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rabbit polyclonal anti plin2 (Proteintech)

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Proteintech rabbit polyclonal anti plin2

(A) BV2 cells were activated for 3, 6, or 16 hours with the dMIX and Tnf , Il-6 , and Ifn β expression quantified by qRT-PCR and normalised to their expression in untreated cells (CTL). Graphs show means±SD (combined from at least N=4); *P < 0.05, **P < 0.01, ****P < 0.0001 in an ordinary one-way ANOVA. Red and blue asterisks indicate respectively significant enrichment or reduction. (B) BV2 cells were stimulated for 3, 6, or 16 hours with dMIX and “core” and “immune” LD proteins expression quantified by qRT-PCR and normalised to their expression in untreated cells (CTL). Graphs show means±SD (combined from at least N=4); ns is not significant, *P < 0.05, **P < 0.01, ****P < 0.0001 in an ordinary one-way ANOVA. Red and blue asterisks indicate respectively significant enrichment or reduction. (C) Representative confocal images (N=3) of BV2 cells treated for 16 hours with 15µg/ml OA to induce mLDs or with the dMIX to induce dLDs. Cells were labelled with anti-Igtp (green) <t>and</t> <t>anti-Plin2</t> (red) antibodies and LipidTox (LD, blue). Scale bar is 20µm. The yellow square marks the region selected for the high magnification panels.

Rabbit Polyclonal Anti Plin2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 305 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti+plin2/ADRP%2FPerilipin+2+Antibody/bio_rxiv__64898__2026__03__12__711356-317-21-26
Average 96 stars, based on 305 article reviews

rabbit polyclonal anti plin2 - by Bioz Stars, 2026-09

96/100 stars

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1) Product Images from "Defensive lipid droplets are PUFA reservoirs driving bacterial clearance and inflammation"

Article Title: Defensive lipid droplets are PUFA reservoirs driving bacterial clearance and inflammation

Journal: bioRxiv

doi: 10.64898/2026.03.12.711356

Figure Legend Snippet: (A) BV2 cells were activated for 3, 6, or 16 hours with the dMIX and Tnf , Il-6 , and Ifn β expression quantified by qRT-PCR and normalised to their expression in untreated cells (CTL). Graphs show means±SD (combined from at least N=4); *P < 0.05, **P < 0.01, ****P < 0.0001 in an ordinary one-way ANOVA. Red and blue asterisks indicate respectively significant enrichment or reduction. (B) BV2 cells were stimulated for 3, 6, or 16 hours with dMIX and “core” and “immune” LD proteins expression quantified by qRT-PCR and normalised to their expression in untreated cells (CTL). Graphs show means±SD (combined from at least N=4); ns is not significant, *P < 0.05, **P < 0.01, ****P < 0.0001 in an ordinary one-way ANOVA. Red and blue asterisks indicate respectively significant enrichment or reduction. (C) Representative confocal images (N=3) of BV2 cells treated for 16 hours with 15µg/ml OA to induce mLDs or with the dMIX to induce dLDs. Cells were labelled with anti-Igtp (green) and anti-Plin2 (red) antibodies and LipidTox (LD, blue). Scale bar is 20µm. The yellow square marks the region selected for the high magnification panels.

Techniques Used: Expressing, Quantitative RT-PCR

(A) Representative confocal images (N=3) of BV2 cells treated with OA (15µg/ml) to induce mLDs or dMIX (containing 15µg/ml of FAs: 40% LA, 35% OA, 23% PA, and 2% ALA). Cells were labelled with anti-Viperin (green) and anti-Plin2 (red) antibodies and LipidTox (LD, blue). Scale bar is 20µm. The yellow square marks the region selected for the high magnification panels.

Figure Legend Snippet: (A) Representative confocal images (N=3) of BV2 cells treated with OA (15µg/ml) to induce mLDs or dMIX (containing 15µg/ml of FAs: 40% LA, 35% OA, 23% PA, and 2% ALA). Cells were labelled with anti-Viperin (green) and anti-Plin2 (red) antibodies and LipidTox (LD, blue). Scale bar is 20µm. The yellow square marks the region selected for the high magnification panels.

