The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

Research Report: Human SAMD8 (UniProt Q96LT4) — functional annotation of SMSr/CPE synthase/PE-PLC

Executive summary

Human SAMD8 encodes sphingomyelin synthase–related protein (SMSr), an endoplasmic reticulum (ER)-resident multi-pass membrane enzyme of the sphingomyelin synthase (SMS) family whose N-terminal SAM (sterile α motif) domain controls oligomerization and ER retention. Historically, SMSr has been studied as a ceramide phosphoethanolamine (CPE) synthase (a “trace” phosphosphingolipid pathway), but recent work (2023) argues that in vivo its dominant role may be phosphatidylethanolamine phospholipase C (PE‑PLC) activity that regulates hepatic PE levels and promotes NAFLD/NASH phenotypes. Key mechanistic themes include (i) SAM-domain–mediated oligomerization controlling ER localization; (ii) coupling to DAG signaling (including via DGKδ interaction) through PLC-like chemistry; and (iii) stress/apoptosis regulation, including caspase‑6 cleavage of SMSr during apoptosis. (cabukusta2017erresidencyof pages 10-13, cabukusta2017ceramidephosphoethanolaminesynthase pages 7-10, chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)

0) Gene/protein verification (critical identity check)

Target identity is consistent across the literature retrieved:
- Gene symbol: SAMD8; protein name used in primary literature: SMSr (sphingomyelin synthase-related protein). (jiang2022sphingomyelinsynthasefamily pages 4-6, cabukusta2017erresidencyof pages 1-2)
- Organism: Human studies include HeLa and other mammalian cell systems expressing human SMSr, and review sources explicitly describe SAMD8 as the gene encoding SMSr. (cabukusta2017ceramidephosphoethanolaminesynthase pages 1-2, jiang2022sphingomyelinsynthasefamily pages 4-6)
- Family/domain match: SMSr is consistently described as a member of the SMS family with a SAM domain (distinguishing it from SMS2) and a conserved catalytic motif consistent with LPP/PLC-like phosphodiesterase chemistry. (jiang2022sphingomyelinsynthasefamily pages 6-8, jiang2022sphingomyelinsynthasefamily pages 3-4)

1) Key concepts and definitions (current understanding)

1.1 SMS family: “sphingomyelin synthases” versus “PLC-like” enzymes

A current conceptual framework (reviewed by Jiang & Chiang, 2022) treats the SMS family as phospholipase C–like enzymes: they can cleave glycerophospholipids to release diacylglycerol (DAG) and a phosphorylated headgroup, and (in the presence of ceramide) transfer the phosphoryl headgroup to ceramide to form SM (from PC) or CPE (from PE). (jiang2022sphingomyelinsynthasefamily pages 11-15, jiang2022sphingomyelinsynthasefamily pages 6-8)

1.2 Ceramide phosphoethanolamine (CPE)

CPE is a sphingomyelin (SM) analog with a phosphoethanolamine headgroup. In mammals it appears to be a low-abundance (“trace”) lipid class compared with SM. (bickert2015functionalcharacterizationof pages 5-6)

1.3 PE-PLC activity

PE-PLC activity (as defined in the 2023 JBC study) is the enzymatic hydrolysis of phosphatidylethanolamine (PE) to generate DAG and the corresponding phosphorylated headgroup; importantly, this is proposed to occur in the absence of ceramide. (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2, chiang2023sphingomyelinsynthase–relatedprotein pages 10-11)

2) Primary biochemical function: enzymatic activities and substrate specificity

2.1 CPE synthase activity (classical model)

Multiple sources characterize SMSr/SAMD8 as a ceramide phosphoethanolamine synthase (CPE synthase)—i.e., it can use PE as a phosphoethanolamine donor and ceramide as acceptor, yielding CPE (often assayed using fluorescent ceramide analogs) and DAG as a coproduct in SMS-family headgroup transfer reactions. (bickert2017biologicalfunctionsof pages 32-35, cabukusta2017erresidencyof pages 14-15)

