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Proteintech plin5
Plin5, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 219 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/plin5/GLUT4+Antibody/pm41780607-137-40-41
Average 96 stars, based on 219 article reviews

plin5 - by Bioz Stars, 2026-09

96/100 stars

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Membrane:

Article Title: Lipid Droplets Metabolism Mediated by ANXA7‐PPARγ Signaling Axis Regulates Spinal Cord Injury Repair in Mice
Article Snippet: .. The membrane was blocked with 5% BSA and incubated with following primary antibodies 4 °C overnight: Annexin A7 (Proteintech, Cat# 10154‐2‐AP), PPARγ (Abcam, Cat# ab178860), GPX4 (Cell signaling technology, Cat# #52 455), NRF2 (Cell signaling technology, Cat# 12721S), PLIN1 (Abcam Cat# ab172907), PLIN2 (Santa Cruz, Cat# sc‐377429), β‐actin (CST, Cat# 4970S), PLIN5 (Proteintech, Cat# 26951‐1‐AP), Histone H3 (Proteintech, 17168‐1‐AP). ..

Incubation:

Article Title: Cardiac lipid droplets differ under pathological and physiological conditions.
Article Snippet: .. Primary antibodies against HSL (Cell Signaling Technology, 4107S), LC3B (Thermo Fisher, #81004-1), or Plin5 (Proteintech, #26951-1-AP) were applied at 1:250 and incubated overnight at 4 °C. .. After washing, sections were incubated with Alexa Fluor 488 donkey anti-rabbit IgG (Life Technologies, A21206; 1:500) for 1 h at room temperature.

Article Title: Cardiac lipid droplets differ under pathological and physiological conditions
Article Snippet: .. Primary antibodies against HSL (Cell Signaling Technology, 4107S), LC3B (Thermo Fisher, #81004-1), or PLIN5 (Proteintech, #26951-1-AP) were applied at 1:250 and incubated overnight at 4°C. .. After washing, sections were incubated with Alexa Fluor 488 donkey anti-rabbit IgG (Life Technologies, A21206; 1:500) for 1 h at room temperature.

Article Title: Lipid Droplets Metabolism Mediated by ANXA7‐PPARγ Signaling Axis Regulates Spinal Cord Injury Repair in Mice
Article Snippet: Cells were seed on the glass‐bottom dishes (NEST Biotechnology Co. Ltd., Wuxi, China) and fixed with 4% paraformaldehyde and permeabilized with 0.1% Triton X‐100 after treatment. .. After blocking with 5% BSA, the samples were incubated with primary antibodies at 4 °C overnight: NRF2 (Cell signaling technology, Cat# 12721S), HO‐1 (Abcam, Cat# ab189491), PPARγ (Abcam, Cat# ab178860), ANXA7 (Proteintech, Cat# 10154‐2‐AP), PLIN5 (Proteintech, Cat# 26951‐1‐AP), PLIN2 (Santa Cruz, Cat# sc‐377429), PLIN1(Abcam, Cat# ab172907), VDAC1 (Proteintech, Cat# 66345‐1‐Ig). ..

Western Blot:

Article Title: Metformin promotes lipid droplet-mitochondria coupling and improves insulin secretion in pancreatic β-cells exposed to lipotoxicity.
Article Snippet: Lipotoxicity that is caused by excess lipid accumulation is a major factor that contributes to gradual impairments of β-cell function and the development of type 2 diabetes.. Metformin has shown protective effects against lipidinduced damage in β-cells, but its specific mechanisms of action within pancreatic islets remain unclear.. The present study comprehensively examined direct effects of metformin on lipid metabolism pathways in INS-1E β-cells that were exposed to lipotoxic stress.

Article Title: Copper-Induced DRP1 Activation Disrupts Mitochondrial-Lipid Droplet Contact to Promote Hepatic Steatosis.
Article Snippet: Copper (Cu) is a vital dietary element for both humans and animals and is widely supplemented in food.. However, excessive consumption of this trace element can adversely affect the overall well-being.. Previous studies have demonstrated that longterm Cu intake can lead to severe hepatotoxicity.