Techniques Used:

Immunofluorescence:

Article Title: PICALM Alzheimer's risk allele causes aberrant lipid droplets in microglia.
Article Snippet: Images were acquired using the Nikon ECLIPSE TE2000-U microscope. .. Primary antibodies used for microglial immunofluorescence and their dilutions for incubation were as follows: rat anti-TREM2 (MABN755, Sigma-Aldrich, 1:100), rabbit anti-CD45 (SAB4502541, Sigma-Aldrich, 1:200), mouse anti-PU1 (89136, Cell Signalling, 1:100), mouse anti-IBA1 (MA5-27726, Thermo Fisher Scientific, 1:100), rabbit anti-P2Y12 (702516, Invitrogen, 1:200), rabbit anti-TMEM119 (AB209064, Abcam, 1:100), rabbit anti-PLIN2 (15294-1-AP, Proteintech, 1:200), rabbit anti-ATP6AP2 (SAB2702080, Sigma-Aldrich, 1:100), rabbit anti-VAMP1 (702787, Thermo Fisher Scientific, 1:100), rabbit anti-HMGCR (SAB4200528, Sigma-Aldrich, 1:100) and mouse anti-CD74 (14-0747-82, Thermo Fisher Scientific, 1:100). .. Secondary antibodies were Alexa 488 donkey anti-rat (A21208, Invitrogen, 1:1,000), Alexa 594 anti-rabbit (A21207, Invitrogen, 1:1,000), Alexa 647 anti-mouse (A32787, Invitrogen, 1:1,000), Alexa donkey 594 anti-mouse (A21203, Invitrogen, 1:1,000) and Alexa donkey 647 anti-rabbit (A32795, Invitrogen, 1:1,000).

Article Title: PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia
Article Snippet: Images were acquired using the Nikon ECLIPSE TE2000-U microscope. .. Primary antibodies used for microglial immunofluorescence and their dilutions for incubation were as follows: rat anti-TREM2 (MABN755, Sigma-Aldrich, 1:100), rabbit anti-CD45 (SAB4502541, Sigma-Aldrich, 1:200), mouse anti-PU1 (89136, Cell Signalling, 1:100), mouse anti-IBA1 (MA5-27726, Thermo Fisher Scientific, 1:100), rabbit anti-P2Y12 (702516, Invitrogen, 1:200), rabbit anti-TMEM119 ( AB209064 , Abcam, 1:100), rabbit anti-PLIN2 (15294-1-AP, Proteintech, 1:200), rabbit anti-ATP6AP2 (SAB2702080, Sigma-Aldrich, 1:100), rabbit anti-VAMP1 (702787, Thermo Fisher Scientific, 1:100), rabbit anti-HMGCR (SAB4200528, Sigma-Aldrich, 1:100) and mouse anti-CD74 (14-0747-82, Thermo Fisher Scientific, 1:100). .. Secondary antibodies were Alexa 488 donkey anti-rat (A21208, Invitrogen, 1:1,000), Alexa 594 anti-rabbit (A21207, Invitrogen, 1:1,000), Alexa 647 anti-mouse (A32787, Invitrogen, 1:1,000), Alexa donkey 594 anti-mouse (A21203, Invitrogen, 1:1,000) and Alexa donkey 647 anti-rabbit (A32795, Invitrogen, 1:1,000).

Incubation:

Article Title: Androgen regulates seasonal changes in triglyceride synthesis through the AR-SREBP1-FASN axis in the scented glands of muskrats (Ondatra zibethicus).
Article Snippet: SREBP1 (sterol regulatory element binding protein 1) plays an important role in maintaining lipid balance in mammals.. Previous research showed that androgen significantly regulated the secretion of lipid-rich musky odor substances from the scented glands of muskrats.. Our investigation provides insights into the pathways through which androgen induces SREBP1 expression and affects seasonal changes in triglyceride synthesis in muskrat scented glands.

Article Title: DNA Damage-Regulated Autophagy Modulator1 (DRAM1)-induced lipophagy facilitates Toxoplasma gondii nutrient acquisition and infection
Article Snippet: Autophagy is a catabolic process that responds to various environmental stresses, such as nutrient deficiency and intracellular pathogen infection.. Toxoplasma gondii is an intracellular parasite that acquires nutrients from the host cells for its proliferation; however, the molecular mechanisms of T. gondii parasites’ nutritional acquisition and metabolism are not fully understood.. Here, we found that T. gondii type I RH strain induced host cell autophagy for nutrient acquisition and growth.