Evidence types in retrieved primary sources:
- In vitro activity assay approach: Cabukusta et al. (2017) describe an activity assay using NBD‑ceramide as acceptor and a defined PE species as donor, followed by extraction and TLC/quantification of NBD-labeled products. This directly operationalizes the headgroup-transfer (CPE synthase) activity in a reconstituted biochemical assay format. (cabukusta2017erresidencyof pages 14-15)
- Catalytic residue constraint: In mice, mutation of a conserved Asp (D348E in SMSr) abolishes SMSr-mediated CPE production in heterologous expression systems, supporting that SMSr’s enzymatic activity depends on conserved SMS-family catalytic residues. (bickert2015functionalcharacterizationof pages 5-6)

2.2 PE-PLC activity (recent model; 2023)

Chiang et al. (2023) provide in vivo biochemical-genetic evidence that SMSr has PE‑PLC activity in liver:
- Smsr knockout (KO) mice have reduced hepatic PE-PLC activity and increased hepatic PE.
- Adenoviral SMSr overexpression increases hepatic PE‑PLC activity and lowers liver PE. (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)

Assay details (substrate and conditions): PE‑PLC activity was measured in liver homogenates using NBD‑PE as substrate, with reaction products separated by TLC to quantify generation of NBD‑DAG. (chiang2023sphingomyelinsynthase–relatedprotein pages 10-11)

2.3 Mechanistic controversy and reconciliation

A key unresolved issue is whether the physiologic “dominant” activity of SMSr is best described as CPE synthase (ceramide-dependent headgroup transfer) or PE‑PLC (ceramide-independent hydrolysis), or whether SMSr can perform both depending on substrate availability/compartmental context.
- The 2022 review explicitly notes in vitro CPE synthase activity while discussing a newer view of SMSr as a PE‑PLC regulating PE levels and generating DAG without ceramide. (jiang2022sphingomyelinsynthasefamily pages 1-3, jiang2022sphingomyelinsynthasefamily pages 11-15)
- Mouse tissue lipidomics show that steady-state CPE is extremely low, which supports the idea that CPE synthesis may be quantitatively minor in many tissues despite clear biochemical capacity. (bickert2015functionalcharacterizationof pages 5-6, bickert2015functionalcharacterizationof pages 12-13)

3) Subcellular localization, topology, and regulation

3.1 ER residency and SAM-domain–mediated oligomerization

Cabukusta et al. (2017, Scientific Reports, Jan 2017) show that SMSr is ER-resident and that ER retention depends on homotypic oligomerization mediated by its SAM domain:
- Crosslinking/native gels indicate SMSr forms trimers and hexamers.
- Mutations disrupting SAM-mediated self-assembly partially redistribute SMSr toward the Golgi; SAM deletion increases Golgi redistribution.
- Curcumin stabilizes SMSr oligomers and promotes ER retention. (cabukusta2017erresidencyof pages 10-13, cabukusta2017erresidencyof pages 1-2)

3.2 Apoptosis-linked regulation: caspase-6 cleavage

Cabukusta et al. (2017, Bioscience Reports, Jul 2017) identify SMSr as a specific substrate of caspase‑6:
- In apoptosis induced by staurosporine or FasL, SMSr undergoes caspase-mediated cleavage.
- Cleavage occurs primarily at Asp120 (and secondarily Asp118), between the SAM domain and the membrane spans, effectively separating the regulatory SAM domain from the catalytic membrane-embedded region.
- Recombinant caspase‑6 cleaves SMSr in vitro; inhibition/knockdown of caspase‑6 reduces cleavage in cells. (cabukusta2017ceramidephosphoethanolaminesynthase pages 7-10, cabukusta2017ceramidephosphoethanolaminesynthase pages 5-7)

4) Biological roles, pathways, and phenotypes

4.1 Ceramide homeostasis and apoptosis suppression (cell-based model)

Primary studies describe SMSr as a negative regulator of ceramide-driven apoptosis, requiring both catalytic function and the SAM domain. In these models, SMSr is proposed to control ER ceramide levels and suppress ceramide-induced mitochondrial apoptosis. (cabukusta2017erresidencyof pages 1-2, cabukusta2017ceramidephosphoethanolaminesynthase pages 1-2)

