Affinage

PLIN5

Perilipin-5 · UniProt Q00G26

Length
463 aa
Mass
50.8 kDa
Annotated
2026-06-10
51 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PLIN5 is a lipid droplet coat protein of oxidative tissues (heart, skeletal muscle, liver, brown adipose) that scaffolds the controlled mobilization of stored triacylglycerol and couples it to mitochondrial fatty acid oxidation (PMID:17130488, PMID:16571721). Its N-terminal PAT-1 plus adjacent 33-mer region targets the protein to the droplet surface and clusters droplets (PMID:16571721, PMID:22675471), while a C-terminal region (residues ~200–463) binds both the lipase ATGL and its co-activator ABHD5/CGI-58, with individual PLIN5 molecules engaging one or the other, implying an oligomeric regulatory complex (PMID:19064991, PMID:21148142). In the basal state PLIN5 restrains lipolysis and promotes triacylglycerol accumulation (PMID:17234449, PMID:22675471), and productive ATGL engagement is sensitized by accessory factors including HSD17β11 (PMID:41238190); the PLIN5–ABHD5 interaction is essential for ATGL activity at PLIN5 droplets, as an ABHD5 mutant that cannot bind PLIN5 fails to mobilize droplet lipid (PMID:19064991). Upon cAMP/PKA-driven lipolytic stimulation PLIN5 acts as a fatty-acid-binding protein that traffics droplet-derived monounsaturated fatty acids to the nucleus, where the MUFAs allosterically activate SIRT1 toward PGC-1α and drive PGC-1α/PPARα transcriptional programs of oxidative metabolism (PMID:31901447, PMID:35470759). PLIN5 also builds lipid droplet–mitochondria contact sites, tethering membranes directly in vitro (PMID:41459334) and channeling fatty acids into β-oxidation through its mitochondrial interaction with the acyl-CoA synthetase FATP4/ACSVL4 (PMID:37290445); phosphorylation at S155 governs contact formation, with the phospho-resistant S155A state favoring contacts and droplet expansion and the phosphomimetic S155E state reducing them (PMID:41872512). In cardiomyocytes PLIN5 additionally interacts with SERCA2 to enhance Ca²⁺ handling and contractility (PMID:36717246). PLIN5 abundance and localization are set post-translationally, being degraded by chaperone-mediated autophagy via LAMP2A to permit droplet breakdown (PMID:32339374) and stabilized/positioned by the kinesin KIF13B for proper mitochondrial localization in the heart (PMID:41531892).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2006 Medium

    Established that PLIN5 is a lipid droplet surface protein of oxidative tissues whose expression promotes triacylglycerol storage while also supporting fatty acid oxidation, defining its dual storage/oxidation role and PPARα-driven regulation.

    Evidence Subcellular fractionation, immunofluorescence and ectopic overexpression with metabolic flux in cardiomyocytes and CHO cells, plus deletion mapping and PPARα-knockout mice

    PMID:16571721 PMID:17130488 PMID:17234449

    Open questions at the time
    • Mechanism coupling storage to oxidation not resolved
    • Identity of interacting lipolytic machinery unknown at this stage
  2. 2008 High

    Identified the PLIN5–ABHD5/CGI-58 interaction at the droplet surface as essential for regulating ATGL activity, explaining how PLIN5 gates lipolysis.

    Evidence Interaction assays in fibroblasts, in situ binding in microdissected cardiac fibers, and ABHD5 E262K mutant functional assays

    PMID:19064991

    Open questions at the time
    • How the interaction is switched on/off by signaling not yet defined
    • Stoichiometry of the droplet complex unknown
  3. 2010 High

    Mapped a C-terminal region that binds ATGL and ABHD5 in a mutually exclusive manner per molecule, establishing PLIN5 as an oligomeric scaffold that differentially controls lipase recruitment.

    Evidence Live-cell interaction and competition assays, chimeric/mutant perilipin analysis, neutral lipid accumulation readouts

    PMID:21148142

    Open questions at the time
    • Oligomeric architecture not structurally resolved
    • Regulation of the binding switch not defined
  4. 2012 Medium

    Confirmed via bidirectional gain/loss-of-function in hepatocytes that PLIN5 restrains lipolysis and triglyceride turnover, and localized the targeting/clustering function to the N-terminal 188 residues.