Article Title: Regulating PPARG Reduces Lipid Accumulation in Microglia and Promotes Functional Recovery After Spinal Cord Injury.
Article Snippet: .. The sections were incubated in PBS with 10% donkey serum and the following primary antibodies for 18 h at 4 °C: goat anti-IBA1 (1:1000; Abcam, ab5076), goat anti-PPARG (1:1000; CST, 81B8), mouse anti-GFAP (1:1000; CST, 3670), rabbit anti-NeuN (1:1000; CST, 24307), rab- bit anti-dMBP (1:1000; Millipore, ab5864), and rabbit anti-PLIN2 (1:200; Proteintech, 15294-1-AP). .. After primary antibody incubation, the sections were washed thrice in PBS, and incubated in PBS with 10% donkey serum and the following secondary antibodies for 1 h at 26 °C: donkey antirabbit Alexa Fluor 555, donkey antirabbit Alexa Fluor 647, and donkey antirabbit Alexa Fluor 405 (all at 1:200 dilution; Invitrogen).

Image Search Results

Enhanced recruitment of Rab5 to lipid droplets (LDs) upon lipophagy stimulation . A , Western blot analysis of Rab5 and EEA1 GTP-pulldown in regular medium (CT) or 4 h HBSS starvation in Hep3B cells. B , quantification of the fold change of GTP-bound/total Rab5 as well as EEA1 from n = 4 independent experiments. C , quantification of total Rab5–β-actin confirming that starvation does not change overall Rab5 expression. D , Western blot analysis of LDs isolated from Hep3B cells by density gradient centrifugation showing abundant levels of Rab5 in isolated LDs following 4 h of HBSS starvation compared with the regular medium (CT). E , quantification of Rab5–Plin2 in the biochemically isolated LDs. F , fluorescence micrograph showing immunofluorescence staining of Hep3B cells expressing Myc-tagged Rab5 ( green ). Cells were treated with oleic acid for 16 h and then either maintained in regular medium (control) or subjected to 4 h of HBSS starvation before being fixed and stained with Oil Red O (ORO; red ) to label LDs. Note the marked increase in Rab5 staining around LDs in HBSS-starved cells versus control ( yellow arrowheads ). Graphs represent mean ± SD from n = 3 to 4 independent experiments. Statistical significance was determined using an unpaired two-tailed t test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. CT, control; EEA1, early endosome antigen 1; HBSS, Hank’s balanced salt solution; Plin2, perilipin-2.

Journal: The Journal of Biological Chemistry

Article Title: Rab5 nucleotide binding promotes oxidative metabolism to fuel hepatocellular carcinoma cell proliferation

doi: 10.1016/j.jbc.2026.111321

Figure Lengend Snippet: Enhanced recruitment of Rab5 to lipid droplets (LDs) upon lipophagy stimulation . A , Western blot analysis of Rab5 and EEA1 GTP-pulldown in regular medium (CT) or 4 h HBSS starvation in Hep3B cells. B , quantification of the fold change of GTP-bound/total Rab5 as well as EEA1 from n = 4 independent experiments. C , quantification of total Rab5–β-actin confirming that starvation does not change overall Rab5 expression. D , Western blot analysis of LDs isolated from Hep3B cells by density gradient centrifugation showing abundant levels of Rab5 in isolated LDs following 4 h of HBSS starvation compared with the regular medium (CT). E , quantification of Rab5–Plin2 in the biochemically isolated LDs. F , fluorescence micrograph showing immunofluorescence staining of Hep3B cells expressing Myc-tagged Rab5 ( green ). Cells were treated with oleic acid for 16 h and then either maintained in regular medium (control) or subjected to 4 h of HBSS starvation before being fixed and stained with Oil Red O (ORO; red ) to label LDs. Note the marked increase in Rab5 staining around LDs in HBSS-starved cells versus control ( yellow arrowheads ). Graphs represent mean ± SD from n = 3 to 4 independent experiments. Statistical significance was determined using an unpaired two-tailed t test. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. CT, control; EEA1, early endosome antigen 1; HBSS, Hank’s balanced salt solution; Plin2, perilipin-2.

Article Snippet: Antibodies against Rab5A (2143S), PLIN2 (95109), and EEA1 (2411S) were purchased from Cell Signaling Technology.