4.2 DAG/PA signaling pathway via DGKδ interaction

Murakami et al. (2020, JBC, Mar 2020) provide evidence that SMSr (via its SAM domain) interacts with DGKδ (diacylglycerol kinase δ), linking SMSr activity to specific phosphatidic acid (PA) pools:
- Co-immunoprecipitation indicates SAMD-dependent binding; deleting SMSr’s SAM domain reduces DGKδ co-precipitation by ~75%.
- In COS-7 cells, SMSr co-expression increases total PA by ~20% and increases specific PA species (>20%) enriched in saturated/monounsaturated acyl chains (e.g., 30:0, 32:1, 32:0, 34:1, 34:2 PA). (murakami2020diacylglycerolkinaseδ pages 5-6, murakami2020diacylglycerolkinaseδ pages 10-11)
- A parallel set of experiments reports SMSr increasing total DG by ~14%, consistent with SMSr supplying DG species upstream of DGK. (murakami2020diacylglycerolkinaseδ pages 6-7)

This supports a pathway-level interpretation where SMSr contributes to DAG generation (via PLC-like chemistry), which is then converted by DGKδ into defined PA species—potentially a ceramide-independent signaling axis. (murakami2020diacylglycerolkinaseδ pages 1-1, murakami2020diacylglycerolkinaseδ pages 10-11)

4.3 In vivo lipid abundance and baseline phenotypes (mouse genetics)

Bickert et al. (2015, Journal of Lipid Research, Apr 2015) show that mammalian CPE pools are extremely small:
- Across mouse tissues, CPE is ~300–1,500-fold lower than SM.
- Absolute CPE reaches ~0.020 mol% of total phospholipid in testis/brain and ~0.002–0.005 mol% in heart/liver. (bickert2015functionalcharacterizationof pages 5-6)

In vivo perturbation of SMSr catalytic activity produced surprisingly mild baseline phenotypes:
- SMSr catalytic inactivation mainly reduced brain CPE (e.g., 40–60% reduction in short-chain CPE species; ~30% lower total CPE in forebrain/cerebellum) but did not show major increases in tissue ceramide/hexosylceramide nor clear organelle defects by EM in liver/brain under baseline conditions. (bickert2015functionalcharacterizationof pages 9-10, bickert2015functionalcharacterizationof pages 12-13)
- Combined inactivation of SMSr and SMS2 reduced but did not eliminate CPE in tissues, implying additional enzymatic sources/pathways. (bickert2015functionalcharacterizationof pages 10-12)

5) Recent developments (prioritizing 2023–2024)

5.1 2023: SMSr as PE-PLC and a driver of NAFLD/NASH

A major 2023 development is the proposal that SMSr is a physiologically relevant PE‑PLC that promotes NAFLD/NASH:
- In a 16-week high-fat diet + fructose model, Smsr-KO mice showed significantly less weight gain, lower plasma triglyceride and cholesterol, and lower hepatic triglyceride accumulation (Oil Red O evidence described). (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)
- Inflammatory signaling was reduced: cytokine array/ELISA showed ~30% reductions in inflammatory cytokines including plasma TNFα and IL-6, and liver expression of Fsp27, PPARγ2, FAS, Tnfα, Timp1 was decreased. (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)
- Anti-fibrotic effects: SMSr deficiency reduced TGFβ1 activity and collagen 1α1 expression and prevented TGFβ1-driven induction of fibrosis genes in experimental contexts. (chiang2023sphingomyelinsynthase–relatedprotein pages 8-9)
- Human association reported: NASH patient liver sections showed higher SMSr protein signal by immunostaining, and patients had reduced plasma PE and reduced PE/PC ratio (descriptive statements in retrieved evidence). (chiang2023sphingomyelinsynthase–relatedprotein pages 8-9)

Interpretation: This work reframes SAMD8/SMSr from a “trace CPE synthase” to a regulator of hepatic PE homeostasis, DAG signaling, and inflammatory/fibrotic pathways relevant to metabolic liver disease. (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)

5.2 2024 landscape

Within the retrieved corpus, 2024 sources largely provide contextual reviews rather than new SAMD8-specific mechanistic primary data; the most concrete SAMD8 advances in the current evidence set are from 2023. (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)