Blocking Assay:

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PLIN5 deficiency inhibits ferroptosis in lipotoxic hepatocytes in vitro and in vivo . (A) Fe 2+ fluorescence intensity in AML12 cells observed using a fluorescence microscope (magnification, ×10), with red indicating Fe 2+ fluorescence and green indicating nuclei. (B) Western blot analysis of GPX4 protein expression in BSA- or PAOA-treated cells was performed, with GAPDH used as an internal control. (C) Fe 2+ content in the livers of mice in the WT HFD group and PLIN5 −/− HFD group was measured (n=5 mice/group). (D) Liver GSH content of mice in each group was detected (n=5 mice/group). (E) Liver MDA content of mice in each group was detected (n=5 mice/group). (F) mRNA levels of GPX4 in the liver tissues of mice in the WT HFD and PLIN5 −/− HFD groups were analyzed by quantitative polymerase chain reaction (n=5 mice/group). (G) Western blot analysis of GPX4 protein expression in the liver tissues of mice from the WT HFD and PLIN5 −/− HFD groups was performed, with tubulin used as an internal control (n=3 mice/group). All experiments were repeated at least three times (n=3). *P<0.05, **P<0.01, ***P<0.001, n.s., not significant. Fe 2+ , ferrous ion; GSH, glutathione; GPX4, GSH peroxidase 4; HFD, high-fat diet; MDA, malondialdehyde; PAOA, palmitic acid and oleic acid; PLIN5, perilipin 5; WT, wild-type.

Journal: Molecular Medicine Reports

Article Title: PLIN5 deficiency ameliorates metabolic dysfunction-associated fatty liver disease by inhibiting ferroptosis

doi: 10.3892/mmr.2025.13714

Figure Lengend Snippet: PLIN5 deficiency inhibits ferroptosis in lipotoxic hepatocytes in vitro and in vivo . (A) Fe 2+ fluorescence intensity in AML12 cells observed using a fluorescence microscope (magnification, ×10), with red indicating Fe 2+ fluorescence and green indicating nuclei. (B) Western blot analysis of GPX4 protein expression in BSA- or PAOA-treated cells was performed, with GAPDH used as an internal control. (C) Fe 2+ content in the livers of mice in the WT HFD group and PLIN5 −/− HFD group was measured (n=5 mice/group). (D) Liver GSH content of mice in each group was detected (n=5 mice/group). (E) Liver MDA content of mice in each group was detected (n=5 mice/group). (F) mRNA levels of GPX4 in the liver tissues of mice in the WT HFD and PLIN5 −/− HFD groups were analyzed by quantitative polymerase chain reaction (n=5 mice/group). (G) Western blot analysis of GPX4 protein expression in the liver tissues of mice from the WT HFD and PLIN5 −/− HFD groups was performed, with tubulin used as an internal control (n=3 mice/group). All experiments were repeated at least three times (n=3). *P<0.05, **P<0.01, ***P<0.001, n.s., not significant. Fe 2+ , ferrous ion; GSH, glutathione; GPX4, GSH peroxidase 4; HFD, high-fat diet; MDA, malondialdehyde; PAOA, palmitic acid and oleic acid; PLIN5, perilipin 5; WT, wild-type.

Article Snippet: Following transfection, the cells were treated with PAOA for 48 h. In addition, in the pcDNA3.1 PLIN5 + ferrostatin-1 (FER-1) group, the cells were transfected with pcDNA3.1 PLIN5 , pretreated with 2 μM FER-1 (cat. no. HY-100579; MedChemExpress) at 37°C in a 5% CO 2 cell culture incubator for 1 h, and then treated with PAOA for an additional 48 h.

Techniques: In Vitro, In Vivo, Fluorescence, Microscopy, Western Blot, Expressing, Control, Real-time Polymerase Chain Reaction

Overexpression of PLIN5 promotes lipid accumulation and ferroptosis in hepatocytes. (A) mRNA levels of PLIN5 levels were detected via quantitative polymerase chain reaction. (B) PLIN5 protein expression was detected via western blotting. (C) LD changes in cells were observed using a microscope (magnification, ×10), with nuclei stained blue and LDs stained red. Quantitative analysis was performed using ImageJ. (D) Fe 2+ fluorescence intensity in cells was observed using a fluorescence microscope (magnification, ×10), with nuclei stained green and Fe 2+ fluorescence stained red, followed by quantitative analysis. (E) MDA levels were detected in the three cell groups. (F) GSH levels were detected in the three groups of cells. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001, n.s., not significant. Fe 2+ , ferrous ion; GSH, glutathione; LD, lipid droplet; MDA, malondialdehyde; PLIN5, perilipin 5; FER-1, ferrostatin-1.

