell Death 2
Partners
ATP6V0CITPR1MDM2MDMXNDUFS2SCYL2STK38TFRC

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 CERS2 (CerS2/LASS2) is the predominant ceramide synthase in oligodendrocytes and Schwann cells, with substrate specificity for very long-chain fatty acid residues (C22–C24). Knockout mice lacking CERS2 show strongly reduced C24:1 ceramide synthase activity in brain and liver, ~50% loss of compacted myelin, 80% loss of myelin basic protein, cerebellar degeneration, and hepatocarcinoma development, establishing CERS2 as required for myelin maintenance and hepatic tumor suppression. Gene-trap knockout mice (loss-of-function), biochemical ceramide synthase activity assays, lipid profiling, histology, lacZ reporter The Journal of biological chemistry High 19801672
2007 CerS2 expression in mouse brain is specifically localized to oligodendrocytes in white matter tracts and is the predominant CerS in Schwann cells of sciatic nerves; its expression peaks transiently during active myelination, consistent with a role in synthesizing very-long-chain dihydroceramides for myelin sphingolipids. Northern blot, real-time RT-PCR, in situ hybridization Histochemistry and cell biology High 17901973
2009 CerS2 knockdown by siRNA reduces very-long-chain ceramides (C24, C24:1) and paradoxically increases long-chain ceramides (C14, C16) through a ceramide synthase-independent mechanism, leading to growth arrest, autophagy induction, and activation of PERK and IRE1 unfolded protein response pathways. siRNA knockdown, mass spectrometry lipid profiling, cell viability assays, western blot for UPR markers The Biochemical journal High 19728861
2016 CERS2 enzymatic activity is regulated by phosphorylation at cytoplasmic C-terminal residues conforming to a CK2 consensus motif; CK2 inhibition (CX-4945) reduced CERS2 phosphorylation and drastically lowered CERS2 catalytic activity (primarily by reducing Vmax) toward C22:0/C24:0-CoA substrates in mouse brain. Pharmacological CK2 inhibition, in vitro ceramide synthase activity assays, phosphorylation site mapping, mutagenesis The Journal of biological chemistry High 26887952
2012 LASS2 (CERS2) directly interacts with the C subunit of vacuolar H+-ATPase (V-ATPase, ATP6V0C) and inhibits V-ATPase activity, thereby increasing intracellular H+ concentration, raising extracellular pH, reducing MMP-2 secretion, and suppressing breast cancer cell invasion; LASS2 overexpression increases chemosensitivity to doxorubicin. Overexpression and knockdown (siRNA), V-ATPase activity assay, pH measurement, invasion assays, co-immunoprecipitation (referenced from prior work), xenograft model Oncogene High 22580606
2013 The homeodomain of LASS2/TMSG1 directly mediates physical interaction with the C subunit of V-ATPase (ATP6V0C); domain-deletion variants lacking the homeodomain fail to regulate V-ATPase activity and intracellular pH, and lose apoptosis-inducing function. Immunoprecipitation, immunofluorescence, immuno-electron microscopy, domain deletion constructs, pH fluorescence probe (BCECF/AM), apoptosis assay Journal of cellular biochemistry High 22991218
2010 LASS2 overexpression in hepatocellular carcinoma cells (HCCLM3) increases intracellular H+ and decreases extracellular H+ via interaction with V-ATPase, induces cytochrome c release from mitochondria, reduces pro-caspase-3, and enhances apoptosis through the mitochondrial pathway. Transient transfection, pH-sensitive fluorescence probes (BCECF/BCECF-AM), Annexin-V/PI flow cytometry, western blot for cytochrome c and caspase-3 Sheng li xue bao : [Acta physiologica Sinica] Medium 20571735
2014 Silencing LASS2/TMSG1 in prostate cancer cell line PC-3M-2B4 increases V-ATPase activity and extracellular H+ concentration, activates secreted MMP-2 and MMP-9, and enhances cell proliferation, invasion in vitro, and lymph node metastasis in vivo. shRNA stable knockdown, V-ATPase activity assay, MMP gelatin zymography, xenograft/lymph node metastasis model Journal of cellular biochemistry High 24453046