6) Current applications and real-world implementations

6.1 Biomarker or stratification potential (metabolic liver disease)

Chiang et al. (2023) report SMSr protein differences in human NASH liver and altered plasma PE/PE:PC ratio, suggesting a potential biomarker axis (SMSr/PE metabolism/inflammation) for NASH stratification or mechanistic monitoring, though clinical validation is not established in the retrieved evidence. (chiang2023sphingomyelinsynthase–relatedprotein pages 8-9)

6.2 Therapeutic targeting concept

Given the 2023 findings, SMSr enzymatic activity (PE-PLC) could be viewed as a potential drug target for NAFLD/NASH. The 2022 review notes D609 as an inhibitor used to inhibit SMSr activity in a dose-dependent manner in their framework, supporting feasibility of pharmacological modulation (as a research tool and potential lead concept). (jiang2022sphingomyelinsynthasefamily pages 6-8)

6.3 Lipid signaling engineering

The DGKδ interaction data indicate SAMD8 can shape specific DAG→PA flux toward saturated/monounsaturated PA species, offering a mechanistically grounded “node” for manipulating lipid signaling outputs in engineered systems (cell models) (murakami2020diacylglycerolkinaseδ pages 10-11, murakami2020diacylglycerolkinaseδ pages 6-7).

7) Expert opinions / authoritative analysis

Jiang & Chiang (2022) explicitly summarize: (i) SMSr is the third SMS-family member, ER-localized and conserved; (ii) SMSr has CPE synthase activity in vitro but not canonical SM synthase activity; and (iii) a newer classification frames SMSr as a PE‑PLC generating DAG and regulating PE levels—while also noting the mismatch between strong cell-based phenotypes and minimal baseline mouse phenotypes, implying physiology is context-dependent and not fully settled. (jiang2022sphingomyelinsynthasefamily pages 4-6, jiang2022sphingomyelinsynthasefamily pages 1-3)

8) Key quantitative statistics (from recent/primary studies)

• CPE abundance in mammals: CPE is ~300–1,500-fold lower than SM across mouse tissues; CPE up to ~0.020 mol% of total phospholipid (brain/testis) and ~0.002–0.005 mol% (heart/liver). (bickert2015functionalcharacterizationof pages 5-6)
• Brain CPE dependence on SMSr: SMSr catalytic inactivation reduces short-chain CPE species by 40–60% and total CPE by ~30% in forebrain/cerebellum. (bickert2015functionalcharacterizationof pages 9-10, bickert2015functionalcharacterizationof pages 12-13)
• NAFLD inflammation reduction with Smsr deficiency (mouse model): inflammatory cytokines reduced by ~30% (including TNFα and IL-6) under the HFD+fructose paradigm. (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)
• SMSr–DGKδ pathway: deleting SMSr SAMD reduces DGKδ co-IP by ~75%; SMSr co-expression increases total PA by ~20% and increases specific PA species (>20%) (30:0, 32:1, 32:0, 34:1, 34:2). (murakami2020diacylglycerolkinaseδ pages 5-6, murakami2020diacylglycerolkinaseδ pages 10-11)
• Apoptosis regulation: caspase-6 cleaves SMSr mainly at Asp120 (secondary Asp118), producing an ~33 kDa fragment in vitro. (cabukusta2017ceramidephosphoethanolaminesynthase pages 5-7)

9) Consolidated evidence map (key sources)

Table: This table summarizes the main primary studies and a key review on human SAMD8/SMSr, covering identity, localization, enzymatic activity, regulation, and phenotypes. It highlights where the literature is consistent and where recent work has introduced mechanistic controversy, especially around CPE synthase versus PE-PLC activity.

