Affinage

CIDEC

Lipid transferase CIDEC · UniProt Q96AQ7

Length
238 aa
Mass
26.8 kDa
Annotated
2026-04-28
100 papers in source corpus 37 papers cited in narrative 36 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CIDEC (also called FSP27) is a lipid droplet (LD)-associated protein that drives unilocular LD formation in adipocytes and hepatocytes by mediating directional, pressure-driven transfer of neutral lipids from smaller to larger LDs at LD-LD contact sites. At these contact sites, the CIDE-N domain undergoes phase separation to form gel-like condensates that create lipid-permeable fusion plates, while the CIDE-C domain is required for LD targeting and fusion; CIDEC simultaneously suppresses lipolysis by directly inhibiting ATGL and sequestering its co-activator CGI-58, and its protein stability is regulated by PCAF-mediated acetylation at K56 (stabilizing) versus HDAC6-mediated deacetylation and AMPK/HSC70-driven proteasomal degradation (PMID:22144693, PMID:34508658, PMID:36800289, PMID:24627478, PMID:35963433, PMID:28287402, PMID:25315694). Perilipin1 interaction with CIDEC markedly enhances lipid transfer activity, and CIDE-N homodimerization is required for function (PMID:23481402). A homozygous truncation mutation (E186X) in the CIDE-C domain causes familial partial lipodystrophy with multilocular white adipocyte LDs (PMID:20049731). Transcription of CIDEC is directly activated by PPARγ in adipocytes, PPARα and CREBH in hepatocytes (the latter driving a liver-specific Fsp27β isoform), and is modulated by insulin/PI3K-JNK2, TNFα/MEK-ERK, and growth hormone signaling (PMID:18396136, PMID:25418138, PMID:25125366, PMID:20154362).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1992 Medium

    Before CIDEC's lipid droplet function was known, the FSP27 promoter was shown to confer adipocyte-specific expression dependent on C/EBP-binding elements, establishing tissue-restricted transcriptional control as a foundational property.

    Evidence Promoter-reporter transfection and DNase I footprinting with adipocyte nuclear extracts

    PMID:1339452

    Open questions at the time
    • Identity of the specific C/EBP family member(s) driving endogenous expression was not resolved
    • No link to lipid metabolism was established at this stage
  2. 2003 Medium

    Cloning of human CIDE-3 (CIDEC) revealed conserved CIDE-N and CIDE-C domains and showed that overexpression induces apoptosis, initially framing the protein within the CIDE cell-death family.

    Evidence DNA fragmentation assay and GFP-fusion localization in 293T cells

    PMID:12429024

    Open questions at the time
    • Apoptotic function was based on overexpression; physiological relevance of cell-death activity remained unclear
    • Lipid droplet association was not yet recognized
  3. 2008 High

    Genetic ablation in mice and PPARγ-dependent transcriptional activation established CIDEC as a major determinant of unilocular LD formation, triglyceride storage, and lipolytic suppression in white adipose tissue and liver, redefining its primary function from apoptosis to lipid metabolism.

    Evidence FSP27 knockout mice with multilocular LD/lean phenotype; ChIP and reporter assays identifying PPARγ PPRE in the Cidec promoter; adenoviral gain/loss-of-function in hepatocytes

    PMID:18396136 PMID:18654663 PMID:18845124

    Open questions at the time
    • Mechanism by which CIDEC promotes LD enlargement (fusion vs. transfer vs. synthesis) was unresolved
    • Relative contribution of lipolysis suppression vs. LD fusion was not separated
  4. 2009 High

    A human homozygous truncation (E186X) in the CIDE-C domain causing partial lipodystrophy provided genetic proof that the CIDE-C domain is essential for LD targeting and function in humans.

    Evidence Human genetic study with cellular validation showing mislocalization and loss of LD enlargement by mutant CIDEC

    PMID:20049731

    Open questions at the time
    • Whether additional CIDEC mutations cause lipodystrophy in other families was unknown
    • Structural basis for CIDE-C domain function remained unresolved
  5. 2011 High

    Live-cell imaging and FRAP revealed that CIDEC concentrates at LD-LD contact sites and mediates directional lipid transfer from smaller to larger LDs driven by Laplace pressure differences, resolving the biophysical mechanism of LD growth.

    Evidence FRAP, live-cell imaging, and biophysical pressure analysis in Fsp27-deficient and Fsp27-overexpressing cells

    PMID:22144693

    Open questions at the time
    • Molecular nature of the pore or channel allowing lipid transfer was unknown
    • Whether other CIDE family members use the same mechanism was untested
  6. 2013 High

    Perilipin1 was identified as a direct activator of CIDEC-mediated lipid transfer through interaction with the CIDE-N domain, and CIDE-N homodimerization was shown to be required for function, defining the key protein-protein interactions governing CIDEC activity.

