Review

plin3 antibody (OriGene)

Name: plin3 antibody
Brand: OriGene
Rating: 90 (1 reviews)

OriGene is a verified supplier

OriGene manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

OriGene plin3 antibody
Plin3 Antibody, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/plin3 antibody/product/OriGene
Average 90 stars, based on 1 article reviews

plin3 antibody - by Bioz Stars, 2026-03

90/100 stars

Images

Image Search Results

m 6 A modification of PLIN3 mRNA is increased by HIV-1 infection in primary CD4 + T cells. Activated primary CD4 + T cells isolated from PBMCs of three donors were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. Total cellular RNA was subjected to meRIP, and the level of m 6 A-modified transcripts in the meRIP was determined relative to ( A ) input or ( B ) mock-infected controls by RT-qPCR. Data are shown as mean ± SD. A two-tailed unpaired t -test was used for statistical analysis ( P values are shown on the figures).

Journal: Journal of Virology

Article Title: Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells

doi: 10.1128/jvi.01536-25

Figure Lengend Snippet: m 6 A modification of PLIN3 mRNA is increased by HIV-1 infection in primary CD4 + T cells. Activated primary CD4 + T cells isolated from PBMCs of three donors were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. Total cellular RNA was subjected to meRIP, and the level of m 6 A-modified transcripts in the meRIP was determined relative to ( A ) input or ( B ) mock-infected controls by RT-qPCR. Data are shown as mean ± SD. A two-tailed unpaired t -test was used for statistical analysis ( P values are shown on the figures).

Article Snippet: Antibodies used for immunoblotting were as follows: HIV-1 p24 (clone #24-2, the AIDS Research and Reference Reagent Program, NIH), GAPDH (AHP1628, Bio-Rad), METTL3 (15073, Proteintech), METTL14 (CL4252, Abcam), PLIN3 (10694-1-AP, Proteintech), and HIV-Ig (3957, the AIDS Research and Reference Reagent Program, NIH).

Techniques: Modification, Infection, Isolation, Quantitative RT-PCR, Two Tailed Test

HIV-1 infection increases PLIN3 mRNA levels but decreases PLIN3 protein levels in primary CD4 + T cells. ( A–D ) Primary CD4 + T cells were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. The HIV-1 reverse transcription inhibitor NVP was used to block viral replication (HIV-1 + NVP). GAPDH was used as a loading control. ( A ) PLIN3 and HIV-1 protein expression were measured by IB. A representative IB is shown. ( B ) Relative levels of PLIN3 protein expression normalized with GAPDH, as shown in ( A ), from three individual donors. ( C ) PLIN3 mRNA levels were measured by RT-qPCR. N = 6 (Mock, HIV-1) or N = 3 (HIV-1 + NVP). ( D ) Cells were treated with actinomycin D at 96 hpi. Samples were collected at the indicated time points, and PLIN3 mRNA levels were detected by RT-qPCR. Data are shown as means ± SD of results from three donors’ cells (raw data in ). Ordinary one-way ANOVA with Dunnett correction (B, and C) and multiple unpaired t -test ( D ) were used for statistical analysis ( P values are shown on figures). ns, not significant. * P < 0.05.

Journal: Journal of Virology

Article Title: Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells

doi: 10.1128/jvi.01536-25

Figure Lengend Snippet: HIV-1 infection increases PLIN3 mRNA levels but decreases PLIN3 protein levels in primary CD4 + T cells. ( A–D ) Primary CD4 + T cells were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. The HIV-1 reverse transcription inhibitor NVP was used to block viral replication (HIV-1 + NVP). GAPDH was used as a loading control. ( A ) PLIN3 and HIV-1 protein expression were measured by IB. A representative IB is shown. ( B ) Relative levels of PLIN3 protein expression normalized with GAPDH, as shown in ( A ), from three individual donors. ( C ) PLIN3 mRNA levels were measured by RT-qPCR. N = 6 (Mock, HIV-1) or N = 3 (HIV-1 + NVP). ( D ) Cells were treated with actinomycin D at 96 hpi. Samples were collected at the indicated time points, and PLIN3 mRNA levels were detected by RT-qPCR. Data are shown as means ± SD of results from three donors’ cells (raw data in ). Ordinary one-way ANOVA with Dunnett correction (B, and C) and multiple unpaired t -test ( D ) were used for statistical analysis ( P values are shown on figures). ns, not significant. * P < 0.05.