References (URLs and publication dates)

The report’s key sources (with URLs and dates) are embedded in the table above and include:
- Cabukusta et al., Scientific Reports (Jan 2017): https://doi.org/10.1038/srep41290 (cabukusta2017erresidencyof pages 10-13)
- Cabukusta et al., Bioscience Reports (Jul 2017): https://doi.org/10.1042/BSR20170867 (cabukusta2017ceramidephosphoethanolaminesynthase pages 7-10)
- Bickert et al., Journal of Lipid Research (Apr 2015): https://doi.org/10.1194/jlr.M055269 (bickert2015functionalcharacterizationof pages 12-13)
- Murakami et al., Journal of Biological Chemistry (Mar 2020): https://doi.org/10.1074/jbc.RA119.012369 (murakami2020diacylglycerolkinaseδ pages 1-1)
- Jiang & Chiang, Advances in Experimental Medicine and Biology (Jan 2022): https://doi.org/10.1007/978-981-19-0394-6_7 (jiang2022sphingomyelinsynthasefamily pages 1-3)
- Chiang et al., Journal of Biological Chemistry (Sep 2023): https://doi.org/10.1016/j.jbc.2023.105162 (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2)

Limitations of this evidence set

Within the retrieved documents, no 2024 primary SAMD8-focused mechanistic study was captured; 2023 provides the main recent primary advance. Additionally, structural data (e.g., high-resolution structures) for SMSr specifically were not present in the retrieved evidence corpus, so mechanistic details are limited to biochemical assays, genetics, topology/oligomerization, and pathway-level lipidomics.

References

1. (cabukusta2017erresidencyof pages 10-13): Birol Cabukusta, Matthijs Kol, Laura Kneller, Angelika Hilderink, Andreas Bickert, John G. M. Mina, Sergei Korneev, and Joost C. M. Holthuis. Er residency of the ceramide phosphoethanolamine synthase smsr relies on homotypic oligomerization mediated by its sam domain. Scientific Reports, Jan 2017. URL: https://doi.org/10.1038/srep41290, doi:10.1038/srep41290. This article has 25 citations and is from a peer-reviewed journal.

2. (cabukusta2017ceramidephosphoethanolaminesynthase pages 7-10): Birol Cabukusta, Niclas T. Nettebrock, Matthijs Kol, Angelika Hilderink, Fikadu G. Tafesse, and Joost C.M. Holthuis. Ceramide phosphoethanolamine synthase smsr is a target of caspase-6 during apoptotic cell death. Bioscience Reports, Jul 2017. URL: https://doi.org/10.1042/bsr20170867, doi:10.1042/bsr20170867. This article has 11 citations and is from a peer-reviewed journal.

3. (chiang2023sphingomyelinsynthase–relatedprotein pages 1-2): Yeun-po Chiang, Zhiqiang Li, Mulin He, Quiana Jones, Meixia Pan, Xianlin Han, and Xian-Cheng Jiang. Sphingomyelin synthase–related protein smsr is a phosphatidylethanolamine phospholipase c that promotes nonalcoholic fatty liver disease. Journal of Biological Chemistry, 299:105162, Sep 2023. URL: https://doi.org/10.1016/j.jbc.2023.105162, doi:10.1016/j.jbc.2023.105162. This article has 7 citations and is from a domain leading peer-reviewed journal.

4. (jiang2022sphingomyelinsynthasefamily pages 4-6): Xian-Cheng Jiang and Yeun-po Chiang. Sphingomyelin synthase family and phospholipase cs. Advances in experimental medicine and biology, 1372:77-86, Jan 2022. URL: https://doi.org/10.1007/978-981-19-0394-6_7, doi:10.1007/978-981-19-0394-6_7. This article has 11 citations and is from a peer-reviewed journal.

5. (cabukusta2017erresidencyof pages 1-2): Birol Cabukusta, Matthijs Kol, Laura Kneller, Angelika Hilderink, Andreas Bickert, John G. M. Mina, Sergei Korneev, and Joost C. M. Holthuis. Er residency of the ceramide phosphoethanolamine synthase smsr relies on homotypic oligomerization mediated by its sam domain. Scientific Reports, Jan 2017. URL: https://doi.org/10.1038/srep41290, doi:10.1038/srep41290. This article has 25 citations and is from a peer-reviewed journal.

6. (cabukusta2017ceramidephosphoethanolaminesynthase pages 1-2): Birol Cabukusta, Niclas T. Nettebrock, Matthijs Kol, Angelika Hilderink, Fikadu G. Tafesse, and Joost C.M. Holthuis. Ceramide phosphoethanolamine synthase smsr is a target of caspase-6 during apoptotic cell death. Bioscience Reports, Jul 2017. URL: https://doi.org/10.1042/bsr20170867, doi:10.1042/bsr20170867. This article has 11 citations and is from a peer-reviewed journal.