    Evidence Overexpression and siRNA in AML12 and primary hepatocytes with serial deletion mapping and metabolic assays

    PMID:22675471

    Open questions at the time
    • Only modest effect on β-oxidation
    • Single-lab domain mapping
  5. 2014 Medium

    Showed PLIN5 redistributes to mitochondria upon contraction-induced lipolysis, providing in vivo evidence for activity-dependent droplet–mitochondria coupling.

    Evidence Mitochondrial isolation and western blotting in an in vivo rat hindlimb stimulation model

    PMID:25318747

    Open questions at the time
    • Molecular tether mediating mitochondrial association not identified
    • Single method for the key finding
  6. 2019 High

    Defined a signaling output for PLIN5 beyond the droplet: it binds and shuttles MUFAs to the nucleus after PKA stimulation, where they allosterically activate SIRT1/PGC-1α/PPARα, linking lipolysis to transcriptional control of oxidative metabolism.

    Evidence Fatty acid binding assays, nuclear fractionation, in vitro SIRT1 activity assays with MUFAs, cAMP/PKA stimulation in cells and animals

    PMID:31901447

    Open questions at the time
    • Mechanism of nuclear import not defined
    • Selectivity for MUFA species over other lipids not fully characterized
  7. 2020 Medium

    Established that PLIN5 abundance is controlled by chaperone-mediated autophagy, providing a degradation route required for lipid droplet breakdown.

    Evidence LAMP2A-knockout mice and LAMP2A-deficient HepG2 cells with droplet and PLIN5 protein quantification

    PMID:32339374

    Open questions at the time
    • CMA recognition motif on PLIN5 not mapped
    • Relationship to phospho-regulation unknown
  8. 2023 High

    Resolved the mitochondrial tether: PLIN5 binds the acyl-CoA synthetase FATP4/ACSVL4 via C-terminal domains to form a minimal contact-inducing interaction that channels fatty acids into β-oxidation during starvation, and identified PKA phosphorylation as a requirement.

    Evidence Reciprocal co-IP in human and murine cells, domain mapping, phosphorylation and fatty acid trafficking assays, organelle contact imaging

    PMID:37290445

    Open questions at the time
    • Which residue(s) drive the phospho-dependence not pinpointed in this study
    • Regulation of contact dynamics over time unclear
  9. 2023 High

    Extended PLIN5 function in the heart to calcium handling by demonstrating a SERCA2 interaction that enhances Ca²⁺ cycling and contractility.

    Evidence Quantitative proteomics, in situ proximity ligation assay, live Ca²⁺ imaging, cardiac-specific overexpression mice

    PMID:36717246

    Open questions at the time
    • Whether interaction is direct or droplet-dependent unclear
    • Link to PLIN5's lipid functions not established
  10. 2025 Medium

    Identified accessory regulators of PLIN5 function: HSD17β11 facilitates PLIN5–ATGL interaction for PKA-stimulated lipolysis, TBC1D15 recruits PLIN5 to mitochondria to promote contacts and nuclear translocation, and KIF13B stabilizes PLIN5 against lysosomal degradation to maintain cardiac mitochondrial localization.

    Evidence Gene deletions and domain-mapped co-IP/interaction assays in human cell lines and mice, lipolysis and lipidomic readouts, AAV9-PLIN5 rescue

    PMID:40334909 PMID:41238190 PMID:41531892

    Open questions at the time
    • Each interaction shown by single labs
    • Integration of these regulators into one pathway not established
  11. 2025 Medium

    Placed PLIN5 upstream of PGC-1α in distinct cell types, where it modulates ROS in vascular smooth muscle and a PGC-1α/Drp1 axis controlling mitochondrial function and insulin secretion in β-cells.

    Evidence Co-IP/interaction assays, knockdown/overexpression in VSMCs and INS-1 cells, Plin5± and db/db mice, promoter binding and ROS/insulin assays

    PMID:35470759 PMID:40884681

    Open questions at the time
    • Whether PLIN5–PGC-1α interaction is direct unresolved
    • Tissue-specificity of the axis not reconciled
  12. 2025 Medium

    Provided in vitro reconstitution evidence that PLIN5 protein alone is sufficient to tether membranes to a lipid droplet monolayer while preventing fusion, confirming a direct mechanical role in contact-site formation.