Techniques: Infection, Reverse Transcription, Blocking Assay, Control, Expressing, Quantitative RT-PCR

$HIV-1 infection increases the levels of PLIN3 mRNA in the nucleus of primary CD4 + T cells. ( A–D ) Activated primary CD4 + T cells from three healthy donors were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. Each dot represents the result from one donor’s cells. Data are shown as means ± SD. ( A ) PLIN3 mRNA levels in total cell lysates were measured by RT-qPCR and normalized with GAPDH. ( B ) MALAT1 lncRNA and HPRT mRNA levels from each fraction were measured by RT-qPCR to confirm successful separation of the nucleus and cytoplasm, respectively. ( C and D ) Cellular RNA was separated into nuclear and cytoplasmic fractions prior to RT-qPCR analysis. PLIN3 mRNA levels from the nuclear and cytoplasmic fractions are shown relative to MALAT1 and HPRT , respectively. A two-tailed unpaired t -test was used for statistical analysis. P value is shown on the figure. ns, not significant.$

Journal: Journal of Virology

Article Title: Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells

doi: 10.1128/jvi.01536-25

Figure Lengend Snippet: HIV-1 infection increases the levels of PLIN3 mRNA in the nucleus of primary CD4 + T cells. ( A–D ) Activated primary CD4 + T cells from three healthy donors were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. Each dot represents the result from one donor’s cells. Data are shown as means ± SD. ( A ) PLIN3 mRNA levels in total cell lysates were measured by RT-qPCR and normalized with GAPDH. ( B ) MALAT1 lncRNA and HPRT mRNA levels from each fraction were measured by RT-qPCR to confirm successful separation of the nucleus and cytoplasm, respectively. ( C and D ) Cellular RNA was separated into nuclear and cytoplasmic fractions prior to RT-qPCR analysis. PLIN3 mRNA levels from the nuclear and cytoplasmic fractions are shown relative to MALAT1 and HPRT , respectively. A two-tailed unpaired t -test was used for statistical analysis. P value is shown on the figure. ns, not significant.

Techniques: Infection, Quantitative RT-PCR, Two Tailed Test

$Polysome profile analysis of HIV-1-infected primary CD4 + T cells from three donors. ( A–E ) Activated primary CD4 + T cells from three healthy donors were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. ( A ) Polysome profile analysis (fractions 1-10, from top to bottom of the sucrose gradient). ( B–D ) Relative mRNA levels of ( B ) HIV-1 gag, ( C ) HPRT, and ( D ) PLIN3 from each fraction were measured by RT-qPCR. ( E ) Relative abundance of PLIN3 and HPRT in combined fractions 9 and 10 was measured by RT-qPCR. A two-tailed unpaired t -test was used for statistical analysis. P value is shown on the figure. ns, not significant. ( B–E ) The total detected quantity of a transcript in all fractions is set to 100% and the proportion of transcript found in each fraction ( B–D ) or combined two fractions ( E ) is represented as a percentage.$

Journal: Journal of Virology

Article Title: Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells

doi: 10.1128/jvi.01536-25

Figure Lengend Snippet: Polysome profile analysis of HIV-1-infected primary CD4 + T cells from three donors. ( A–E ) Activated primary CD4 + T cells from three healthy donors were mock-infected or infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. ( A ) Polysome profile analysis (fractions 1-10, from top to bottom of the sucrose gradient). ( B–D ) Relative mRNA levels of ( B ) HIV-1 gag, ( C ) HPRT, and ( D ) PLIN3 from each fraction were measured by RT-qPCR. ( E ) Relative abundance of PLIN3 and HPRT in combined fractions 9 and 10 was measured by RT-qPCR. A two-tailed unpaired t -test was used for statistical analysis. P value is shown on the figure. ns, not significant. ( B–E ) The total detected quantity of a transcript in all fractions is set to 100% and the proportion of transcript found in each fraction ( B–D ) or combined two fractions ( E ) is represented as a percentage.