7. (jiang2022sphingomyelinsynthasefamily pages 6-8): Xian-Cheng Jiang and Yeun-po Chiang. Sphingomyelin synthase family and phospholipase cs. Advances in experimental medicine and biology, 1372:77-86, Jan 2022. URL: https://doi.org/10.1007/978-981-19-0394-6_7, doi:10.1007/978-981-19-0394-6_7. This article has 11 citations and is from a peer-reviewed journal.

8. (jiang2022sphingomyelinsynthasefamily pages 3-4): Xian-Cheng Jiang and Yeun-po Chiang. Sphingomyelin synthase family and phospholipase cs. Advances in experimental medicine and biology, 1372:77-86, Jan 2022. URL: https://doi.org/10.1007/978-981-19-0394-6_7, doi:10.1007/978-981-19-0394-6_7. This article has 11 citations and is from a peer-reviewed journal.

9. (jiang2022sphingomyelinsynthasefamily pages 11-15): Xian-Cheng Jiang and Yeun-po Chiang. Sphingomyelin synthase family and phospholipase cs. Advances in experimental medicine and biology, 1372:77-86, Jan 2022. URL: https://doi.org/10.1007/978-981-19-0394-6_7, doi:10.1007/978-981-19-0394-6_7. This article has 11 citations and is from a peer-reviewed journal.

10. (bickert2015functionalcharacterizationof pages 5-6): Andreas Bickert, Christina Ginkel, Matthijs Kol, Katharina vom Dorp, Holger Jastrow, Joachim Degen, René L. Jacobs, Dennis E. Vance, Elke Winterhager, Xian-Cheng Jiang, Peter Dörmann, Pentti Somerharju, Joost C.M. Holthuis, and Klaus Willecke. Functional characterization of enzymes catalyzing ceramide phosphoethanolamine biosynthesis in mice[s]. Journal of Lipid Research, 56:821-835, Apr 2015. URL: https://doi.org/10.1194/jlr.m055269, doi:10.1194/jlr.m055269. This article has 56 citations and is from a peer-reviewed journal.

11. (chiang2023sphingomyelinsynthase–relatedprotein pages 10-11): Yeun-po Chiang, Zhiqiang Li, Mulin He, Quiana Jones, Meixia Pan, Xianlin Han, and Xian-Cheng Jiang. Sphingomyelin synthase–related protein smsr is a phosphatidylethanolamine phospholipase c that promotes nonalcoholic fatty liver disease. Journal of Biological Chemistry, 299:105162, Sep 2023. URL: https://doi.org/10.1016/j.jbc.2023.105162, doi:10.1016/j.jbc.2023.105162. This article has 7 citations and is from a domain leading peer-reviewed journal.

12. (bickert2017biologicalfunctionsof pages 32-35): A Bickert. Biological functions of sphingomyelin synthase related protein and ceramide synthase 4 investigated with transgenic mouse mutants. Unknown journal, 2017.

13. (cabukusta2017erresidencyof pages 14-15): Birol Cabukusta, Matthijs Kol, Laura Kneller, Angelika Hilderink, Andreas Bickert, John G. M. Mina, Sergei Korneev, and Joost C. M. Holthuis. Er residency of the ceramide phosphoethanolamine synthase smsr relies on homotypic oligomerization mediated by its sam domain. Scientific Reports, Jan 2017. URL: https://doi.org/10.1038/srep41290, doi:10.1038/srep41290. This article has 25 citations and is from a peer-reviewed journal.

14. (jiang2022sphingomyelinsynthasefamily pages 1-3): Xian-Cheng Jiang and Yeun-po Chiang. Sphingomyelin synthase family and phospholipase cs. Advances in experimental medicine and biology, 1372:77-86, Jan 2022. URL: https://doi.org/10.1007/978-981-19-0394-6_7, doi:10.1007/978-981-19-0394-6_7. This article has 11 citations and is from a peer-reviewed journal.