    Evidence Reciprocal Co-IP, FRAP-based lipid transfer quantification, domain mutagenesis, and crystal structure of CIDE-N homodimer at 2.0 Å

    PMID:23399566 PMID:23481402 PMID:24025675

    Open questions at the time
    • How Plin1 binding mechanistically enhances lipid transfer rate was not determined
    • Role of CIDE-N dimerization in phase separation was not yet appreciated
  7. 2014 High

    CIDEC was shown to directly inhibit ATGL lipolytic activity via its C-terminal region (aa 120–220), establishing a dual mechanism — LD fusion plus lipolysis suppression — for triglyceride storage, while AMPK activation was found to trigger CIDEC ubiquitination and proteasomal degradation via HSC70.

    Evidence Co-IP and domain mapping of CIDEC-ATGL interaction in ATGL KO rescue; AICAR/phenformin treatment with cycloheximide chase and HSC70 knockdown

    PMID:24627478 PMID:25315694

    Open questions at the time
    • E3 ubiquitin ligase responsible for AMPK-triggered CIDEC degradation was not identified (CHIP was excluded)
    • Structural basis for CIDEC-ATGL inhibitory interaction was lacking
  8. 2015 Medium

    Tissue-specific transcriptional programs were delineated: PPARα directly activates Cidec in hepatocytes during fasting, and CREBH drives a liver-specific Fsp27β isoform from a distinct promoter, explaining how the same gene is induced in both adipose and liver contexts.

    Evidence ChIP, reporter assays, adenoviral shRNA in vivo for PPARα; promoter identification and constitutively active CREBH reporter assays for Fsp27β

    PMID:25125366 PMID:25418138

    Open questions at the time
    • Functional differences between Fsp27α and Fsp27β isoforms beyond expression pattern were not fully characterized
    • Whether PPARα and CREBH cooperate on the same promoter was untested
  9. 2017 High

    Post-translational regulation of CIDEC stability was resolved: PCAF acetylates K56 to stabilize CIDEC, while HDAC6 deacetylates K56 to destabilize it; dietary fatty acids shift the PCAF/HDAC6 balance toward acetylation on the ER, linking nutritional status to CIDEC protein levels.

    Evidence Acetylation site mutagenesis, adipocyte-specific Hdac6 KO mice, Co-IP of CIDEC-PCAF and CIDEC-HDAC6, LD fusion assays in obese animal models

    PMID:28287402

    Open questions at the time
    • Whether K56 acetylation affects CIDEC phase separation or interaction with Plin1/ATGL was not tested
    • Deacetylation-independent degradation pathways were not addressed
  10. 2018 Medium

    A polybasic RKKR motif in the CIDEC linker was found to interact with acidic phospholipids and act as an autoinhibitory element that restrains LD fusion, adding a lipid-dependent regulatory layer to CIDEC activity.

    Evidence Charge-reversal mutagenesis, phospholipid binding assays, and LD size quantification

    PMID:30361435

    Open questions at the time
    • How RKKR motif regulation integrates with Plin1 activation or acetylation status was not explored
    • In vivo significance of this autoinhibitory mechanism was not tested
  11. 2021 High

    The molecular basis of the LD-LD contact site was resolved: CIDEC-N undergoes phase separation via multivalent homomeric interactions to form gel-like condensates that constitute the lipid-permeable fusion plate, establishing phase separation as the organizing principle for CIDEC-mediated lipid transfer.

    Evidence In vitro reconstitution of CIDEC-N phase separation, live-cell FRAP at LDCS, functional deletion mutants disrupting phase separation

    PMID:34508658

    Open questions at the time
    • Whether Plin1, ATGL, or CGI-58 partition into or are excluded from the condensate was not determined
    • Structural details of the lipid-permeable pore within the condensate are unknown
  12. 2022 High

    CIDEC's lipolysis-suppressive function was extended beyond ATGL to its co-activator CGI-58: CIDEC sequesters CGI-58, reducing free fatty acid release and lipotoxicity, with in vivo validation showing adipose-specific CIDEC transgenic mice are protected from HFD-induced glucose intolerance.

    Evidence Co-IP of CIDEC-CGI-58, adipose-specific transgenic and E186X mutant mice, lipidomics, recombinant CIDEC on human adipose tissue ex vivo

    PMID:35963433

    Open questions at the time
    • Whether CIDEC binds CGI-58 and ATGL simultaneously or competitively was not resolved
    • Stoichiometry of the CIDEC-CGI-58 complex is unknown
  13. 2023 High

    Cryo-electron tomography visualized the LD-LD interface architecture, showing that CIDEC-mediated lipid transfer occurs through closely apposed phospholipid monolayers with exponential transfer kinetics sensitive to inter-monolayer distance, providing direct structural evidence for the transfer mechanism.