    Evidence Artificial lipid droplet monolayers with PLIN5, LUV attachment/fusion assays with dual fluorescence

    PMID:41459334

    Open questions at the time
    • Artificial system not validated in cells
    • Does not address regulation by phosphorylation or partners
  13. 2026 High

    Defined S155 phosphorylation as the molecular switch governing droplet–mitochondria contacts and lipotoxicity in vivo, with phospho-resistant S155A enhancing contacts and protecting against Western-diet damage and phosphomimetic S155E reducing them.

    Evidence S155A/S155E variant overexpression, single-cell tissue imaging, spatial proteomics, mouse dietary models

    PMID:41872512

    Open questions at the time
    • Kinase/phosphatase dynamics at S155 in vivo not fully mapped
    • Reconciliation with PKA-activated lipolysis model incomplete
  14. 2026 Medium

    Demonstrated an essential physiological role for PLIN5 in adaptive thermogenesis through acute brown-adipocyte-specific deletion.

    Evidence Doxycycline-inducible BAT-specific knockout mice, cold challenge, thermogenic gene expression, mitochondrial EM and respiration (preprint)

    PMID:41509390

    Open questions at the time
    • Preprint not yet peer-reviewed
    • Molecular mechanism linking PLIN5 to cristae and uncoupled respiration not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How PLIN5 integrates its competing functions — lipolysis gating, mitochondrial tethering, nuclear lipid signaling, and Ca²⁺ handling — into a single phosphorylation- and partner-regulated decision at the droplet surface remains unresolved.
  • No integrated structural model of the PLIN5 oligomeric complex
  • Spatiotemporal coordination between cytosolic, mitochondrial, and nuclear PLIN5 pools unknown
  • Phospho-code beyond S155 and its upstream kinases/phosphatases incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 1
Localization
GO:0005739 mitochondrion 3 GO:0005811 lipid droplet 3 GO:0005634 nucleus 2
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-74160 Gene expression (Transcription) 1 R-HSA-9612973 Autophagy 1
Partners
ABHD5FATP4HSD17B11KIF13BPGC-1ALPHAPNPLA2SERCA2TBC1D15