Journal: Molecular Medicine Reports

Article Title: PLIN5 deficiency ameliorates metabolic dysfunction-associated fatty liver disease by inhibiting ferroptosis

doi: 10.3892/mmr.2025.13714

Figure Lengend Snippet: Overexpression of PLIN5 promotes lipid accumulation and ferroptosis in hepatocytes. (A) mRNA levels of PLIN5 levels were detected via quantitative polymerase chain reaction. (B) PLIN5 protein expression was detected via western blotting. (C) LD changes in cells were observed using a microscope (magnification, ×10), with nuclei stained blue and LDs stained red. Quantitative analysis was performed using ImageJ. (D) Fe 2+ fluorescence intensity in cells was observed using a fluorescence microscope (magnification, ×10), with nuclei stained green and Fe 2+ fluorescence stained red, followed by quantitative analysis. (E) MDA levels were detected in the three cell groups. (F) GSH levels were detected in the three groups of cells. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001, n.s., not significant. Fe 2+ , ferrous ion; GSH, glutathione; LD, lipid droplet; MDA, malondialdehyde; PLIN5, perilipin 5; FER-1, ferrostatin-1.

Techniques: Over Expression, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Microscopy, Staining, Fluorescence

PLIN5 affects ferroptosis through ATF3/CHOP/CHAC1 signaling. (A) DEGs in mouse liver tissues from the PLIN5 −/− HFD group are shown compared to those in the WT HFD group (red dots represent upregulated genes, whereas blue dots represent downregulated genes). (B) DEGs associated with ferroptosis in the PLIN5 −/− HFD and WT HFD groups were analyzed (log 2 FC>1, P<0.05). (C) KEGG pathway and GO term enrichment analyses of different genes were performed. (D) mRNA levels of PRC1, LTF, GDPD5, FSCN1, MYC, ATF3 and PLIN2 in the liver tissues of WT HFD and PLIN5 −/− HFD mice were measured (n=5 mice/group). (E) mRNA levels of ATF3, CHOP and CHAC1 in the liver tissues of mice in each group were detected (n=5 mice/group). (F) Western blot analysis of ATF3, CHOP and CHAC1 protein expression in the liver tissues of mice from the WT HFD and PLIN5 −/− HFD groups was performed, with tubulin as the internal reference. Semi-quantitative analysis performed using ImageJ (n=3 mice/group). All experiments were repeated at least three times (n=3). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001, n.s., not significant. ATF3, activating transcription factor 3; CHAC1, cation transport regulator-like protein 1; CHOP, C/EBP homologous protein; DEGs, differentially expressed genes; FC, fold-change; FSCN1 , fascin actin-bundling protein 1; GDPD5 , glycerophosphodiester phosphodiesterase domain containing 5; GPX4 , glutathione peroxidase 4; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; ND, normal diet; LTF , lactotransferrin; PLIN , perilipin; PRC1 , protein regulator of cytokinesis 1; WT, wild-type; BP, biological process; CC, cellular component; MF, molecular function.

Journal: Molecular Medicine Reports

Article Title: PLIN5 deficiency ameliorates metabolic dysfunction-associated fatty liver disease by inhibiting ferroptosis