    Evidence Electron cryo-tomography of LD-LD contacts combined with quantitative live fluorescence microscopy of lipid transfer kinetics

    PMID:36800289

    Open questions at the time
    • Atomic-resolution structure of the CIDEC condensate at the contact site is lacking
    • Whether a proteinaceous pore exists or lipid transfer occurs purely through monolayer proximity remains unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions include: (1) the atomic-level structure of the CIDEC phase-separated fusion plate and whether it forms a discrete pore; (2) how post-translational modifications (acetylation, ubiquitination, phospholipid binding) regulate phase separation properties; (3) whether CIDEC condensates selectively partition or exclude regulatory partners such as Plin1, ATGL, and CGI-58.
  • No high-resolution structure of the intact CIDEC condensate at LD-LD contacts
  • Interplay between acetylation/AMPK degradation and phase separation is untested
  • Comprehensive interactome of the CIDEC condensate is not defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 2 GO:0140313 molecular sequestering activity 2
Localization
GO:0005811 lipid droplet 7 GO:0005783 endoplasmic reticulum 2 GO:0005829 cytosol 1
Pathway
R-HSA-1430728 Metabolism 7 R-HSA-162582 Signal Transduction 3 R-HSA-5357801 Programmed Cell Death 2

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 FSP27/CIDEC localizes to lipid droplets in white adipocytes and promotes formation of unilocular lipid droplets; ablation results in multilocular lipid droplets, increased lipolysis, decreased triacylglycerol storage, and increased mitochondrial biogenesis in white adipose tissue. FSP27 knockout mice, siRNA depletion in cultured adipocytes, ectopic expression in COS cells, in vivo phenotypic analysis The Journal of clinical investigation High 18654663
2011 Fsp27 is focally enriched at the lipid droplet-lipid droplet contact site (LDCS) and mediates directional net lipid transfer from smaller to larger LDs, driving LD growth via a pressure-difference mechanism. Live-cell imaging, FRAP/photobleaching, Fsp27-deficient adipocytes, Fsp27-overexpressing cells, biophysical analysis of LD internal pressure The Journal of cell biology High 22144693
2013 Perilipin1 (Plin1) interacts with the CIDE-N domain of Fsp27 and markedly increases Fsp27-mediated lipid exchange, lipid transfer, and lipid droplet growth; CIDE-N homodimerization is required for Fsp27 activity and Plin1 can restore activity of CIDE-N homodimerization-defective mutants. Co-immunoprecipitation, FRAP, live-cell imaging, domain mutagenesis, siRNA depletion Nature communications High 23481402
2013 Human FSP27 (CIDEC) interacts with PLIN1 via its C-terminal domain (aa 120–220) in primary human adipocytes, and co-expression of FSP27 and PLIN1 increases average lipid droplet size and promotes unilocular adipocyte formation. Co-localization by immunofluorescence, co-immunoprecipitation, deletion mapping, triglyceride/glycerol assays in human adipocytes Biochemical and biophysical research communications Medium 23399566
2009 A truncation mutation in the CIDE-C domain of human CIDEC (E186X) causes partial lipodystrophy with multilocular lipid droplets; the mutant protein is mistargeted and fails to increase lipid droplet size in transfected cells, establishing the CIDE-C domain as necessary for LD targeting and function. Human genetics (homozygous truncation mutation), transfection of mutant vs. WT CIDEC in cells, lipid droplet size assay EMBO molecular medicine High 20049731
2011 FSP27 promotes LD clustering (requiring aa 173–220) followed by their fusion into enlarged droplets (requiring aa 120–210), with LD enlargement—but not clustering—associated with triglyceride accumulation. GFP-fusion deletion mutants, fluorescence microscopy, triglyceride quantification in HeLa cells PloS one Medium 22194867
2009 The FSP27 CIDE-C domain (aa 174–192) is required for lipid droplet localization and apoptosis induction (via caspase-9 and mitochondrial cytochrome c release); the CIDE-C domain also mediates heterodimerization with CIDEA. eGFP-FSP27 deletion constructs, caspase activity assays, cytochrome c release, co-immunoprecipitation, Western blot American journal of physiology. Endocrinology and metabolism Medium 19843876
2014 FSP27 (aa 120–220) directly interacts with ATGL (adipose triglyceride lipase) to inhibit its lipolytic activity and promote triglyceride storage; FSP27 depletion increases lipolysis and impairs insulin signaling via reduced AKT phosphorylation. Co-immunoprecipitation, domain deletion mapping, siRNA knockdown, lipolysis assays, AKT phosphorylation assays in human adipocytes and ATGL KO mouse fibroblasts The Journal of biological chemistry High 24627478
2017 HDAC6 deacetylates CIDEC at K56 (acetylated by PCAF), leading to CIDEC destabilization and reduced lipid droplet fusion; dietary fatty acids promote CIDEC acetylation by dissociating CIDEC from HDAC6 and increasing CIDEC-PCAF association on the ER, requiring conversion of FAs to triacylglycerols. Co-immunoprecipitation, acetylation site mutagenesis, adipocyte-specific Hdac6 KO mice, lipid droplet fusion assays, in vivo obese animal models The Journal of clinical investigation High 28287402