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 PLIN5 (OXPAT/MLDP/LSDP5) localizes to the surface of lipid droplets in oxidative tissues and co-localizes with adipophilin (ADRP) on lipid droplets in primary cardiomyocytes. Ectopic expression promotes fatty acid-induced triacylglycerol accumulation and long-chain fatty acid oxidation. Subcellular fractionation, immunofluorescence co-localization in primary cardiomyocytes, ectopic overexpression with metabolic flux assays Diabetes Medium 17130488
2006 PLIN5 (LSDP5) associates with lipid storage droplets when ectopically expressed as YFP or FLAG fusion proteins, and forced expression in CHO cells inhibits lipolysis of intracellular lipid droplets. Fluorescent fusion protein expression, lipid droplet fractionation, lipolysis assay in CHO cells Biochimica et biophysica acta Medium 17234449
2006 PLIN5 (MLDP) is enriched on lipid droplet surfaces in the heart; the N-terminal PAT-1 domain plus the adjacent 33-mer domain are required for lipid droplet targeting. Expression is regulated by PPARalpha and induced by fasting. GFP fusion protein overexpression, deletion analysis, subcellular fractionation, PPARalpha knockout mice The Journal of biological chemistry Medium 16571721
2008 PLIN5 (Mldp) binds ABHD5 (CGI-58, the co-activator of ATGL) on the surface of lipid droplets in cardiac muscle fibers. This interaction is dynamic, enhanced by oleic acid treatment in a triglyceride-synthesis-dependent manner, and essential for ATGL activity at PLIN5-containing lipid droplets; an ABHD5 mutant (E262K) that cannot bind PLIN5 fails to prevent lipid droplet accumulation in cells expressing PLIN5. Protein interaction assays in transfected fibroblasts, microdissected cardiac muscle fiber co-localization, in situ binding assays, mutant ABHD5 functional assays The Journal of biological chemistry High 19064991
2010 PLIN5 binds both ATGL and ABHD5, but individual PLIN5 molecules bind either ATGL or ABHD5 but not both simultaneously, suggesting an oligomeric complex at the droplet surface. The C-terminal 64 amino acids (residues 200–463) are necessary and sufficient for binding both ATGL and ABHD5, and the C-terminal region is critical for the differential binding of ATGL to PLIN5 versus PLIN1. A mutant PLIN5 that binds ABHD5 but not ATGL is defective in preventing neutral lipid accumulation. Protein interaction assays in live cells, in situ binding, chimeric/mutant perilipin analysis, neutral lipid accumulation assays The Journal of biological chemistry High 21148142
2012 PLIN5 (LSDP5) overexpression in hepatocytes enhances lipid accumulation and inhibits lipolysis; knockdown decreases triglyceride content, stimulates lipolysis, and modestly increases mitochondrial fatty acid β-oxidation. The lipid droplet-targeting and droplet-clustering domain maps to the N-terminal 188 amino acids. Overexpression and siRNA knockdown in AML12 hepatocytes and primary hepatocytes, serial deletion mapping, triglyceride and lipolysis assays PloS one Medium 22675471
2014 PLIN5 content is increased in isolated skeletal muscle mitochondria (~1.6-fold) following 30 min of contraction-induced lipolysis in rat hindlimb, whereas PLIN3 mitochondrial content is unchanged. An association between PLIN3 and PLIN5 was detected and was unaltered by contraction. Mitochondrial isolation by differential centrifugation, western blotting, in vivo hindlimb stimulation model Physiological reports Medium 25318747
2019 PLIN5 is a fatty-acid-binding protein that preferentially binds lipid droplet-derived monounsaturated fatty acids (MUFAs) and traffics them to the nucleus following cAMP/PKA-mediated lipolytic stimulation. Nuclear PLIN5 facilitates SIRT1-dependent PGC-1α/PPARα signaling. MUFAs were identified as the first endogenous allosteric activators of SIRT1 toward select substrates including PGC-1α. Fatty acid binding assays, nuclear fractionation, SIRT1 activity assays with MUFAs, cAMP/PKA stimulation, cell and animal model experiments Molecular cell High 31901447
2020 PLIN5 is a substrate of chaperone-mediated autophagy (CMA); its degradation through CMA (via LAMP2A) is required for lipid droplet breakdown. Disruption of CMA (LAMP2A deletion) leads to PLIN5 accumulation and impaired lipid droplet breakdown but not increased lipid droplet formation. LAMP2A-knockout mice, LAMP2A-deficient HepG2 cells (L2A−), lipid droplet quantification, PLIN5 protein measurement Liver international Medium 32339374
2023 PLIN5 interacts with the acyl-CoA synthetase FATP4 (ACSVL4) on mitochondria to promote lipid droplet-to-mitochondria fatty acid trafficking and β-oxidation during starvation. Phosphorylation of PLIN5 (by PKA during starvation) and an intact mitochondrial tethering domain are required for efficient fatty acid channeling. The C-terminal domains of PLIN5 and FATP4 constitute a minimal protein interaction sufficient to induce organelle contacts. Co-immunoprecipitation in human and murine cells, domain mapping, PLIN5 phosphorylation assays, fatty acid trafficking assays, β-oxidation measurements, organelle contact imaging Developmental cell High 37290445