doi: 10.3892/mmr.2025.13714

Figure Lengend Snippet: PLIN5 affects ferroptosis through ATF3/CHOP/CHAC1 signaling. (A) DEGs in mouse liver tissues from the PLIN5 −/− HFD group are shown compared to those in the WT HFD group (red dots represent upregulated genes, whereas blue dots represent downregulated genes). (B) DEGs associated with ferroptosis in the PLIN5 −/− HFD and WT HFD groups were analyzed (log 2 FC>1, P<0.05). (C) KEGG pathway and GO term enrichment analyses of different genes were performed. (D) mRNA levels of PRC1, LTF, GDPD5, FSCN1, MYC, ATF3 and PLIN2 in the liver tissues of WT HFD and PLIN5 −/− HFD mice were measured (n=5 mice/group). (E) mRNA levels of ATF3, CHOP and CHAC1 in the liver tissues of mice in each group were detected (n=5 mice/group). (F) Western blot analysis of ATF3, CHOP and CHAC1 protein expression in the liver tissues of mice from the WT HFD and PLIN5 −/− HFD groups was performed, with tubulin as the internal reference. Semi-quantitative analysis performed using ImageJ (n=3 mice/group). All experiments were repeated at least three times (n=3). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001, n.s., not significant. ATF3, activating transcription factor 3; CHAC1, cation transport regulator-like protein 1; CHOP, C/EBP homologous protein; DEGs, differentially expressed genes; FC, fold-change; FSCN1 , fascin actin-bundling protein 1; GDPD5 , glycerophosphodiester phosphodiesterase domain containing 5; GPX4 , glutathione peroxidase 4; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; ND, normal diet; LTF , lactotransferrin; PLIN , perilipin; PRC1 , protein regulator of cytokinesis 1; WT, wild-type; BP, biological process; CC, cellular component; MF, molecular function.

Techniques: Western Blot, Expressing

PLIN5 affects ferroptosis via ATF3/CHOP/CHAC1 signaling. The mRNA expression levels of (A) GPX4 , (B) ATF3 , (C) CHOP and (D) CHAC1 in cells from each group were measured. (E) Western blot analysis of GPX4, ATF3, CHOP and CHAC1 protein expression in cells from different groups was performed, normalized to tubulin as an internal control. Semi-quantitative analysis was performed using ImageJ. All experiments were repeated at least three times. *P<0.05, **P<0.01, ***P<0.001, n.s., not significant. ATF3, activating transcription factor 3; CHAC1, cation transport regulator-like protein 1; CHOP, C/EBP homologous protein; FER-1, ferrostatin-1; GPX4 , glutathione peroxidase 4; PAOA, palmitic acid and oleic acid; PLIN5 , perilipin 5.

Journal: Molecular Medicine Reports

Article Title: PLIN5 deficiency ameliorates metabolic dysfunction-associated fatty liver disease by inhibiting ferroptosis

doi: 10.3892/mmr.2025.13714

Figure Lengend Snippet: PLIN5 affects ferroptosis via ATF3/CHOP/CHAC1 signaling. The mRNA expression levels of (A) GPX4 , (B) ATF3 , (C) CHOP and (D) CHAC1 in cells from each group were measured. (E) Western blot analysis of GPX4, ATF3, CHOP and CHAC1 protein expression in cells from different groups was performed, normalized to tubulin as an internal control. Semi-quantitative analysis was performed using ImageJ. All experiments were repeated at least three times. *P<0.05, **P<0.01, ***P<0.001, n.s., not significant. ATF3, activating transcription factor 3; CHAC1, cation transport regulator-like protein 1; CHOP, C/EBP homologous protein; FER-1, ferrostatin-1; GPX4 , glutathione peroxidase 4; PAOA, palmitic acid and oleic acid; PLIN5 , perilipin 5.

Techniques: Expressing, Western Blot, Control

Knockdown of ATF3 alleviates lipid accumulation and ferroptosis induced by overexpression of PLIN5 . (A) ATF3 mRNA expression in AML12 cells was analyzed by quantitative polymerase chain reaction 48 h after transfection with shATF3 plasmid. (B) Semi-quantitative analysis of ATF3 protein expression in AML12 cells 48 h after transfection with shATF3 plasmid was performed, normalized to tubulin as an internal control, using ImageJ. (C) LDs were observed in cells from different intervention groups using a microscope (magnification, ×10), with nuclei stained blue and LDs stained red and quantitative analysis was performed using ImageJ. (D) Fe 2+ fluorescence intensity in cells from different intervention groups was observed using a fluorescence microscope, with nuclei stained green and Fe 2+ fluorescence stained red, followed by quantitative analysis. (E) MDA content was measured in cells from different intervention groups. (F) GSH content was measured in cells from different intervention groups. All experiments were repeated at least three times. *P<0.05, **P<0.01, ***P<0.001, n.s., not significant. ATF3, activating transcription factor 3; Fe 2+ , ferrous ion; GSH, glutathione; LD, lipid droplet; MDA, malondialdehyde; NC, negative control; PAOA, palmitic acid and oleic acid; PLIN5 , perilipin 5; sh, short hairpin.