2008 Fsp27 expression in ob/ob mouse liver is directly transcriptionally activated by PPARγ (functional PPAR response element in the Fsp27 promoter); hepatic Fsp27 promotes triglyceride accumulation and lipid droplet formation. Chromatin immunoprecipitation, reporter assay, adenovirus-mediated overexpression and shRNA knockdown in hepatocytes in vitro and in vivo Cell metabolism High 18396136
2008 Cidec transcription is directly activated by PPARγ2 via a PPRE at −219/−207 of the Cidec promoter in adipocytes. Chromatin immunoprecipitation, luciferase reporter assay, gel shift assay, promoter mutagenesis Biochemical and biophysical research communications Medium 18845124
2015 CIDEC/Fsp27 is a direct transcriptional target of PPARα in hepatocytes; adenoviral silencing of hepatic Fsp27 abolishes fasting-induced liver steatosis without altering plasma lipids, and synergizes with PPARα agonists to reduce diet-induced hepatosteatosis. ChIP, reporter assay, adenoviral shRNA silencing in vivo, pharmacological PPARα activation Hepatology (Baltimore, Md.) Medium 25418138
2015 The liver-enriched transcription factor CREBH activates transcription of a liver-specific Fsp27β isoform (10 extra N-terminal amino acids) from a distinct promoter; Fsp27β localizes to lipid droplet surfaces, suppresses lipolysis, and promotes lipid droplet enlargement and TG accumulation in liver. Promoter identification, reporter assay with constitutively active CREBH, adenoviral overexpression, lipid droplet imaging in hepatocytes Hepatology (Baltimore, Md.) Medium 25125366
2012 Fsp27/CIDEC is a CREB target gene in the liver; early fasting induction involves the PKA-CREB-CRTC2 signaling pathway (induced by forskolin, blocked by CREB inhibition); pharmacological or genetic inhibition of fatty acid oxidation increases Fsp27 expression during fasting. Promoter reporter assay with CREB, forskolin stimulation, Sirt1 KO animals, etomoxir/Hmgcs2 interference in vivo and in HepG2 cells Journal of lipid research Medium 23220584
2021 Cidec undergoes phase separation via multivalent homomeric interactions of its N-terminal domain at LD-LD contact sites, forming gel-like condensates that create lipid-permeable fusion plates for LD fusion; phase separation is required for LD fusion activity. In vitro phase separation reconstitution, live-cell imaging, fluorescence recovery experiments, deletion mutants, in vivo LDCS analysis Developmental cell High 34508658
2023 Cidec-mediated lipid transfer between LDs occurs through closely apposed phospholipid monolayers at LD-LD interfaces, follows exponential kinetics, and is slowed by increasing the distance between monolayers, as visualized by electron cryo-tomography. Electron cryo-tomography, quantitative live fluorescence microscopy of lipid transfer kinetics Cell reports High 36800289
2013 Crystal structure of the CIDE-N domain of FSP27 at 2.0 Å resolution reveals a biologically important homodimeric interface similar to the CAD/ICAD heterodimeric complex, providing a structural basis for FSP27-mediated LD growth. X-ray crystallography at 2.0 Å resolution Biochemical and biophysical research communications Medium 24025675
2018 A polybasic RKKR motif in the linker region of CIDEC interacts with acidic phospholipids via electrostatic attraction to inhibit LD fusion; deletion or mutation of the RKKR motif disrupts protein-lipid interaction and results in enhanced LD fusion and supersized LDs. Targeted deletion and GFP-fusion constructs, fluorescence microscopy, phospholipid binding assays The Journal of biological chemistry Medium 30361435
2014 AMPK activation induces ubiquitination and proteasomal degradation of FSP27, resulting in LD multilocularization; HSC70 is identified as a novel FSP27-binding protein that promotes FSP27 degradation, while CHIP (E3 ubiquitin ligase) is not required. AICAR/phenformin treatment, AMPKα1 knockdown, proteasome inhibition, mass spectrometry, co-immunoprecipitation of endogenous proteins, cycloheximide chase, siRNA knockdown of HSC70 and CHIP American journal of physiology. Endocrinology and metabolism Medium 25315694
2015 Cidec interacts with AMPKα1 and promotes its degradation via the ubiquitin-proteasome pathway, thereby promoting adipocyte differentiation; the interaction was confirmed by yeast two-hybrid, co-immunoprecipitation, and co-localization. Yeast two-hybrid, co-immunoprecipitation, immunofluorescence co-localization, proteasome inhibition assay Biochimica et biophysica acta Medium 26367078
2018 Growth hormone downregulates FSP27 expression by activating MEK/ERK signaling, which phosphorylates PPARγ at Ser273 and promotes its nuclear-to-cytosol translocation; FSP27 overexpression inhibits PPARγ Ser273 phosphorylation and promotes nuclear retention, thus suppressing GH-induced lipolysis. Selective inhibitors, constitutively active MEK1 mutant, immunofluorescence, subcellular fractionation, reporter assay, human adipose-derived stromal vascular cells, human subjects American journal of physiology. Endocrinology and metabolism Medium 30325658
2016 TNF-α downregulates CIDEC transcription through MEK/ERK-dependent phosphorylation and nuclear export of PPARγ in human adipocytes. MEK/ERK inhibitors, constitutively active MEK1, immunofluorescence, subcellular fractionation, luciferase reporter assay Obesity (Silver Spring, Md.) Medium 27062372
2014 CIDEC translocates from the ER to lipid droplets in response to fatty acid stimulation; the N-terminal domain (aa 1–173) mediates LD localization while the C-terminal domain (aa 174–238) is necessary for LD fusion; aa 106–173 contains an ER-binding domain. CIDEC deletion mutant analysis, immunofluorescence, subcellular fractionation in HepG2 cells Genes to cells : devoted to molecular & cellular mechanisms Medium 25255829