Techniques: Western Blot, Expressing, Isolation, Gradient Centrifugation, Fluorescence, Immunofluorescence, Staining, Control, Two Tailed Test

Journal: bioRxiv

Article Title: Defensive lipid droplets are PUFA reservoirs driving bacterial clearance and inflammation

doi: 10.64898/2026.03.12.711356

Figure Lengend Snippet: (A) BV2 cells were activated for 3, 6, or 16 hours with the dMIX and Tnf , Il-6 , and Ifn β expression quantified by qRT-PCR and normalised to their expression in untreated cells (CTL). Graphs show means±SD (combined from at least N=4); *P < 0.05, **P < 0.01, ****P < 0.0001 in an ordinary one-way ANOVA. Red and blue asterisks indicate respectively significant enrichment or reduction. (B) BV2 cells were stimulated for 3, 6, or 16 hours with dMIX and “core” and “immune” LD proteins expression quantified by qRT-PCR and normalised to their expression in untreated cells (CTL). Graphs show means±SD (combined from at least N=4); ns is not significant, *P < 0.05, **P < 0.01, ****P < 0.0001 in an ordinary one-way ANOVA. Red and blue asterisks indicate respectively significant enrichment or reduction. (C) Representative confocal images (N=3) of BV2 cells treated for 16 hours with 15µg/ml OA to induce mLDs or with the dMIX to induce dLDs. Cells were labelled with anti-Igtp (green) and anti-Plin2 (red) antibodies and LipidTox (LD, blue). Scale bar is 20µm. The yellow square marks the region selected for the high magnification panels.

Article Snippet: Primary antibodies were diluted in blocking solution: mouse monoclonal anti-Viperin (1:100, ab107359, Abcam), mouse monoclonal anti-Igtp (1:100, sc-136317, Santa Cruz Biotechnology), rabbit polyclonal anti-Plin2 (1:200, 15294-1-AP, Proteintech).

Techniques: Expressing, Quantitative RT-PCR

Journal: bioRxiv

Article Title: Defensive lipid droplets are PUFA reservoirs driving bacterial clearance and inflammation

doi: 10.64898/2026.03.12.711356

Figure Lengend Snippet: (A) Representative confocal images (N=3) of BV2 cells treated with OA (15µg/ml) to induce mLDs or dMIX (containing 15µg/ml of FAs: 40% LA, 35% OA, 23% PA, and 2% ALA). Cells were labelled with anti-Viperin (green) and anti-Plin2 (red) antibodies and LipidTox (LD, blue). Scale bar is 20µm. The yellow square marks the region selected for the high magnification panels.

Techniques:

a , AlphaFold3-predicted structure of murine CLCC1 dimer (aa50-165), with two alpha-helices cross-linked by interchain disulfide bonds (C67, C81), and residues 91-165 clamped together mainly based on hydrophobic interactions. b , Schematics of different CLCC1 constructs. FL, full length. ΔNTD, amino 19-165 required for CLCC1 dimerization deleted. c , CLCC1 lacking NTD (ΔNTD) fails to oligomerize. Huh7 cells were infected with AAVs expressing CLCC1-FLAG or ΔNTD CLCC1-FLAG, prior to blue native PAGE (upper) or SDS-PAGE (lower) analysis. d , Non-reducing PAGE analysis of CLCC1-FLAG or ΔNTD CLCC1-FLAG in samples as in ( c ). e , CLCC1 lacking NTD (ΔNTD) fails to localize to the ER encircling geLDs. TMEM41B-deficient Huh7 cells infected with AAVs expressing CLCC1-FLAG or ΔNTD CLCC1-FLAG, were co-stained with anti-FLAG antibodies and LipidTox, prior to confocal microscopy. Scale bar, 5 μm. f , Re-Introduction of CLCC1 FL but not ΔNTD CLCC1 suppresses geLDs in CLCC1-deficient Huh7 cells. CLCC1-deficient Huh7 cells infected with AAVs expressing CLCC1-FLAG or ΔNTD CLCC1-FLAG, were co-stained with anti-FLAG antibodies, anti-Plin2 antibodies and LipidTox, prior to confocal microscopy. Scale bar, 5 μm. g , IB analysis of the same cell sets as in ( e ). For b-f , representative of results of at least 3 biologically independent replicates are shown. For gel source data, see Supplementary Fig. .