2021 CerS2-derived very-long-chain ceramides (C24, C24:1, C26:1) mediate oncogene-induced senescence downstream of SK1 knockdown in MCF10A cells expressing oncogenic K-Ras; siRNA knockdown of CerS2 blocks the increase of VLC ceramides induced by SK1 knockdown and reverses p21 induction. siRNA knockdown (CerS2 and SK1), lipidomic mass spectrometry, p21/SA-β-gal senescence assays, fumonisin B1 inhibition Cell death & disease Medium 33414460
2021 LASS2 phosphorylation at serine-248 is essential for promoting β-catenin degradation; LASS2 interacts physically with STK38, SCYL2, and ATP6V0C to promote ubiquitin-proteasome-dependent degradation of β-catenin. The S248A dephosphorylation mutant fails to suppress Wnt/β-catenin signaling and enhances prostate cancer growth and metastasis in vivo. Co-immunoprecipitation, site-directed mutagenesis (S248A), ubiquitin-proteasome pathway assays, xenograft in vivo model Journal of cellular biochemistry Medium 33852174
2024 LASS2 (CERS2) directly interacts with transferrin receptor (TFRC) as identified by co-IP LC-MS in thyroid, breast, and liver cancer cells; LASS2 overexpression regulates iron homeostasis and ferroptosis status, inhibiting tumor cell migration, invasion and EMT through this TFRC interaction. Co-IP coupled LC-MS, protein-protein docking, co-immunoprecipitation western blot, immunofluorescence, proximity ligation assay, transcriptomics/proteomics/metabolomics, ferroptosis pathway assays Cancer cell international Medium 38419028
2024 LASS2 inhibits PP2A activity and physically dissociates PP2A from β-catenin in bladder cancer stem cells, preventing β-catenin dephosphorylation and accumulating cytosolic phospho-β-catenin, which decreases transcription of ABCC2 and CD44, thereby reducing stem-like properties and restoring cisplatin sensitivity. Co-immunoprecipitation, LC-MS, luciferase reporter assay, chromatin immunoprecipitation, pathway reporter array, gain/loss-of-function, cell- and patient-derived xenograft models BMC medicine Medium 38191448
2018 LASS2 overexpression inhibits ERK phosphorylation, which acts upstream of Drp1 phosphorylation, to promote mitochondrial fusion over fission; LASS2 depletion increases p-Drp1, causing mitochondrial fission and increased cancer cell invasion and chemoresistance in bladder cancer cells. Plasmid transfection and siRNA knockdown, MitoTracker staining, JC-1 staining, ERK inhibitor (PD98059), Drp1 inhibitor (Mdivi), western blot Journal of Cancer Medium 29581781
2021 Nrf2 transcriptionally activates LASS2 (CERS2) by binding antioxidant response elements (AREs) in the LASS2 promoter, as demonstrated by luciferase reporter assays; elevated Nrf2/LASS2 expression promotes progestin resistance in endometrial cancer cells. Luciferase reporter assay (ARE-containing LASS2 promoter), siRNA knockdown, western blot, flow cytometry American journal of translational research Medium 33841656
2023 LASS2 interacts directly with MDM2 and MDMX, disrupting p53 degradation; LASS2 overexpression also promotes p53 phosphorylation at Ser15 and acetylation at Lys373, facilitating nuclear translocation of p53, thereby exerting tumor-suppressive effects in a p53-dependent manner in liver cancer cells. Co-immunoprecipitation, gene set enrichment analysis, western blot for p53 modifications, overexpression/knockdown functional assays Cell death discovery Medium 37963859
2020 LASS2 interacts with NDUFS2 (complex I subunit) as identified by co-IP and LC-MS; this interaction promotes mitochondrial ROS production, activates AMPK phosphorylation, and inhibits lipogenesis, reducing hepatocyte lipid accumulation. Co-IP, LC-MS, siRNA knockdown and overexpression, western blot for AMPK/ACC phosphorylation, lipid content assays Biochemical and biophysical research communications Medium 32279995
2017 LASS2 knockdown in liver-specific knockout mice delayed liver regeneration after partial hepatectomy, with reduced PCNA, Ki67, cyclin A, CDK2, p-Rb, and CDK4/cyclin D1 complex formation; co-immunoprecipitation confirmed decreased CDK4/cyclin D1 interaction in LASS2-deficient livers. Liver-specific conditional Cre-LoxP knockout, partial hepatectomy model, co-immunoprecipitation (CDK4/cyclin D1), IHC, western blot Biochemical and biophysical research communications Medium 28958935