2022 CIDEC regulates ATGL enzymatic activity by interacting with its activator CGI-58, reducing free fatty acid release and lipotoxicity in adipocytes; adipose-specific CIDEC transgenic mice are protected from HFD-induced glucose intolerance, while the E186X variant abolishes this protection. Transgenic mouse model (Ad-CIDECtg and Ad-CIDECmut), transcriptomics, lipidomics, Co-IP of CIDEC-CGI-58, recombinant CIDEC treatment of human adipose tissue, triglyceride breakdown assays The Journal of biological chemistry High 35963433
2023 CIDEC interacts with endothelial VEGFA-VEGFR2 signaling; endothelial-specific CIDEC expression reduces VEGFA and VEGFR2 degradation, increasing VEGFR2 activation, improved insulin signaling/eNOS activation, and vascular relaxation. Endothelial-specific CIDEC transgenic mice, insulin signaling assays, eNOS activation, vascular relaxation measurements, VEGF pathway analysis Diabetes Medium 36256836
2022 Small intestine-specific CIDEC knockout reduces body fat, liver TG, and hepatic steatosis; mechanistically, CIDEC promotes phosphatidic acid synthesis by interacting with 1-acylglycerol-3-phosphate-O-acyltransferase (AGPAT) to accelerate TG accumulation in intestinal cells. Cre/LoxP intestine-specific KO mice, Co-IP of CIDEC-AGPAT, metabolic phenotyping, phosphatidic acid measurement International journal of biological sciences Medium 36263170
2023 Paxillin family proteins Hic-5 and LPXN interact with CIDEC and inhibit its proteasomal ubiquitination/degradation, thereby stabilizing CIDEC protein, enlarging LDs, and promoting lipid storage in adipocytes. HTRF-based high-throughput screening, Co-IP, ubiquitination assays, proteasome inhibition, LD morphology in adipocytes The Journal of biological chemistry Medium 38159847
2010 Insulin upregulates CIDEC expression in human adipocytes via a PI3K-JNK2-dependent pathway, and CIDEC depletion abolishes insulin-induced lipid droplet enlargement and increases glycerol release. PI3K/Akt/JNK inhibitors, siRNA knockdown of JNK1/JNK2, lipid droplet imaging, glycerol release assay Journal of lipid research Medium 20154362 21636835
2016 FSP27 negatively regulates AMPK activity and ATGL expression in adipocytes; CIDEC knockdown in LPS-treated renal tubular epithelial cells restores phospho-AMPKα and suppresses NF-κB pathway activation and inflammatory cytokine production. CIDEC siRNA knockdown, Western blot for p-AMPKα, NF-κB pathway reporters, cytokine measurement Inflammation Low 29959627
2017 Gp78 (membrane E3 ubiquitin ligase) co-localizes and physically interacts with CIDEC on the surface of lipid droplets, and this interaction promotes lipid accumulation in hepatocytes. Co-immunoprecipitation, immunofluorescence co-localization, overexpression/knockdown in AML12 cells Molecular medicine reports Low 28656280
2016 FSP27 negatively regulates the AMPK-signaling axis; negatively charged residues (D215, E218, E219, E220) in the polar C-terminal region of FSP27 are essential for LD enlargement, while the N-terminal domain (aa 1–130) accelerates but is not required for LD growth. FSP27 domain deletion and charge-reversal mutagenesis, LD size quantification FEBS letters Medium 26921608
2003 Human CIDE-3 (CIDEC), a homologue of mouse FSP27, contains conserved CIDE-N and CIDE-C domains and induces apoptosis (DNA fragmentation) upon overexpression in 293T cells; GFP-tagged CIDE-3 localizes to cytosolic corpuscles; an alternative splice isoform (CIDE-3α, lacking exon 3) retains apoptosis-inducing activity. DNA fragmentation assay, GFP fusion protein localization, RT-PCR, transfection in 293T cells The Biochemical journal Medium 12429024
2010 CIDE-3 (CIDEC) interacts with LITAF (lipopolysaccharide-induced tumor necrosis factor) in hepatic cells, identified by yeast two-hybrid screening; overexpressed CIDE-3 induces apoptosis in hepatocellular carcinoma cells. Yeast two-hybrid, flow cytometry apoptosis assay, overexpression in SMMC-7721 cells Medical oncology (Northwood, London, England) Low 20957525
1992 The FSP27 promoter confers adipocyte-specific expression; a palindromic sequence (TTCGAAA) is required for adipocyte-specific expression and is bound by C/EBP and C/EBP-like proteins as demonstrated by DNase I footprinting. Promoter-reporter transfection, DNase I footprinting with nuclear extracts The Journal of biological chemistry Medium 1339452
2025 CIDEC acts as a metabolic gatekeeper in liver regeneration: its depletion after peak LD accumulation promotes TG mobilization and fatty acid oxidation-driven regeneration; overexpression of CIDEC or DGAT2 exacerbates TG retention and impairs regeneration. CIDEC depletion/overexpression in mice, lipidomics, transcriptomics, FAO inhibition experiments, chronic steatosis model Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 41255220
2025 N-terminal domain of CIDEC (CIDEC-N) undergoes phase separation in vitro; in vitro reconstitution confirmed that multivalent homomeric CIDEC-N interactions are sufficient to drive phase separation, providing a biochemical basis for LDCS condensate formation. Recombinant protein purification, in vitro phase separation assay, concentration-dependent droplet formation STAR protocols Medium 40232936