Journal: Nature

Article Title: CLCC1 governs ER bilayer equilibration to maintain lipid homeostasis

doi: 10.1038/s41586-026-10161-y

Figure Lengend Snippet: a , AlphaFold3-predicted structure of murine CLCC1 dimer (aa50-165), with two alpha-helices cross-linked by interchain disulfide bonds (C67, C81), and residues 91-165 clamped together mainly based on hydrophobic interactions. b , Schematics of different CLCC1 constructs. FL, full length. ΔNTD, amino 19-165 required for CLCC1 dimerization deleted. c , CLCC1 lacking NTD (ΔNTD) fails to oligomerize. Huh7 cells were infected with AAVs expressing CLCC1-FLAG or ΔNTD CLCC1-FLAG, prior to blue native PAGE (upper) or SDS-PAGE (lower) analysis. d , Non-reducing PAGE analysis of CLCC1-FLAG or ΔNTD CLCC1-FLAG in samples as in ( c ). e , CLCC1 lacking NTD (ΔNTD) fails to localize to the ER encircling geLDs. TMEM41B-deficient Huh7 cells infected with AAVs expressing CLCC1-FLAG or ΔNTD CLCC1-FLAG, were co-stained with anti-FLAG antibodies and LipidTox, prior to confocal microscopy. Scale bar, 5 μm. f , Re-Introduction of CLCC1 FL but not ΔNTD CLCC1 suppresses geLDs in CLCC1-deficient Huh7 cells. CLCC1-deficient Huh7 cells infected with AAVs expressing CLCC1-FLAG or ΔNTD CLCC1-FLAG, were co-stained with anti-FLAG antibodies, anti-Plin2 antibodies and LipidTox, prior to confocal microscopy. Scale bar, 5 μm. g , IB analysis of the same cell sets as in ( e ). For b-f , representative of results of at least 3 biologically independent replicates are shown. For gel source data, see Supplementary Fig. .

Article Snippet: The following primary antibodies were used for IB: rabbit polyclonal anti-PLIN2 (Cell Signaling Technology, 45535, 1:1,000), rabbit polyclonal anti-HSD17B13 (ABclonal, A6256, 1:1,000), rabbit polyclonal anti-ATGL (Cell Signaling Technology, 2138, 1:1,000), rabbit polyclonal anti-SigmaR1 (Proteintech, 15168-1-AP, 1:1,000), rabbit polyclonal anti-calnexin (Proteintech, 10427-2-AP, 1:1,000), rabbit polyclonal anti-APOB (Proteintech, 20578-1-AP, 1:1,000), rabbit polyclonal anti-ApoE (Fitzgerald, 10R-10633, 1:1,000), mouse monoclonal anti APOE (Cell Signaling technology, 74417, 1:1,000), rabbit polyclonal anti-APOA1 (Fitzgerald, 70R-15769, 1:1,000), rabbit polyclonal anti-LIPIN1 (Proteintech, 27026-1-AP, 1:1,000), rabbit polyclonal anti-FASN (Proteintech, 10624-2-AP, 1:1,000), rabbit polyclonal anti-ACC1 (Proteintech, 21923-1-AP, 1:1,000), mouse monoclonal anti-MTP (Santa Cruz Biotechnology, sc-135994, 1:1,000), mouse monoclonal anti-PDI (BD transduction Laboratories, 610946, 1:1,000), rabbit polyclonal anti-BIP (Proteintech, 11587-1-AP, 1:1,000), rabbit polyclonal anti-tubulin (Proteintech, 11224-1-AP, 1:1,000), rabbit polyclonal anti-torsin A/DYT1 (Abcam, ab34540, 1:1,000), rabbit polyclonal anti-CES3 (Proteintech, 14587-1-AP, 1:1,000), rabbit polyclonal anti-REEP5 (Proteintech, 14643-1-AP, 1:1,000), mouse monoclonal anti-Flag (M2) (Sigma-Aldrich, F1804, 1:500). rabbit anti-GM130 antibody (Proteintech, 11308-1-AP, 1:1,000), rabbit polyclonal antibody against the N-terminal epitope of human TMEM41B (residues 1–109) were produced by the Proteintech Group ( www.ptglab.com ), the rabbit anti-serum was collected and purified by NHS beads conjugated with His-tagged human TMEM41B (residues 1–109), followed by washing with PBS containing 0.15% Triton X-100, eluted with 50 mM glycine (pH 2.5) and neutralized with Tris-HCl pH 8.0.