Techniques: Infection, Quantitative RT-PCR, Two Tailed Test

Knockdown of PLIN3 in primary CD4 + T cells decreases HIV-1 production but increases viral infectivity. ( A–D ) Primary CD4 + T cells were transduced with lentiviral vectors expressing non-targeting (Ctrl) or PLIN3 small guide (sg) RNA to achieve partial stable knockdown of PLIN3. Cells were then infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. ( A ) Relative levels of PLIN3 expression and HIV-1 infection were measured by IB in cells from three independent donors. ( B ) Relative quantification of PLIN3 protein expression is shown in ( A ). ( C ) Relative levels of HIV-1 protein expression are shown in ( A ). ( D ) Cell supernatant p24 levels from HIV-1-infected cells were quantified by ELISA. ( E ) TZM-bl cells were infected with HIV-1 collected from sgCtrl or sgPLIN3 cell culture supernatants. Luciferase activity was measured at 48 hpi. ( F–H ) Primary activated CD4 + T cells from one additional donor were nucleofected with control crRNA or one of three different crRNAs specifically targeting PLIN3 . ( F ) Western blot analysis of PLIN3 knockdown efficiency. GAPDH was used as a loading control. Relative PLIN3 levels were normalized to GAPDH. ( G ) The cells used in ( F ) were subsequently infected with HIV-1 NL4-3 at an MOI of 1 for 96 h, and p24 levels in the supernatant were measured by ELISA. ( H ) TZM-bl cells were infected with HIV-1 collected from Ctrl or crPLIN3 cell culture supernatants. Luciferase activity was measured at 48 hpi and normalized to protein amounts. Data are shown as means ± SD from three individual donors or 2–4 technical replicates. A two-tailed unpaired t -test ( B ), multiple unpaired t -test ( C–E ), and one-way ANOVA ( G and H ) were used for statistical analysis ( P values are shown on figures). ns, not significant.

Journal: Journal of Virology

Article Title: Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells

doi: 10.1128/jvi.01536-25

Figure Lengend Snippet: Knockdown of PLIN3 in primary CD4 + T cells decreases HIV-1 production but increases viral infectivity. ( A–D ) Primary CD4 + T cells were transduced with lentiviral vectors expressing non-targeting (Ctrl) or PLIN3 small guide (sg) RNA to achieve partial stable knockdown of PLIN3. Cells were then infected with HIV-1 NL4–3 at an MOI of 1 for 96 h. ( A ) Relative levels of PLIN3 expression and HIV-1 infection were measured by IB in cells from three independent donors. ( B ) Relative quantification of PLIN3 protein expression is shown in ( A ). ( C ) Relative levels of HIV-1 protein expression are shown in ( A ). ( D ) Cell supernatant p24 levels from HIV-1-infected cells were quantified by ELISA. ( E ) TZM-bl cells were infected with HIV-1 collected from sgCtrl or sgPLIN3 cell culture supernatants. Luciferase activity was measured at 48 hpi. ( F–H ) Primary activated CD4 + T cells from one additional donor were nucleofected with control crRNA or one of three different crRNAs specifically targeting PLIN3 . ( F ) Western blot analysis of PLIN3 knockdown efficiency. GAPDH was used as a loading control. Relative PLIN3 levels were normalized to GAPDH. ( G ) The cells used in ( F ) were subsequently infected with HIV-1 NL4-3 at an MOI of 1 for 96 h, and p24 levels in the supernatant were measured by ELISA. ( H ) TZM-bl cells were infected with HIV-1 collected from Ctrl or crPLIN3 cell culture supernatants. Luciferase activity was measured at 48 hpi and normalized to protein amounts. Data are shown as means ± SD from three individual donors or 2–4 technical replicates. A two-tailed unpaired t -test ( B ), multiple unpaired t -test ( C–E ), and one-way ANOVA ( G and H ) were used for statistical analysis ( P values are shown on figures). ns, not significant.

Techniques: Knockdown, Infection, Transduction, Expressing, Quantitative Proteomics, Enzyme-linked Immunosorbent Assay, Cell Culture, Luciferase, Activity Assay, Control, Western Blot, Two Tailed Test

Summary and proposed model. In primary CD4 + T cells, HIV-1 infection promotes the interaction between METTL3 and METTL14. HIV-1 infection increases m 6 A level and nuclear accumulation of PLIN3 mRNA but reduces PLIN3 protein expression and translation efficiency. Knockdown of PLIN3 in primary CD4 + T cells decreases HIV-1 release but increases viral infectivity in TZM-bl cells. Ctrl, control; KD, knockdown.