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 FSP27 contributes to efficient energy storage in murine white adipocytes by promoting the formation of unilocular lipid droplets. The Journal of clinical investigation 333 18654663
2011 Fsp27 promotes lipid droplet growth by lipid exchange and transfer at lipid droplet contact sites. The Journal of cell biology 304 22144693
2008 Hepatic steatosis in leptin-deficient mice is promoted by the PPARgamma target gene Fsp27. Cell metabolism 292 18396136
2008 Up-regulation of mitochondrial activity and acquirement of brown adipose tissue-like property in the white adipose tissue of fsp27 deficient mice. PloS one 223 18682832
2013 Perilipin1 promotes unilocular lipid droplet formation through the activation of Fsp27 in adipocytes. Nature communications 211 23481402
2009 Partial lipodystrophy and insulin resistant diabetes in a patient with a homozygous nonsense mutation in CIDEC. EMBO molecular medicine 211 20049731
2015 Fat-Specific Protein 27/CIDEC Promotes Development of Alcoholic Steatohepatitis in Mice and Humans. Gastroenterology 121 26099526
2013 FSP27 and PLIN1 interaction promotes the formation of large lipid droplets in human adipocytes. Biochemical and biophysical research communications 112 23399566
2011 FSP27 promotes lipid droplet clustering and then fusion to regulate triglyceride accumulation. PloS one 108 22194867
2003 Molecular cloning and characterization of CIDE-3, a novel member of the cell-death-inducing DNA-fragmentation-factor (DFF45)-like effector family. The Biochemical journal 103 12429024
2014 Fat-specific protein 27 (FSP27) interacts with adipose triglyceride lipase (ATGL) to regulate lipolysis and insulin sensitivity in human adipocytes. The Journal of biological chemistry 100 24627478
1992 Cloning and transcriptional regulation of a novel adipocyte-specific gene, FSP27. CAAT-enhancer-binding protein (C/EBP) and C/EBP-like proteins interact with sequences required for differentiation-dependent expression. The Journal of biological chemistry 98 1339452
2015 Transcriptional activation of Fsp27 by the liver-enriched transcription factor CREBH promotes lipid droplet growth and hepatic steatosis. Hepatology (Baltimore, Md.) 90 25125366
2015 Insulin resistance and white adipose tissue inflammation are uncoupled in energetically challenged Fsp27-deficient mice. Nature communications 87 25565658
2018 FTO promotes SREBP1c maturation and enhances CIDEC transcription during lipid accumulation in HepG2 cells. Biochimica et biophysica acta. Molecular and cell biology of lipids 72 29486327
2009 Functional analysis of FSP27 protein regions for lipid droplet localization, caspase-dependent apoptosis, and dimerization with CIDEA. American journal of physiology. Endocrinology and metabolism 72 19843876
2015 CIDEC/FSP27 is regulated by peroxisome proliferator-activated receptor alpha and plays a critical role in fasting- and diet-induced hepatosteatosis. Hepatology (Baltimore, Md.) 70 25418138
2017 HDAC6-mediated acetylation of lipid droplet-binding protein CIDEC regulates fat-induced lipid storage. The Journal of clinical investigation 67 28287402
2008 Assessment of fat-specific protein 27 in the adipocyte lineage suggests a dual role for FSP27 in adipocyte metabolism and cell death. American journal of physiology. Endocrinology and metabolism 60 18198355
2008 Transcriptional activation of Cidec by PPARgamma2 in adipocyte. Biochemical and biophysical research communications 59 18845124
2008 Lipid droplets: FSP27 knockout enhances their sizzle. The Journal of clinical investigation 52 18654644
2018 Growth hormone acts along the PPARγ-FSP27 axis to stimulate lipolysis in human adipocytes. American journal of physiology. Endocrinology and metabolism 48 30325658
2011 Loss of mitogen-activated protein kinase phosphatase-1 protects from hepatic steatosis by repression of cell death-inducing DNA fragmentation factor A (DFFA)-like effector C (CIDEC)/fat-specific protein 27. The Journal of biological chemistry 48 21521693
2021 A gel-like condensation of Cidec generates lipid-permeable plates for lipid droplet fusion. Developmental cell 43 34508658
2012 Comparison of brown and white adipose tissue fat fractions in ob, seipin, and Fsp27 gene knockout mice by chemical shift-selective imaging and (1)H-MR spectroscopy. American journal of physiology. Endocrinology and metabolism 41 23149622
2010 Human adenovirus 36 decreases fatty acid oxidation and increases de novo lipogenesis in primary cultured human skeletal muscle cells by promoting Cidec/FSP27 expression. International journal of obesity (2005) 41 20440297