15. (bickert2015functionalcharacterizationof pages 12-13): Andreas Bickert, Christina Ginkel, Matthijs Kol, Katharina vom Dorp, Holger Jastrow, Joachim Degen, René L. Jacobs, Dennis E. Vance, Elke Winterhager, Xian-Cheng Jiang, Peter Dörmann, Pentti Somerharju, Joost C.M. Holthuis, and Klaus Willecke. Functional characterization of enzymes catalyzing ceramide phosphoethanolamine biosynthesis in mice[s]. Journal of Lipid Research, 56:821-835, Apr 2015. URL: https://doi.org/10.1194/jlr.m055269, doi:10.1194/jlr.m055269. This article has 56 citations and is from a peer-reviewed journal.

16. (cabukusta2017ceramidephosphoethanolaminesynthase pages 5-7): Birol Cabukusta, Niclas T. Nettebrock, Matthijs Kol, Angelika Hilderink, Fikadu G. Tafesse, and Joost C.M. Holthuis. Ceramide phosphoethanolamine synthase smsr is a target of caspase-6 during apoptotic cell death. Bioscience Reports, Jul 2017. URL: https://doi.org/10.1042/bsr20170867, doi:10.1042/bsr20170867. This article has 11 citations and is from a peer-reviewed journal.

17. (murakami2020diacylglycerolkinaseδ pages 5-6): Chiaki Murakami, Fumi Hoshino, Hiromichi Sakai, Yasuhiro Hayashi, Atsushi Yamashita, and Fumio Sakane. Diacylglycerol kinase δ and sphingomyelin synthase–related protein functionally interact via their sterile α motif domains. Journal of Biological Chemistry, 295:2932-2947, Mar 2020. URL: https://doi.org/10.1074/jbc.ra119.012369, doi:10.1074/jbc.ra119.012369. This article has 29 citations and is from a domain leading peer-reviewed journal.

18. (murakami2020diacylglycerolkinaseδ pages 10-11): Chiaki Murakami, Fumi Hoshino, Hiromichi Sakai, Yasuhiro Hayashi, Atsushi Yamashita, and Fumio Sakane. Diacylglycerol kinase δ and sphingomyelin synthase–related protein functionally interact via their sterile α motif domains. Journal of Biological Chemistry, 295:2932-2947, Mar 2020. URL: https://doi.org/10.1074/jbc.ra119.012369, doi:10.1074/jbc.ra119.012369. This article has 29 citations and is from a domain leading peer-reviewed journal.

19. (murakami2020diacylglycerolkinaseδ pages 6-7): Chiaki Murakami, Fumi Hoshino, Hiromichi Sakai, Yasuhiro Hayashi, Atsushi Yamashita, and Fumio Sakane. Diacylglycerol kinase δ and sphingomyelin synthase–related protein functionally interact via their sterile α motif domains. Journal of Biological Chemistry, 295:2932-2947, Mar 2020. URL: https://doi.org/10.1074/jbc.ra119.012369, doi:10.1074/jbc.ra119.012369. This article has 29 citations and is from a domain leading peer-reviewed journal.

20. (murakami2020diacylglycerolkinaseδ pages 1-1): Chiaki Murakami, Fumi Hoshino, Hiromichi Sakai, Yasuhiro Hayashi, Atsushi Yamashita, and Fumio Sakane. Diacylglycerol kinase δ and sphingomyelin synthase–related protein functionally interact via their sterile α motif domains. Journal of Biological Chemistry, 295:2932-2947, Mar 2020. URL: https://doi.org/10.1074/jbc.ra119.012369, doi:10.1074/jbc.ra119.012369. This article has 29 citations and is from a domain leading peer-reviewed journal.

21. (bickert2015functionalcharacterizationof pages 9-10): Andreas Bickert, Christina Ginkel, Matthijs Kol, Katharina vom Dorp, Holger Jastrow, Joachim Degen, René L. Jacobs, Dennis E. Vance, Elke Winterhager, Xian-Cheng Jiang, Peter Dörmann, Pentti Somerharju, Joost C.M. Holthuis, and Klaus Willecke. Functional characterization of enzymes catalyzing ceramide phosphoethanolamine biosynthesis in mice[s]. Journal of Lipid Research, 56:821-835, Apr 2015. URL: https://doi.org/10.1194/jlr.m055269, doi:10.1194/jlr.m055269. This article has 56 citations and is from a peer-reviewed journal.