Techniques: Construct, Infection, Expressing, Blue Native PAGE, SDS Page, Staining, Confocal Microscopy

a , Confocal microscopy of CRISPR/-Cas9-mediated LacZ targeting Huh7 cells (CTL) infected with AAVs expressing GFP-CB5 (left) or GFP-Plin2 (right) with DMSO (upper) or 50 nM of MTP inhibitor lomitapide (lower) treatments for 24 h. Cells were stained with LipidTox prior to confocal microscopy. Scale bar, 5 μm. b , Confocal microscopy of CRISPR/-Cas9-mediated TMEM41B KO Huh7 cells with treatments and staining procedures as in (a). For a and b , Representative results of 3 biologically independent experiments were shown. Scale bar, 5 μm. c , Quantification of the geLD/total LD area ratio (CB5 positive) and cLD/total LD area ratio (Plin2 positive) from ( b ). Data are presented as mean ± s.e.m. n = 5 cells for CB5 and 6 for Plin2 in both DMSO or MTPi group. Statistical significance was determined by unpaired two-tailed Student’s t test. d , Confocal microscopy of the indicated Huh7 cells treated with DMSO, or 50 nM of the MTP inhibitor lomitapide for 72 h, followed by co-staining with LipidTox, anti-APOE antibody and anti-Plin2 antibody. Scale bar, 5 μm. Representative results of 3 biologically independent replicates are shown. e , IB analysis of cell lysates from indicated Huh7 cells treated with the MTP inhibitor lomitapide (50 nM) or implitapide (5 μM) for 72 h. Representative results of 3 biologically independent replicates are shown. For gel source data, see Supplementary Fig. .

Journal: Nature

Article Title: CLCC1 governs ER bilayer equilibration to maintain lipid homeostasis

doi: 10.1038/s41586-026-10161-y

Figure Lengend Snippet: a , Confocal microscopy of CRISPR/-Cas9-mediated LacZ targeting Huh7 cells (CTL) infected with AAVs expressing GFP-CB5 (left) or GFP-Plin2 (right) with DMSO (upper) or 50 nM of MTP inhibitor lomitapide (lower) treatments for 24 h. Cells were stained with LipidTox prior to confocal microscopy. Scale bar, 5 μm. b , Confocal microscopy of CRISPR/-Cas9-mediated TMEM41B KO Huh7 cells with treatments and staining procedures as in (a). For a and b , Representative results of 3 biologically independent experiments were shown. Scale bar, 5 μm. c , Quantification of the geLD/total LD area ratio (CB5 positive) and cLD/total LD area ratio (Plin2 positive) from ( b ). Data are presented as mean ± s.e.m. n = 5 cells for CB5 and 6 for Plin2 in both DMSO or MTPi group. Statistical significance was determined by unpaired two-tailed Student’s t test. d , Confocal microscopy of the indicated Huh7 cells treated with DMSO, or 50 nM of the MTP inhibitor lomitapide for 72 h, followed by co-staining with LipidTox, anti-APOE antibody and anti-Plin2 antibody. Scale bar, 5 μm. Representative results of 3 biologically independent replicates are shown. e , IB analysis of cell lysates from indicated Huh7 cells treated with the MTP inhibitor lomitapide (50 nM) or implitapide (5 μM) for 72 h. Representative results of 3 biologically independent replicates are shown. For gel source data, see Supplementary Fig. .

Techniques: Confocal Microscopy, CRISPR, Infection, Expressing, Staining, Two Tailed Test

Journal: Nature

Article Title: Lesion-remote astrocytes govern microglia-mediated white matter repair