2021 The rs267738 SNP in CERS2 (encoding an E115A substitution) is a partial loss-of-function variant: homozygous knock-in mice generated by CRISPR show reduced liver CERS2 ceramide synthase activity, worsened diet-induced glucose intolerance, and hepatic steatosis. CRISPR knock-in mouse model, in vitro ceramide synthase activity assay, lipidomics, metabolic phenotyping (glucose tolerance test) The Journal of clinical endocrinology and metabolism High 33705551
2025 Whole-body Cers2 knockout and rs267738 knock-in mice exhibit glucose intolerance and impaired insulin secretion in vivo; islets isolated from these mice show reduced β-cell function with decreased glucose-stimulated insulin secretion ex vivo, linking CERS2 activity and very-long-chain sphingolipid biosynthesis to β-cell function. Cers2 knockout and CRISPR knock-in mouse models, glucose tolerance tests, ex vivo islet insulin secretion assays, metabolomics Science advances High 39792658
2025 CERS2 physically interacts with the ER calcium channel IP3R1; the small-molecule CerS2 agonist DH20931 promotes this interaction, enhancing ER-mitochondria proximity and facilitating Ca2+ flux into mitochondria, triggering mitochondrial dysfunction and apoptosis. Additionally, VLCC accumulation from CerS2 activation induces ER stress via ATF4/CHOP/PUMA pathway. Co-immunoprecipitation, Ca2+ flux measurements, ER-mitochondria proximity assays, small-molecule agonist (DH20931), LC-MS ceramide quantification, fluorescence-coupled enzymatic assays, xenograft models Molecular cancer therapeutics Medium 42012500
2025 Phosphorylation of LASS2 at serine-348 (identified by mass spectrometry) is essential for regulation of V-ATPase activity; the LASS2 S348A dephosphorylation mutant fails to suppress V-ATPase activity, increases extracellular H+ and active MMP-2, and significantly enhances prostate cancer cell invasion and migration. Protein phosphatase inhibitor calyculin A reduced growth and invasion of metastatic prostate cancer cells. Mass spectrometry phospho-site mapping, site-directed mutagenesis (S348A), V-ATPase activity assay, MMP-2 zymography, invasion assays, calyculin A pharmacological inhibition Beijing da xue xue bao. Yi xue ban Medium 41399074
2014 CerS2 deletion in mice results in bulk loss of sulfatides containing C23/C24 acyl chains in the kidney, with compensatory upregulation of C16–C20 acyl chain sulfatides; phytosphingosine-containing cortical sulfatides are completely depleted without compensation, establishing CerS2 as uniquely required for these species. CerS2 knockout mice, imaging mass spectrometry (IMS), LC-MS/MS lipid profiling, regional mRNA expression analysis Journal of lipid research Medium 25267995

Source papers

Stage 0 corpus · 61 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Adult ceramide synthase 2 (CERS2)-deficient mice exhibit myelin sheath defects, cerebellar degeneration, and hepatocarcinomas. The Journal of biological chemistry 247 19801672
2009 Disruption of ceramide synthesis by CerS2 down-regulation leads to autophagy and the unfolded protein response. The Biochemical journal 121 19728861
2012 miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injury. Journal of cell science 110 22393241
2007 Differential expression of (dihydro)ceramide synthases in mouse brain: oligodendrocyte-specific expression of CerS2/Lass2. Histochemistry and cell biology 92 17901973
2012 LASS2 enhances chemosensitivity of breast cancer by counteracting acidic tumor microenvironment through inhibiting activity of V-ATPase proton pump. Oncogene 85 22580606
2016 Enzyme Activities of the Ceramide Synthases CERS2-6 Are Regulated by Phosphorylation in the C-terminal Region. The Journal of biological chemistry 73 26887952
2015 miR-9 promotes cell proliferation and inhibits apoptosis by targeting LASS2 in bladder cancer. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 59 26150338
2015 CERS2 suppresses tumor cell invasion and is associated with decreased V-ATPase and MMP-2/MMP-9 activities in breast cancer. Journal of cellular biochemistry 56 25213553
2014 Silencing of LASS2/TMSG1 enhances invasion and metastasis capacity of prostate cancer cell. Journal of cellular biochemistry 39 24453046