2023 PLIN5 interacts with SERCA2 (sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2) in cardiomyocytes. Cardiac-specific PLIN5 overexpression in mice increases intracellular Ca2+ release during contraction, Ca2+ removal during relaxation, and SERCA2 function, resulting in improved cardiac contractility. Quantitative proteomics, in situ proximity ligation assay, live imaging of Ca2+ dynamics in cardiomyocytes, cardiac-specific overexpression mouse model Life science alliance High 36717246
2025 HSD17β11 facilitates the interaction between PLIN5 and ATGL, enabling efficient PKA-stimulated lipolysis in human cell lines. HSD17β11 deletion increases lipid droplet size and number due to impaired lipolysis. HSD17β11 deletion in human cell lines, co-immunoprecipitation/interaction assays for PLIN5-ATGL, lipolysis assays with PKA stimulation Journal of lipid research Medium 41238190
2025 TBC1D15 is recruited to mitochondrial membranes in hepatocytes in response to alcohol exposure, where it recruits PLIN5 through its 10–180 aa domain, promoting mitochondria-lipid droplet contacts and facilitating PKA-induced nuclear translocation of PLIN5. TBC1D15 domain mapping, co-immunoprecipitation, immunofluorescence, hepatocyte-specific overexpression mouse model, PKA inhibition Metabolism: clinical and experimental Medium 40334909
2026 PLIN5 phosphorylation at S155 regulates mitochondria-lipid droplet contact formation in hepatocytes: the phosphorylation-resistant S155A variant enhances organelle contacts and lipid droplet expansion, while the phosphomimetic S155E variant reduces contacts and yields fewer, smaller lipid droplets. S155A overexpression in Western-diet-fed mice reduced lipotoxicity. PLIN5 phosphorylation variant overexpression (S155A, S155E), single-cell tissue imaging (scPhenomics), spatial proteomics, mouse dietary models Nature metabolism High 41872512
2025 KIF13B stabilizes PLIN5 by preventing its lysosomal degradation. Loss of KIF13B disrupts the mitochondrial localization of PLIN5, impairing cardiac lipid homeostasis and mitochondrial function. AAV9-mediated PLIN5 restoration in Kif13b-knockout mice rescued cardiac dysfunction. Kif13b knockout mice, AAV9-PLIN5 gene therapy rescue, western blotting for PLIN5 localization, immunofluorescence, lipidomics Research (Washington, D.C.) Medium 41531892
2022 Plin5 interacts with PGC-1α in vascular smooth muscle cells; Plin5 knockdown attenuates this interaction, increases ROS, and promotes VSMC proliferation and migration. Overexpression of PGC-1α suppresses PDGF-BB-induced ROS, proliferation, and migration in Plin5-deficient VSMCs, placing Plin5 upstream of PGC-1α in ROS regulation. Co-immunoprecipitation/interaction assay, Plin5 knockdown mice (Plin5±), VSMC isolation, ROS measurement, proliferation/migration assays, NAC rescue Bioengineered Medium 35470759
2025 PLIN5 knockdown in INS-1 β-cells promotes apoptosis and reduces insulin secretion through lipid accumulation and mitochondrial dysfunction, mediated by decreased PGC-1α and increased Drp1 levels. Reduced PLIN5 decreases binding of PGC-1α to the Drp1 promoter region, and PLIN5 overexpression reverses high-glucose-induced damage via this PGC-1α/Drp1 axis. PLIN5 knockdown and overexpression in INS-1 cells and db/db mice, chromatin interaction assay (PGC-1α binding to Drp1 promoter), mitochondrial function assays, insulin secretion measurement Endocrine Medium 40884681
2025 In vitro, PLIN5 incorporated into an artificial lipid droplet monolayer promotes stable attachment of large unilamellar vesicles (mimicking organelle bilayer membranes) to the droplet surface while preventing membrane fusion, demonstrating a direct role of PLIN5 protein in promoting organelle contact site formation. In vitro reconstitution with artificial lipid droplets, PLIN5-coated monolayers, LUV attachment/fusion assays with dual fluorescence labeling Biochemistry and biophysics reports Medium 41459334
2024 PLIN5 phosphorylation at S155 is increased in the lipid droplet fraction of fasted mouse liver compared to fed state (measured by mass spectrometry). The phosphorylation-resistant S155A knock-in mice show reduced IRS2 expression in liver upon fasting, suggesting phospho-PLIN5 contributes to hepatic IRS2-mediated insulin signaling, but S155 phosphorylation is dispensable for upregulation of lipid metabolism genes during fasting. Mass spectrometry quantification of phospho-PLIN5, Phos-tag gels, whole-body S155A knock-in mice, RNA sequencing, qPCR of liver gene expression bioRxivpreprint Medium bio_10.1101_2024.11.09.622792
2026 Acute deletion of PLIN5 specifically in brown adipocytes of adult mice causes reduced thermogenic gene expression, decreased mitochondrial cristae density, impaired uncoupled BAT mitochondrial respiration, and cold intolerance, establishing an essential role of BAT PLIN5 in adaptive thermogenesis. Doxycycline-inducible BAT-specific PLIN5 knockout mice, cold exposure challenge, thermogenic gene expression, transmission electron microscopy of mitochondria, mitochondrial respiration assays bioRxivpreprint Medium 41509390