2016 Polychlorinated biphenyls exposure-induced insulin resistance is mediated by lipid droplet enlargement through Fsp27. Archives of toxicology 34 27837308
2012 Fsp27/CIDEC is a CREB target gene induced during early fasting in liver and regulated by FA oxidation rate. Journal of lipid research 34 23220584
2016 TNF-α downregulates CIDEC via MEK/ERK pathway in human adipocytes. Obesity (Silver Spring, Md.) 33 27062372
2010 Differential roles of CIDEA and CIDEC in insulin-induced anti-apoptosis and lipid droplet formation in human adipocytes. Journal of lipid research 32 20154362
2018 Growth hormone controls lipolysis by regulation of FSP27 expression. The Journal of endocrinology 31 30400015
2017 Amelioration of diet-induced steatohepatitis in mice following combined therapy with ASO-Fsp27 and fenofibrate. Journal of lipid research 28 28874443
2015 Effects of a High Fat Diet and Voluntary Wheel Running Exercise on Cidea and Cidec Expression in Liver and Adipose Tissue of Mice. PloS one 27 26176546
2011 Differential regulation of CIDEA and CIDEC expression by insulin via Akt1/2- and JNK2-dependent pathways in human adipocytes. Journal of lipid research 27 21636835
2018 Dietary fat-associated osteoarthritic chondrocytes gain resistance to lipotoxicity through PKCK2/STAMP2/FSP27. Bone research 25 30002945
2019 Pgc1a is responsible for the sex differences in hepatic Cidec/Fsp27β mRNA expression in hepatic steatosis of mice fed a Western diet. American journal of physiology. Endocrinology and metabolism 24 31846369
2018 Effects of a high energy and low protein diet on hepatic and plasma characteristics and Cidea and Cidec mRNA expression in liver and adipose tissue of laying hens with fatty liver hemorrhagic syndrome. Animal science journal = Nihon chikusan Gakkaiho 23 30523654
2022 Ban-xia-xie-xin-tang ameliorates hepatic steatosis by regulating Cidea and Cidec expression in HFD-fed mice. Phytomedicine : international journal of phytotherapy and phytopharmacology 22 35908522
2023 The architecture of Cidec-mediated interfaces between lipid droplets. Cell reports 20 36800289
2022 Human CIDEC transgene improves lipid metabolism and protects against high-fat diet-induced glucose intolerance in mice. The Journal of biological chemistry 20 35963433
2019 Mouse Fat-Specific Protein 27 (FSP27) expressed in plant cells localizes to lipid droplets and promotes lipid droplet accumulation and fusion. Biochimie 18 31400447
2015 Cidec promotes the differentiation of human adipocytes by degradation of AMPKα through ubiquitin-proteasome pathway. Biochimica et biophysica acta 18 26367078
2010 Cide-a and Cide-c are induced in the progression of hepatic steatosis and inhibited by eicosapentaenoic acid. Prostaglandins, leukotrienes, and essential fatty acids 18 20542418
2022 Small Intestine-specific Knockout of CIDEC Improves Obesity and Hepatic Steatosis by Inhibiting Synthesis of Phosphatidic Acid. International journal of biological sciences 17 36263170
2014 Effects of pioglitazone mediated activation of PPAR-γ on CIDEC and obesity related changes in mice. PloS one 17 25210844
2013 Molecular basis for homo-dimerization of the CIDE domain revealed by the crystal structure of the CIDE-N domain of FSP27. Biochemical and biophysical research communications 17 24025675
2010 CIDE-3 interacts with lipopolysaccharide-induced tumor necrosis factor, and overexpression increases apoptosis in hepatocellular carcinoma. Medical oncology (Northwood, London, England) 17 20957525
2018 Polybasic RKKR motif in the linker region of lipid droplet (LD)-associated protein CIDEC inhibits LD fusion activity by interacting with acidic phospholipids. The Journal of biological chemistry 16 30361435
2014 Regulation of FSP27 protein stability by AMPK and HSC70. American journal of physiology. Endocrinology and metabolism 16 25315694
2020 Eicosapentaenoic and docosapentaenoic acids lessen the expression of PPARγ/Cidec affecting adipogenesis in cultured 3T3-L1 adipocytes. Acta histochemica 15 31955908
2008 Molecular cloning, chromosomal location and expression pattern of porcine CIDEa and CIDEc. Molecular biology reports 15 18311595
2017 The effects of cell death-inducing DNA fragmentation factor-α-like effector C (CIDEC) on milk lipid synthesis in mammary glands of dairy cows. Journal of dairy science 14 28284693
2021 CIDEC silencing attenuates diabetic nephropathy via inhibiting apoptosis and promoting autophagy. Journal of diabetes investigation 13 33655702
2018 CIDEC Is Involved in LPS-Induced Inflammation and Apoptosis in Renal Tubular Epithelial Cells. Inflammation 13 29959627