Journal: Molecular Medicine Reports

Article Title: PLIN5 deficiency ameliorates metabolic dysfunction-associated fatty liver disease by inhibiting ferroptosis

doi: 10.3892/mmr.2025.13714

Figure Lengend Snippet: Knockdown of ATF3 alleviates lipid accumulation and ferroptosis induced by overexpression of PLIN5 . (A) ATF3 mRNA expression in AML12 cells was analyzed by quantitative polymerase chain reaction 48 h after transfection with shATF3 plasmid. (B) Semi-quantitative analysis of ATF3 protein expression in AML12 cells 48 h after transfection with shATF3 plasmid was performed, normalized to tubulin as an internal control, using ImageJ. (C) LDs were observed in cells from different intervention groups using a microscope (magnification, ×10), with nuclei stained blue and LDs stained red and quantitative analysis was performed using ImageJ. (D) Fe 2+ fluorescence intensity in cells from different intervention groups was observed using a fluorescence microscope, with nuclei stained green and Fe 2+ fluorescence stained red, followed by quantitative analysis. (E) MDA content was measured in cells from different intervention groups. (F) GSH content was measured in cells from different intervention groups. All experiments were repeated at least three times. *P<0.05, **P<0.01, ***P<0.001, n.s., not significant. ATF3, activating transcription factor 3; Fe 2+ , ferrous ion; GSH, glutathione; LD, lipid droplet; MDA, malondialdehyde; NC, negative control; PAOA, palmitic acid and oleic acid; PLIN5 , perilipin 5; sh, short hairpin.

Techniques: Knockdown, Over Expression, Expressing, Real-time Polymerase Chain Reaction, Transfection, Plasmid Preparation, Control, Microscopy, Staining, Fluorescence, Negative Control

(a) Western blot for PLIN5, Actin, TIM23 and TOM20 from whole cell lysate and pure mitochondria with and without treatment with Proteinase K from control or BKOPLIN5 mice housed at 23 or 6 °C for 16 hours.

Journal: bioRxiv

Article Title: Acute deletion of PLIN5 in brown adipocytes causes mitochondrial dysfunction and cold intolerance

doi: 10.64898/2025.12.31.697198

Figure Lengend Snippet: (a) Western blot for PLIN5, Actin, TIM23 and TOM20 from whole cell lysate and pure mitochondria with and without treatment with Proteinase K from control or BKOPLIN5 mice housed at 23 or 6 °C for 16 hours.

Article Snippet: We used the following primary antibodies: PLIN5 (Progen Cat # GP31), GDI (Bickel Lab) [ ], Histone H3 (Cell signaling Cat # 9717), Cox4 (Cell signaling Cat# 4850), TIM23 (Cell signaling Cat # 34822), TOM20 (Santa Cruz sc-11021), Actin (Cell Signaling Cat# 4967).

Techniques: Western Blot, Control

(a) Schematic representation for the strategy for doxycycline-inducible disruption of Plin5 gene. (b) Western blot (WB) depicting PLIN5 in BAT (left panel) and quantification (right panel) and (c) iWAT (left panel) and quantification (right panel) in BiKOPLIN5 and control mice housed at 23 °C or 6 °C for 7 days. (d) WB depicting PLIN5 from liver (left panel) and heart (right panel) of Control or BiKOPLIN5 mice. For WB experiments, mice were housed at the indicated temperatures and administered Dox for 7 days.”

Journal: bioRxiv

Article Title: Acute deletion of PLIN5 in brown adipocytes causes mitochondrial dysfunction and cold intolerance

doi: 10.64898/2025.12.31.697198

Figure Lengend Snippet: (a) Schematic representation for the strategy for doxycycline-inducible disruption of Plin5 gene. (b) Western blot (WB) depicting PLIN5 in BAT (left panel) and quantification (right panel) and (c) iWAT (left panel) and quantification (right panel) in BiKOPLIN5 and control mice housed at 23 °C or 6 °C for 7 days. (d) WB depicting PLIN5 from liver (left panel) and heart (right panel) of Control or BiKOPLIN5 mice. For WB experiments, mice were housed at the indicated temperatures and administered Dox for 7 days.”

Techniques: Disruption, Western Blot, Control

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