Source papers

Stage 0 corpus · 51 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 OXPAT/PAT-1 is a PPAR-induced lipid droplet protein that promotes fatty acid utilization. Diabetes 269 17130488
2006 LSDP5 is a PAT protein specifically expressed in fatty acid oxidizing tissues. Biochimica et biophysica acta 203 17234449
2010 Interactions of perilipin-5 (Plin5) with adipose triglyceride lipase. The Journal of biological chemistry 187 21148142
2006 MLDP, a novel PAT family protein localized to lipid droplets and enriched in the heart, is regulated by peroxisome proliferator-activated receptor alpha. The Journal of biological chemistry 179 16571721
2019 Lipid Droplet-Derived Monounsaturated Fatty Acids Traffic via PLIN5 to Allosterically Activate SIRT1. Molecular cell 142 31901447
2008 Functional interactions between Mldp (LSDP5) and Abhd5 in the control of intracellular lipid accumulation. The Journal of biological chemistry 122 19064991
2023 PLIN5 interacts with FATP4 at membrane contact sites to promote lipid droplet-to-mitochondria fatty acid transport. Developmental cell 112 37290445
2009 Adipocyte differentiation-related protein and OXPAT in rat and human skeletal muscle: involvement in lipid accumulation and type 2 diabetes mellitus. The Journal of clinical endocrinology and metabolism 83 19602560
2013 Inactivation of Plin4 downregulates Plin5 and reduces cardiac lipid accumulation in mice. American journal of physiology. Endocrinology and metabolism 82 23423172
2017 Plin5 alleviates myocardial ischaemia/reperfusion injury by reducing oxidative stress through inhibiting the lipolysis of lipid droplets. Scientific reports 80 28218306
2015 Unraveling the roles of PLIN5: linking cell biology to physiology. Trends in endocrinology and metabolism: TEM 74 25682370
2020 Disruption of Plin5 degradation by CMA causes lipid homeostasis imbalance in NAFLD. Liver international : official journal of the International Association for the Study of the Liver 56 32339374
2014 Lipocalin-2 (LCN2) regulates PLIN5 expression and intracellular lipid droplet formation in the liver. Biochimica et biophysica acta 50 25086218
2012 LSDP5 enhances triglyceride storage in hepatocytes by influencing lipolysis and fatty acid β-oxidation of lipid droplets. PloS one 44 22675471
2016 Decoration of intramyocellular lipid droplets with PLIN5 modulates fasting-induced insulin resistance and lipotoxicity in humans. Diabetologia 42 26864436
2022 Plin5 Bidirectionally Regulates Lipid Metabolism in Oxidative Tissues. Oxidative medicine and cellular longevity 40 35401929
2019 Targeting PLIN2/PLIN5-PPARγ: Sulforaphane Disturbs the Maturation of Lipid Droplets. Molecular nutrition & food research 30 31325205
2019 MicroRNA-370 protects against myocardial ischemia/reperfusion injury in mice following sevoflurane anesthetic preconditioning through PLIN5-dependent PPAR signaling pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 28 30856533
2011 Subcellular localization of skeletal muscle lipid droplets and PLIN family proteins OXPAT and ADRP at rest and following contraction in rat soleus muscle. American journal of physiology. Regulatory, integrative and comparative physiology 28 22012700
2022 Plin5, a New Target in Diabetic Cardiomyopathy. Oxidative medicine and cellular longevity 23 35509833
2021 Leptin Reduces Plin5 m6A Methylation through FTO to Regulate Lipolysis in Piglets. International journal of molecular sciences 18 34638947
2014 Higher PLIN5 but not PLIN3 content in isolated skeletal muscle mitochondria following acute in vivo contraction in rat hindlimb. Physiological reports 18 25318747
2022 Plin5 inhibits proliferation and migration of vascular smooth muscle cell through interacting with PGC-1α following vascular injury. Bioengineered 15 35470759
2023 Cardiac Plin5 interacts with SERCA2 and promotes calcium handling and cardiomyocyte contractility. Life science alliance 13 36717246
2021 Dapagliflozin Mediates Plin5/PPARα Signaling Axis to Attenuate Cardiac Hypertrophy. Frontiers in pharmacology 12 34630108