doi: 10.1038/s41586-025-09887-y

Figure Lengend Snippet: a , High magnification image of IBA1 + /TREM2 + WDM used for 3D reconstruction in main Fig. . b , Relative proportions of IBA1 + microglia that are TREM2 + from WT and Ccn1 c-KO Wallerian degenerating dorsal column white matter (Data from WT Healthy (n = 4), cKO Healthy (n = 3), WT 7dpi (n = 6), cKO 7dpi (n = 6), WT 28dpi (n = 6), cKO 28dpi (n = 5), WT 90dpi (n = 6), cKO 90dpi (n = 6), 2–5 sections per mouse. c , d , High magnification image of IBA1 + / Gpnmb + or Igf1 + WDM used for 3D reconstruction in main Fig. and . e , Cholesterol efflux measured from cultured primary mouse microglia following stimulation with positive control (Abcam 196985) or vehicle (BSA) (n = 6 experimental replicates from independent cultures; Students t-test, ** P ≤ 0.05). f , Microglia lipid species distribution across treatment groups. Note that in both WT and Ccn1- cKO animals, the total microglia lipidome is reduced at 28 dpi. , Heat map showing relative (Z-scored) levels of all significant lipid subtypes detected by unbiased microglia lipidomic analysis. h , i , Lipid pathway enrichment of the WT and Ccn1- cKO injury response highlighting a shift in the predominant lipid pathways employed after iSCI. j , Direct pairwise comparison of WT and Ccn1- cKO microglia lipid profile for healthy and iSCI, including lipid droplet- and myelin-associated lipid subtypes (Log 2 fold-change FDR P ≤ 0.01). k , Schematic of ceramide to sphingomyelin conversion mediated by sphingomyelin synthase predicted by Biopan lipid pathway analysis comparing the iSCI and healthy Ccn1 cKO animals (z-score 1.921). l , Plots show percentage maximum summed intensity for sphingomyelin (SM) and ceramide (CER) in both WT and Ccn1- cKO mice. m , High magnification image of IBA1 + /BODIPY + WDM used for 3D reconstruction in in main Fig. . n , Quantification of the proportion of BODIPY containing microglia from WT or Ccn1- cKO Wallerian degenerating dorsal column white matter (Data from WT Healthy (n = 4), cKO Healthy (n = 3), WT 7dpi (n = 4), cKO 7dpi (n = 4), WT 28dpi (n = 6), cKO 28dpi (n = 5), WT 90dpi (n = 6), cKO 90 dpi (n = 6), 1–6 sections per mouse). o , p , High magnification 3D image reconstruction and quantification of PLIN2 + lipid droplets within IBA1 + WDM nodules from WT and Ccn1 cKO Wallerian degenerating dorsal column white matter (Data from WT Healthy (n = 4), cKO Healthy (n = 3), WT 7dpi (n = 4), cKO 7dpi (n = 4), WT 28dpi (n = 6), cKO 28dpi (n = 5), WT 90dpi (n = 6), cKO 90 dpi (n = 6), 4–6 sections/mouse). q , High magnification image of IBA1 + /PLIN2 + WDM used for 3D reconstruction in panel o. r , Proportions of IBA1 + microglia that are PLIN2 + from WT and Ccn1- cKO Wallerian degenerating dorsal column white matter(Data from WT Healthy (n = 4), cKO Healthy (n = 3), WT 7dpi (n = 4), cKO 7dpi (n = 4), WT 28dpi (n = 6), cKO 28dpi (n = 5), WT 90dpi (n = 6), cKO 90 dpi (n = 6),; 1–6 sections per mouse). s , High magnification image of IBA1 + / Abca1 + WDM used for 3D reconstruction in main Fig. . Bar graphs show mean ± SEM. In graphs of histological count or continuous data, colored data points represent the mean value for each biological replicate (individual mouse), while grey data points indicate replicate measurements from individual tissue sections/cells. Unless stated otherwise, statistical analyses were performed using two-way ANOVA with Holm-Sidak, * P ≤ 0.05, ** P ≤ 0.002, *** P ≤ 0.0002, **** P ≤ 0.0001. Exact P values can be found in source data. Scale bars, 10 µm.

Article Snippet: Primary antibodies include: Rat-CD18 (1:100, Invitrogen), Rat-GFAP (1:1,000, Thermofisher), Rabbit-GFAP (1:1,000, Dako), Goat-IBA1 (1:1,000, Abcam), Rabbit-IBA1 (1:1,000, Wako), Rabbit-LPL (1:50, Abcam), Rabbit-PLIN2 (1:500, Progen), Goat-SOX9 (1:200, R&D system), Mouse- (1:3,000, Biolegend), Sheep-TREM2 (1:250, R&D systems), Rabbit-YAP1 (1:200, Protintech).

Techniques: Cell Culture, Positive Control, Comparison

Review

rabbit polyclonal anti plin2 (Proteintech)

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1) Product Images from "Defensive lipid droplets are PUFA reservoirs driving bacterial clearance and inflammation"

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