2022 Metformin Inhibits Lipid Droplets Fusion and Growth via Reduction in Cidec and Its Regulatory Factors in Rat Adipose-Derived Stem Cells. International journal of molecular sciences 12 35682666
2017 Cidec differentially regulates lipid deposition and secretion through two tissue-specific isoforms. Gene 12 29080839
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2024 Exosomes as nanostructures deliver miR-204 in alleviation of mitochondrial dysfunction in diabetic nephropathy through suppressing methyltransferase-like 7A-mediated CIDEC N6-methyladenosine methylation. Aging 10 38334961
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2021 Cell death-inducing DFFA-like effector C/CIDEC gene silencing alleviates diabetic cardiomyopathy via upregulating AMPKa phosphorylation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 10 33913563
2020 Eicosapentaenoic acid-enriched phospholipids suppressed lipid accumulation by specific inhibition of lipid droplet-associated protein FSP27 in mice. Journal of the science of food and agriculture 10 31919850
2019 Plasticity of histone modifications around Cidea and Cidec genes with secondary bile in the amelioration of developmentally-programmed hepatic steatosis. Scientific reports 10 31745102
2014 Translocation of CIDEC in hepatocytes depends on fatty acids. Genes to cells : devoted to molecular & cellular mechanisms 10 25255829
2022 AMPK-PPARγ-Cidec Axis Drives the Fasting-Induced Lipid Droplet Aggregation in the Liver of Obese Mice. Frontiers in nutrition 9 35859752
2021 Inhibition of cell death inducing DNA fragmentation factor-α-like effector c (CIDEC) by tumor necrosis factor-α induces lipolysis and inflammation in calf adipocytes. Journal of dairy science 9 33685683
2016 Regulation of PPARγ and CIDEC expression by adenovirus 36 in adipocyte differentiation. Molecular and cellular biochemistry 9 27995415
2018 Therapeutic silencing of FSP27 reduces the progression of atherosclerosis in Ldlr-/- mice. Atherosclerosis 8 29859472
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2019 Involvement of PPARγ/FSP27 in the pathogenic mechanism underlying insulin resistance: tipping the balance between lipogenesis and fat storage in adult catch-up growth rats. Nutrition & metabolism 7 30792748
2016 Negatively-charged residues in the polar carboxy-terminal region in FSP27 are indispensable for expanding lipid droplets. FEBS letters 7 26921608
2015 Haplotypes in the promoter region of the CIDEC gene associated with growth traits in Nanyang cattle. Scientific reports 7 26189824
2024 Attenuation of brown adipocyte whitening in high-fat diet-induced obese rats: Effects of melatonin and β-hydroxybutyrate on Cidea, Fsp27 and MT1 expression. Diabetes, obesity & metabolism 6 39118207
2024 CIDEC/FSP27 exacerbates obesity-related abdominal aortic aneurysm by promoting perivascular adipose tissue inflammation. Life metabolism 6 39872985
2017 Single nucleotide polymorphisms in CIDEC gene are associated with metabolic syndrome components risks and antihypertensive drug efficacy. Oncotarget 6 28415694
2016 Alcohol and fat promote steatohepatitis: a critical role for fat-specific protein 27/CIDEC. Journal of investigative medicine : the official publication of the American Federation for Clinical Research 6 27342423
2023 Rare CIDEC coding variants enriched in age-related macular degeneration patients with small low-luminance deficit cause lipid droplet and fat storage defects. PloS one 5 37079518
2022 Fsp27 plays a crucial role in muscle performance. American journal of physiology. Endocrinology and metabolism 5 35157807
2013 Cell death-inducing DFFA-like effector c (CIDEC/Fsp27) gene: molecular cloning, sequence characterization, tissue distribution and polymorphisms in Chinese cattles. Molecular biology reports 5 24065549
2023 Paxillin family proteins Hic-5 and LPXN promote lipid storage by regulating the ubiquitination degradation of CIDEC. The Journal of biological chemistry 4 38159847
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2025 CIDEC Restricts Liver Regeneration by Disturbing Lipid Droplet Triglyceride Turnover. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2 41255220
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2025 Comparative effect of high intensity interval training and moderate intensity continuous training on metabolic improvements and regulation of Cidea and Cidec in obese C57BL/6 mice. PloS one 1 40305497
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2013 Crystallization and preliminary X-ray crystallographic studies of the CIDE-N domain of CIDE-3. Acta crystallographica. Section F, Structural biology and crystallization communications 1 24192364
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