Journal: Journal of Virology

Article Title: Single-base m 6 A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4 + T cells

doi: 10.1128/jvi.01536-25

Figure Lengend Snippet: Summary and proposed model. In primary CD4 + T cells, HIV-1 infection promotes the interaction between METTL3 and METTL14. HIV-1 infection increases m 6 A level and nuclear accumulation of PLIN3 mRNA but reduces PLIN3 protein expression and translation efficiency. Knockdown of PLIN3 in primary CD4 + T cells decreases HIV-1 release but increases viral infectivity in TZM-bl cells. Ctrl, control; KD, knockdown.

Techniques: Infection, Expressing, Knockdown, Control

Differential expression of PLIN3 and its prognostic potential across various cancers. ( A ) Comparison of PLIN3 levels in tumor versus normal tissue samples from GTEx and TCGA databases. ( B ) PLIN3 mRNA expression in paired tumor and normal samples from TCGA. ( C ) PLIN3 expression profiles across various organs comparing tumor and normal tissues. ( D ) Diagnostic ROC curves evaluating PLIN3 as a biomarker across multiple cancers. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Differential expression of PLIN3 and its prognostic potential across various cancers. ( A ) Comparison of PLIN3 levels in tumor versus normal tissue samples from GTEx and TCGA databases. ( B ) PLIN3 mRNA expression in paired tumor and normal samples from TCGA. ( C ) PLIN3 expression profiles across various organs comparing tumor and normal tissues. ( D ) Diagnostic ROC curves evaluating PLIN3 as a biomarker across multiple cancers. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Article Snippet: After deparaffinization and blocking with 5% bovine serum albumin, sections were treated with primary antibodies against PLIN3 (1:500, Proteintech; 10694-1-AP) and either CD163 (1:500, ImmunoWay, YM6146) or CD68 (1:500, ImmunoWay, YM3050).

Techniques: Quantitative Proteomics, Comparison, Expressing, Diagnostic Assay, Biomarker Discovery

Differential analysis of PLIN3 protein levels. ( A ) Wilcoxon Rank Sum Tests to compare the statistical differences in expression levels between the tumor and normal groups from the CPTAC dataset. ( B ) IHC images of PLIN3 staining sourced from the Human Protein Atlas. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Differential analysis of PLIN3 protein levels. ( A ) Wilcoxon Rank Sum Tests to compare the statistical differences in expression levels between the tumor and normal groups from the CPTAC dataset. ( B ) IHC images of PLIN3 staining sourced from the Human Protein Atlas. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Techniques: Expressing, Staining

Survival analysis correlating PLIN3 expression with patient outcomes in pan-cancer. ( A–D ) Forest plots displaying the prognostic significance of PLIN3 for OS, DSS, DFI, and PFI via univariate Cox regression analysis. ( E ) Kaplan-Meier plots for OS, with the red and blue lines representing high and low PLIN3 expression groups, respectively. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Survival analysis correlating PLIN3 expression with patient outcomes in pan-cancer. ( A–D ) Forest plots displaying the prognostic significance of PLIN3 for OS, DSS, DFI, and PFI via univariate Cox regression analysis. ( E ) Kaplan-Meier plots for OS, with the red and blue lines representing high and low PLIN3 expression groups, respectively. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Techniques: Expressing

Genetic alterations of PLIN3 across various cancers. ( A ) Overview of PLIN3 mutation types using data from the COSMIC database. ( B ) Mutation frequency of PLIN3 across different cancer types. ( C ) Detailed mapping of PLIN3 genetic alterations, including sites and numbers, sourced from cBioPortal. ( D ) Histogram depicting the frequency of somatic copy number alterations of PLIN3 in each cancer type. ( E ) Analysis of differential PLIN3 expression across various CNV types in pan-cancer. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Genetic alterations of PLIN3 across various cancers. ( A ) Overview of PLIN3 mutation types using data from the COSMIC database. ( B ) Mutation frequency of PLIN3 across different cancer types. ( C ) Detailed mapping of PLIN3 genetic alterations, including sites and numbers, sourced from cBioPortal. ( D ) Histogram depicting the frequency of somatic copy number alterations of PLIN3 in each cancer type. ( E ) Analysis of differential PLIN3 expression across various CNV types in pan-cancer. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Techniques: Mutagenesis, Expressing