22. (bickert2015functionalcharacterizationof pages 10-12): Andreas Bickert, Christina Ginkel, Matthijs Kol, Katharina vom Dorp, Holger Jastrow, Joachim Degen, René L. Jacobs, Dennis E. Vance, Elke Winterhager, Xian-Cheng Jiang, Peter Dörmann, Pentti Somerharju, Joost C.M. Holthuis, and Klaus Willecke. Functional characterization of enzymes catalyzing ceramide phosphoethanolamine biosynthesis in mice[s]. Journal of Lipid Research, 56:821-835, Apr 2015. URL: https://doi.org/10.1194/jlr.m055269, doi:10.1194/jlr.m055269. This article has 56 citations and is from a peer-reviewed journal.

23. (chiang2023sphingomyelinsynthase–relatedprotein pages 8-9): Yeun-po Chiang, Zhiqiang Li, Mulin He, Quiana Jones, Meixia Pan, Xianlin Han, and Xian-Cheng Jiang. Sphingomyelin synthase–related protein smsr is a phosphatidylethanolamine phospholipase c that promotes nonalcoholic fatty liver disease. Journal of Biological Chemistry, 299:105162, Sep 2023. URL: https://doi.org/10.1016/j.jbc.2023.105162, doi:10.1016/j.jbc.2023.105162. This article has 7 citations and is from a domain leading peer-reviewed journal.

24. (murakami2020diacylglycerolkinaseδ pages 3-4): Chiaki Murakami, Fumi Hoshino, Hiromichi Sakai, Yasuhiro Hayashi, Atsushi Yamashita, and Fumio Sakane. Diacylglycerol kinase δ and sphingomyelin synthase–related protein functionally interact via their sterile α motif domains. Journal of Biological Chemistry, 295:2932-2947, Mar 2020. URL: https://doi.org/10.1074/jbc.ra119.012369, doi:10.1074/jbc.ra119.012369. This article has 29 citations and is from a domain leading peer-reviewed journal.

Artifacts

• Edison artifact artifact-00

Citations

1. bickert2015functionalcharacterizationof pages 5-6
2. cabukusta2017erresidencyof pages 14-15
3. bickert2015functionalcharacterizationof pages 10-12
4. jiang2022sphingomyelinsynthasefamily pages 6-8
5. cabukusta2017ceramidephosphoethanolaminesynthase pages 5-7
6. cabukusta2017erresidencyof pages 10-13
7. cabukusta2017ceramidephosphoethanolaminesynthase pages 7-10
8. bickert2015functionalcharacterizationof pages 12-13
9. jiang2022sphingomyelinsynthasefamily pages 1-3
10. jiang2022sphingomyelinsynthasefamily pages 4-6
11. cabukusta2017erresidencyof pages 1-2
12. cabukusta2017ceramidephosphoethanolaminesynthase pages 1-2
13. jiang2022sphingomyelinsynthasefamily pages 3-4
14. jiang2022sphingomyelinsynthasefamily pages 11-15
15. bickert2017biologicalfunctionsof pages 32-35
16. bickert2015functionalcharacterizationof pages 9-10
17. s
18. https://doi.org/10.1038/srep41290
19. https://doi.org/10.1042/BSR20170867
20. https://doi.org/10.1194/jlr.M055269
21. https://doi.org/10.1016/j.jbc.2023.105162
22. https://doi.org/10.1074/jbc.RA119.012369
23. https://doi.org/10.1007/978-981-19-0394-6_7
24. https://doi.org/10.1038/srep41290,
25. https://doi.org/10.1042/bsr20170867,
26. https://doi.org/10.1016/j.jbc.2023.105162,
27. https://doi.org/10.1007/978-981-19-0394-6_7,
28. https://doi.org/10.1194/jlr.m055269,
29. https://doi.org/10.1074/jbc.ra119.012369,