2016 The asialoglycoprotein receptor suppresses the metastasis of hepatocellular carcinoma via LASS2-mediated inhibition of V-ATPase activity. Cancer letters 36 27241665
2012 Silencing of a novel tumor metastasis suppressor gene LASS2/TMSG1 promotes invasion of prostate cancer cell in vitro through increase of vacuolar ATPase activity. Journal of cellular biochemistry 36 22573553
2018 MicroRNA-98 promotes drug resistance and regulates mitochondrial dynamics by targeting LASS2 in bladder cancer cells. Experimental cell research 35 30463687
2014 A gene variant in CERS2 is associated with rate of increase in albuminuria in patients with diabetes from ONTARGET and TRANSCEND. PloS one 32 25238615
2015 AGPAT9 suppresses cell growth, invasion and metastasis by counteracting acidic tumor microenvironment through KLF4/LASS2/V-ATPase signaling pathway in breast cancer. Oncotarget 30 26110566
2016 Repression of the miR-93-enhanced sensitivity of bladder carcinoma to chemotherapy involves the regulation of LASS2. OncoTargets and therapy 28 27099514
2013 A novel tumor metastasis suppressor gene LASS2/TMSG1 interacts with vacuolar ATPase through its homeodomain. Journal of cellular biochemistry 28 22991218
2014 Renal sulfatides: sphingoid base-dependent localization and region-specific compensation of CerS2-dysfunction. Journal of lipid research 23 25267995
2014 LASS2/TMSG1 inhibits growth and invasion of breast cancer cell in vitro through regulation of vacuolar ATPase activity. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 23 25501280
2016 LASS2 inhibits growth and invasion of bladder cancer by regulating ATPase activity. Oncology letters 22 28356943
2018 LASS2 regulates invasion and chemoresistance via ERK/Drp1 modulated mitochondrial dynamics in bladder cancer cells. Journal of Cancer 21 29581781
2013 Enhancement of DEN-induced liver tumourigenesis in hepatocyte-specific Lass2-knockout mice coincident with upregulation of the TGF-β1-Smad4-PAI-1 axis. Oncology reports 21 24337404
2013 Expression of a tumor-associated gene, LASS2, in the human bladder carcinoma cell lines BIU-87, T24, EJ and EJ-M3. Experimental and therapeutic medicine 17 23407876
2010 [LASS2 interacts with V-ATPase and inhibits cell growth of hepatocellular carcinoma]. Sheng li xue bao : [Acta physiologica Sinica] 17 20571735
2019 miR-3622a promotes proliferation and invasion of bladder cancer cells by downregulating LASS2. Gene 16 30898713
2017 Secretory pathway optimization of CHO producer cells by co-engineering of the mitosRNA-1978 target genes CerS2 and Tbc1D20. Metabolic engineering 16 28088541
2017 Silencing of vacuolar ATPase c subunit ATP6V0C inhibits the invasion of prostate cancer cells through a LASS2/TMSG1-independent manner. Oncology reports 16 29138865
2021 Targeting sphingosine kinase 1 (SK1) enhances oncogene-induced senescence through ceramide synthase 2 (CerS2)-mediated generation of very-long-chain ceramides. Cell death & disease 15 33414460
2019 Clinical and pathological significance of Homo sapiens ceramide synthase 2 (CerS-2) in diverse human cancers. Bioscience reports 15 30988071
2021 Characterizing a Common CERS2 Polymorphism in a Mouse Model of Metabolic Disease and in Subjects from the Utah CAD Study. The Journal of clinical endocrinology and metabolism 14 33705551
2018 Overexpression of LASS2 inhibits proliferation and causes G0/G1 cell cycle arrest in papillary thyroid cancer. Cancer cell international 14 30302058
2019 LASS2 inhibits proliferation and induces apoptosis in HepG2 cells by affecting mitochondrial dynamics, the cell cycle and the nuclear factor‑κB pathways. Oncology reports 13 30896811
2015 Overexpression of a Novel Tumor Metastasis Suppressor Gene TMSG1/LASS2 Induces Apoptosis via a Caspase-dependent Mitochondrial Pathway. Journal of cellular biochemistry 11 25735224
2024 LASS2 suppresses metastasis in multiple cancers by regulating the ferroptosis signalling pathway through interaction with TFRC. Cancer cell international 10 38419028
2021 LASS2 mediates Nrf2-driven progestin resistance in endometrial cancer. American journal of translational research 10 33841656
2021 Phosphorylated LASS2 inhibits prostate carcinogenesis via negative regulation of Wnt/β-catenin signaling. Journal of cellular biochemistry 10 33852174