Associations of PLIN3 with DNA repair, stemness, and epigenetic modifications. ( A ) Heatmap illustrating correlations between PLIN3 and five MMR-related genes. ( B ) Lollipop chart detailing the correlation of PLIN3 levels with DNA methylation-based stem scores. ( C ) Bar chart showing the correlation of PLIN3 levels with RNA methylation-based stem scores. ( D ) Heatmap of the relationships between PLIN3 levels and RNA modifications. ( E ) Heatmap displaying associations of PLIN3 with four methyltransferases. ( F ) Radar chart presenting the Spearman correlation between PLIN3 expression levels and TMB across pan-cancer. ( G ) Radar chart showing the Spearman correlation between PLIN3 expression levels and MSI across pan-cancer. ( H ) Heatmap displaying relationships between PLIN3 expression and ESTIMATE, Immune, and Stromal scores, with statistical significance indicated as *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Associations of PLIN3 with DNA repair, stemness, and epigenetic modifications. ( A ) Heatmap illustrating correlations between PLIN3 and five MMR-related genes. ( B ) Lollipop chart detailing the correlation of PLIN3 levels with DNA methylation-based stem scores. ( C ) Bar chart showing the correlation of PLIN3 levels with RNA methylation-based stem scores. ( D ) Heatmap of the relationships between PLIN3 levels and RNA modifications. ( E ) Heatmap displaying associations of PLIN3 with four methyltransferases. ( F ) Radar chart presenting the Spearman correlation between PLIN3 expression levels and TMB across pan-cancer. ( G ) Radar chart showing the Spearman correlation between PLIN3 expression levels and MSI across pan-cancer. ( H ) Heatmap displaying relationships between PLIN3 expression and ESTIMATE, Immune, and Stromal scores, with statistical significance indicated as *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Techniques: DNA Methylation Assay, Methylation, Expressing

Functional analysis of PLIN3 in human cancers using GSEA. Bubble plot illustrating differential enrichment of hallmark gene sets between PLIN3-high and -low tumor patients. Circle size corresponds to the magnitude of the P-value, while color transitions from red to white to blue indicate the strength of NES. The red boxes highlight key pathways that are significantly enriched in PLIN3-high tumor patients, emphasizing their potential biological importance in cancer progression. Abbreviation list of tumor cohorts from TCGA is given in Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Functional analysis of PLIN3 in human cancers using GSEA. Bubble plot illustrating differential enrichment of hallmark gene sets between PLIN3-high and -low tumor patients. Circle size corresponds to the magnitude of the P-value, while color transitions from red to white to blue indicate the strength of NES. The red boxes highlight key pathways that are significantly enriched in PLIN3-high tumor patients, emphasizing their potential biological importance in cancer progression. Abbreviation list of tumor cohorts from TCGA is given in Supplementary Table 1 .

Techniques: Functional Assay

Correlation analysis between PLIN3 expression and immune cell infiltration. ( A ) Heatmap showing correlations between PLIN3 mRNA expression and the expression of chemokines, chemokine receptors, immune-inhibitors, immune-stimulatory, and MHC genes. ( B ) Heatmaps displaying correlations between PLIN3 expression and infiltration levels of various immune cells. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Correlation analysis between PLIN3 expression and immune cell infiltration. ( A ) Heatmap showing correlations between PLIN3 mRNA expression and the expression of chemokines, chemokine receptors, immune-inhibitors, immune-stimulatory, and MHC genes. ( B ) Heatmaps displaying correlations between PLIN3 expression and infiltration levels of various immune cells. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Techniques: Expressing