2020 Isolated Plin5-deficient cardiomyocytes store less lipid droplets than normal, but without increased sensitivity to hypoxia. Biochimica et biophysica acta. Molecular and cell biology of lipids 12 33373698
2019 Plin5/p-Plin5 Guards Diabetic CMECs by Regulating FFAs Metabolism Bidirectionally. Oxidative medicine and cellular longevity 12 31772713
2025 TBC1D15 protects alcohol-induced liver injury in female mice through PLIN5-mediated mitochondrial and lipid droplet contacting. Metabolism: clinical and experimental 9 40334909
2017 Plin5 deficiency promotes atherosclerosis progression through accelerating inflammation, apoptosis and oxidative stress. Journal of cellular biochemistry 9 29215758
2024 PLIN5 Suppresses Lipotoxicity and Ferroptosis in Cardiomyocyte via Modulating PIR/NF-κB Axis. International heart journal 8 38749744
2020 EPA/DHA Concentrate by Urea Complexation Decreases Hyperinsulinemia and Increases Plin5 in the Liver of Mice Fed a High-Fat Diet. Molecules (Basel, Switzerland) 8 32698439
2020 Methylation of PLIN5 is a crucial biomarker and is involved in ovarian cancer development. Translational cancer research 8 35117648
2023 Lipid-Independent Regulation of PLIN5 via IL-6 through the JAK/STAT3 Axis in Hep3B Cells. International journal of molecular sciences 7 37108378
2022 Hepatic PLIN5 Deficiency Impairs Lipogenesis through Mitochondrial Dysfunction. International journal of molecular sciences 7 36555245
2021 Role of Plin5 Deficiency in Progression of Non-Alcoholic Fatty Liver Disease Induced by a High-Fat Diet in Mice. Journal of comparative pathology 7 34886991
2020 Involvement of activation of PLIN5-Sirt1 axis in protective effect of glycycoumarin on hepatic lipotoxicity. Biochemical and biophysical research communications 7 32448510
2024 PLIN5 contributes to lipophagy of hepatic stellate cells induced by inorganic arsenic. Ecotoxicology and environmental safety 5 39700776
2025 Plin5: A potential therapeutic target for type 2 diabetes mellitus. Diabetology & metabolic syndrome 3 40176076
2026 PLIN5 phosphorylation orchestrates mitochondria lipid-droplet coupling to control hepatic lipid flux and steatosis. Nature metabolism 2 41872512
2026 KIF13B Attenuates Sepsis-Induced Myocardial Dysfunction through the Stabilization of PLIN5. Research (Washington, D.C.) 1 41531892
2025 PLIN5 regulates lipid metabolism via PGC-1α/Drp1 signaling in islet β-cells. Endocrine 1 40884681
2024 Differential Plin5 response to high-fat diet in cardiomyocytes isolated from young and aged mice. Mechanisms of ageing and development 1 39510385
2010 [Construction of eukaryotic fusion expression vectors of LSDP5 and cellular localization]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 1 20423650
2026 Acute deletion of PLIN5 in brown adipocytes causes mitochondrial dysfunction and cold intolerance. bioRxiv : the preprint server for biology 0 41509390
2026 MLDP-AS: an optimized next-generation sequencing assay for enhanced detection of technically challenging variants in expanded carrier screening. Journal of translational medicine 0 41691275
2026 Targeting LRH-1 alleviates diabetes-induced lipotoxicity in podocytes: role of PLIN5-mediated lipid droplet turnover. Renal failure 0 42135621
2025 PLIN5 deficiency ameliorates metabolic dysfunction‑associated fatty liver disease by inhibiting ferroptosis. Molecular medicine reports 0 41104863
2025 PLIN5 affects the fibrosis and progression of pancreatic cancer via modulation of pancreatic stellate cells. Life sciences 0 41187900
2025 HSD17β11 regulates PLIN5-ATGL mediated lipolysis, but not hepatic lipid metabolism in mice. Journal of lipid research 0 41238190
2025 PLIN5 Promotes Lipid Reconstitution in Goat Intramuscular Fat via the PPARγ Signaling Pathway. Biology 0 41300337
2025 Influence of PLIN5 and lipid composition on lipid droplet contact sites with other organelles. Biochemistry and biophysics reports 0 41459334

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