2019 Evaluation of CERS2 Gene as a Potential Biomarker for Bladder Cancer. Disease markers 10 31636736
2018 Hsa-miR-3658 Promotes Cell Proliferation, Migration and Invasion by Effecting LASS2 in Bladder Cancer. Clinical laboratory 10 29739079
2024 Identifying MSMO1, ELOVL6, AACS, and CERS2 related to lipid metabolism as biomarkers of Parkinson's disease. Scientific reports 9 39080336
2017 The role of LASS2 in regulating bladder cancer cell tumorigenicity in a nude mouse model. Oncology letters 9 29113153
2022 Hsa-miR-221-3p promotes proliferation and migration in HER2-positive breast cancer cells by targeting LASS2 and MBD2. Histology and histopathology 8 35734966
2018 Hepatocyte-specific deletion of LASS2 protects against diet-induced hepatic steatosis and insulin resistance. Free radical biology & medicine 8 29626628
2021 MicroRNA-20a Targeting LASS2 Promotes the Proliferation, Invasiveness and Migration of Bladder Cancer. Clinical laboratory 7 34383404
2017 Liver-specific deletion of LASS2 delayed regeneration of mouse liver after partial hepatectomy. Biochemical and biophysical research communications 7 28958935
2025 Reduced circulating sphingolipids and CERS2 activity are linked to T2D risk and impaired insulin secretion. Science advances 6 39792658
2024 LASS2 enhances chemosensitivity to cisplatin by inhibiting PP2A-mediated β-catenin dephosphorylation in a subset of stem-like bladder cancer cells. BMC medicine 6 38191448
2022 LASS2 impairs proliferation of glioma stem cells and migration and invasion of glioma cells mainly via inhibition of EMT and apoptosis promotion. Journal of Cancer 6 35517425
2020 LASS2 regulates hepatocyte steatosis by interacting with NDUFS2/OXPHOS related proteins. Biochemical and biophysical research communications 5 32279995
2005 Expression of LASS2 controlled by LAG1 or ADH1 promoters cannot functionally complement Lag1p. Microbiological research 4 16765836
2023 LASS2 enhances p53 protein stability and nuclear import to suppress liver cancer progression through interaction with MDM2/MDMX. Cell death discovery 3 37963859
2022 LASS2 overexpression enhances early apoptosis of lung cancer cells through the caspase‑dependent pathway. Oncology reports 3 36300249
2024 Downregulation of CerS4 Instead of CerS2 in Liver Effectively Alleviates Hepatic Insulin Resistance in HFD Male Mice. Endocrinology 2 39233348
2020 Association of rs8444 polymorphism in the LASS2 3'-UTR and bladder cancer risk in Chinese population. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) 2 31577563
2014 [LASS2/TMSG1 gene silencing promotes the invasiveness and metastatic of human prostatic carcinoma cells through increase in vacuolar ATPase activity]. Zhonghua bing li xue za zhi = Chinese journal of pathology 2 24842017
2019 [Novel tumor metastasis suppressorgene LASS2/TMSG1 S248A mutant promotes invasion of prostate cancer cells through increasing ATP6V0C expression]. Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 1 30996356
2026 Discovery of a potential CERS2 inhibitor: hit compound identification via structure-based virtual screening and molecular dynamics simulations. Molecular diversity 0 41483315
2026 CerS2 is a druggable target in triple-negative breast cancer. Molecular cancer therapeutics 0 42012500
2025 Expression of LASS2 Can be Regulated by Dihydroartemisinin to Regulate Cisplatin Chemosensitivity in Bladder Cancer Cells. Current pharmaceutical biotechnology 0 38757331
2025 CerS2 is a druggable target in triple-negative breast cancer. bioRxiv : the preprint server for biology 0 40894709
2025 [Effect of dephosphorylation of tumor metastasis suppressor gene LASS2 on vacuolar ATPase activity and invasiveness of prostate cancer]. Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 0 41399074
2023 [LASS2/TMSG1 overexpression inhibits proliferation and promotes apoptosis of human lung cancer A549 cells possibly by upregulating ceramide and p38 MAPK to activate a signaling cascade]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 0 36946034
2003 [Study of the expression membrane protein LASS2]. Sheng wu gong cheng xue bao = Chinese journal of biotechnology 0 15969039