PLIN3 as a Potential Marker of M2 Macrophage Infiltration. ( A ) Heatmap showing PLIN3 gene expression across various microdomains in pan-cancer spatial transcriptomic sections. Rows represent different datasets, each labeled in a color specific to the disease type. Columns represent different cell types, with the color intensity on the right scale indicating data values—darker red signifies higher values, and lighter colors indicate lower values. Gray indicates that the cell type is absent in the microregion. The red boxes highlight PLIN3’s widespread expression in macrophage and malignant cell types. ( B ) Spearman correlation analysis used to calculate the correlation between cell content across all spots and between cell content and gene expression levels. Red lines indicate positive correlations, green lines indicate negative correlations, and gray lines indicate non-significant correlations. Line thickness represents the magnitude of the correlation coefficient ( C ) Spatial transcriptomics exploring co-localization patterns of PLIN3 with CD68 and CD163, color-coded by expression levels. Each dot represents a microdomain (spot) with deeper red indicating higher gene expression. ( D ) Expression of PLIN3 in cancer-specific single-cell clusters analyzed using the TISCH database. The red boxes highlight PLIN3’s widespread expression in monocyte, macrophage and malignant cell types. ( E-F ) UMAP plots detailing cell type distributions and PLIN3 intensity in KIRC ( E ) and NSCLC ( F ). Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: PLIN3 as a Potential Marker of M2 Macrophage Infiltration. ( A ) Heatmap showing PLIN3 gene expression across various microdomains in pan-cancer spatial transcriptomic sections. Rows represent different datasets, each labeled in a color specific to the disease type. Columns represent different cell types, with the color intensity on the right scale indicating data values—darker red signifies higher values, and lighter colors indicate lower values. Gray indicates that the cell type is absent in the microregion. The red boxes highlight PLIN3’s widespread expression in macrophage and malignant cell types. ( B ) Spearman correlation analysis used to calculate the correlation between cell content across all spots and between cell content and gene expression levels. Red lines indicate positive correlations, green lines indicate negative correlations, and gray lines indicate non-significant correlations. Line thickness represents the magnitude of the correlation coefficient ( C ) Spatial transcriptomics exploring co-localization patterns of PLIN3 with CD68 and CD163, color-coded by expression levels. Each dot represents a microdomain (spot) with deeper red indicating higher gene expression. ( D ) Expression of PLIN3 in cancer-specific single-cell clusters analyzed using the TISCH database. The red boxes highlight PLIN3’s widespread expression in monocyte, macrophage and malignant cell types. ( E-F ) UMAP plots detailing cell type distributions and PLIN3 intensity in KIRC ( E ) and NSCLC ( F ). Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Techniques: Marker, Gene Expression, Labeling, Expressing

Investigation of PLIN3’s role in regulating malignancy in LUAD tumor cells. ( A ) Fluorescent staining of tumor tissues showing CD68 (red) and PLIN3 (green), with DAPI (blue) for counterstaining. ( B ) Fluorescent images of tumor tissues with CD163 (red) and PLIN3 (green), counterstained with DAPI (blue). ( C ) PLIN3 mRNA expression levels in transfected cells. ( D ) Colony formation assay to evaluate the impact of PLIN3 on tumor cell proliferation. ( E ) Wound healing assay assessing the effect of PLIN3 knockdown on tumor cell migration.

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Investigation of PLIN3’s role in regulating malignancy in LUAD tumor cells. ( A ) Fluorescent staining of tumor tissues showing CD68 (red) and PLIN3 (green), with DAPI (blue) for counterstaining. ( B ) Fluorescent images of tumor tissues with CD163 (red) and PLIN3 (green), counterstained with DAPI (blue). ( C ) PLIN3 mRNA expression levels in transfected cells. ( D ) Colony formation assay to evaluate the impact of PLIN3 on tumor cell proliferation. ( E ) Wound healing assay assessing the effect of PLIN3 knockdown on tumor cell migration.

Techniques: Staining, Expressing, Transfection, Colony Assay, Wound Healing Assay, Knockdown, Migration

Drug Sensitivity Analysis. ( A ) Bubble plot illustrating correlations between PLIN3 expressions and drug sensitivity across various databases. A p-value < 0.05 was considered statistically significant. ( B ) The heatmap illustrates potential compounds that target PLIN3, identified using CMap analysis across various cancers. ( C ) Identification of PLIN3-targeting compounds through CMap analysis for LUAD. ( D ) 3D molecular docking illustrations showing interactions between PLIN3 and compound clofibrate. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Journal: Journal of Inflammation Research

Article Title: The Role of PLIN3 in Prognosis and Tumor-Associated Macrophage Infiltration: A Pan-Cancer Analysis

doi: 10.2147/JIR.S509245

Figure Lengend Snippet: Drug Sensitivity Analysis. ( A ) Bubble plot illustrating correlations between PLIN3 expressions and drug sensitivity across various databases. A p-value < 0.05 was considered statistically significant. ( B ) The heatmap illustrates potential compounds that target PLIN3, identified using CMap analysis across various cancers. ( C ) Identification of PLIN3-targeting compounds through CMap analysis for LUAD. ( D ) 3D molecular docking illustrations showing interactions between PLIN3 and compound clofibrate. Abbreviation list of tumor cohorts from TCGA is given in. Supplementary Table 1 .

Techniques:

Review

Structured Review

Images

Similar Products

Image Search Results