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anti gdf15 blocking antibody  (MedChemExpress)


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    Structured Review

    MedChemExpress anti gdf15 blocking antibody
    A: UMAP of 6 individual clinical UM “and healthy” scRNA-seq datasets. Data shows major cell types identified and then <t>GDF15</t> expression in the UM cells (malignant cells) B: Violin plots showing expression of GDF15 in a scRNA-Seq analysis of human Class 1 and Class 2 UM. C: Western Blot showing the expression of BAP1, PRAME and GDF15 in a panel of UM cell lines. D: Silencing of BAP1 is associated with increased expression of GDF15 in Mel202 and 92.1 UM cells. BAP1 was silenced using siRNA and resulting lysates probed for expression of BAP1 and GDF15. E: ChIP-Seq analysis of Mel202 cells expressing BAP1 or silenced for BAP1 demonstrates an increase in H3K27ac at the GDF15 promoter following BAP1 knockdown. F: Analysis of GDF15 secretion by ELISA assay demonstrates that co-culture of UM cells with HSCs is associated with increased GDF15 expression, even in UM cell lines with high basal expression of GDF15. Cell lines derived from primary or metastatic specimens are indicated.
    Anti Gdf15 Blocking Antibody, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+gdf15/Ponsegromab/pmc13343499-157-12-18
    Average 94 stars, based on 7 article reviews
    anti gdf15 blocking antibody - by Bioz Stars, 2026-11
    94/100 stars

    Images

    1) Product Images from "GDF15 Reprograms the Microenvironment to Drive Liver Metastasis of Uveal Melanoma"

    Article Title: GDF15 Reprograms the Microenvironment to Drive Liver Metastasis of Uveal Melanoma

    Journal: Cancer research

    doi: 10.1158/0008-5472.CAN-25-0536

    A: UMAP of 6 individual clinical UM “and healthy” scRNA-seq datasets. Data shows major cell types identified and then GDF15 expression in the UM cells (malignant cells) B: Violin plots showing expression of GDF15 in a scRNA-Seq analysis of human Class 1 and Class 2 UM. C: Western Blot showing the expression of BAP1, PRAME and GDF15 in a panel of UM cell lines. D: Silencing of BAP1 is associated with increased expression of GDF15 in Mel202 and 92.1 UM cells. BAP1 was silenced using siRNA and resulting lysates probed for expression of BAP1 and GDF15. E: ChIP-Seq analysis of Mel202 cells expressing BAP1 or silenced for BAP1 demonstrates an increase in H3K27ac at the GDF15 promoter following BAP1 knockdown. F: Analysis of GDF15 secretion by ELISA assay demonstrates that co-culture of UM cells with HSCs is associated with increased GDF15 expression, even in UM cell lines with high basal expression of GDF15. Cell lines derived from primary or metastatic specimens are indicated.
    Figure Legend Snippet: A: UMAP of 6 individual clinical UM “and healthy” scRNA-seq datasets. Data shows major cell types identified and then GDF15 expression in the UM cells (malignant cells) B: Violin plots showing expression of GDF15 in a scRNA-Seq analysis of human Class 1 and Class 2 UM. C: Western Blot showing the expression of BAP1, PRAME and GDF15 in a panel of UM cell lines. D: Silencing of BAP1 is associated with increased expression of GDF15 in Mel202 and 92.1 UM cells. BAP1 was silenced using siRNA and resulting lysates probed for expression of BAP1 and GDF15. E: ChIP-Seq analysis of Mel202 cells expressing BAP1 or silenced for BAP1 demonstrates an increase in H3K27ac at the GDF15 promoter following BAP1 knockdown. F: Analysis of GDF15 secretion by ELISA assay demonstrates that co-culture of UM cells with HSCs is associated with increased GDF15 expression, even in UM cell lines with high basal expression of GDF15. Cell lines derived from primary or metastatic specimens are indicated.

    Techniques Used: Expressing, Western Blot, ChIP-sequencing, Knockdown, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Derivative Assay

    A: RNA-seq analysis of HSCs (LX2) treated with GDF15 (1μg/ml, 24 hr) identifies increased expression of genes encoding multiple ECM proteins ( COL7A1 ), and molecules involved in angiogenesis ( VCAM1, ANGPLT4, PDGFB, FLT1 ). B: Pathway analysis identifies GDF15 to increase expression of genes involved in inflammatory signaling ( TNFA, IFNγ, IL6 ), angiogenesis (hypoxia, angiogenesis) and metabolism. C: Human primary HSCs (HHStec) were stimulated with either GDF15 (1μg/ml) or SPP1 (osteopontin, (1μg/ml)) for 24 hr and Western Blotting used to determine expression of IL-8 and phospho-STAT3. D: HSC (HHStec cells) were grown in monoculture, MP41 cells were grown in monoculture, HSC+MP41 cells were grown in co-culture, HSCs were treated with conditioned media (CM) from MP41 cells or GDF15 (1μg/ml) for 24 hr before probing for the expression of COL1A1 and PDGFRB by Western Blot. E: Immunofluorescence staining of COL1A1 in HSCs (HHStec) cells treated with basal media or conditioned media from MP41 or UMM061 cells. F: CellChat analysis of human UM samples identifies HSC-derived collagens as being a potential outgoing signal to multiple immune subtypes and UM cells.
    Figure Legend Snippet: A: RNA-seq analysis of HSCs (LX2) treated with GDF15 (1μg/ml, 24 hr) identifies increased expression of genes encoding multiple ECM proteins ( COL7A1 ), and molecules involved in angiogenesis ( VCAM1, ANGPLT4, PDGFB, FLT1 ). B: Pathway analysis identifies GDF15 to increase expression of genes involved in inflammatory signaling ( TNFA, IFNγ, IL6 ), angiogenesis (hypoxia, angiogenesis) and metabolism. C: Human primary HSCs (HHStec) were stimulated with either GDF15 (1μg/ml) or SPP1 (osteopontin, (1μg/ml)) for 24 hr and Western Blotting used to determine expression of IL-8 and phospho-STAT3. D: HSC (HHStec cells) were grown in monoculture, MP41 cells were grown in monoculture, HSC+MP41 cells were grown in co-culture, HSCs were treated with conditioned media (CM) from MP41 cells or GDF15 (1μg/ml) for 24 hr before probing for the expression of COL1A1 and PDGFRB by Western Blot. E: Immunofluorescence staining of COL1A1 in HSCs (HHStec) cells treated with basal media or conditioned media from MP41 or UMM061 cells. F: CellChat analysis of human UM samples identifies HSC-derived collagens as being a potential outgoing signal to multiple immune subtypes and UM cells.

    Techniques Used: Expressing, RNA Sequencing, Western Blot, Co-Culture Assay, Immunofluorescence, Staining, Derivative Assay

    A: CellChat analysis of scRNA-Seq from human UM identifies endothelial cells as being a major target of secreted GDF15. B: Exogenous GDF15 and IL8 increase vascular network formation. HUVEC cells were plated on Matrigel and treated with basal media, IL-8 or GDF15 (both 1μg/ml for 0–24 hr). C: Scoring of endothelial network formation data from B. D: Conditioned media (CM) from UM-HSC co-cultures increases vascular network formation. HUVECs were plated onto Matrigel and treated with basal media or CM from MP41, UMM061 and MM28 cells grown in co-culture with LX2 cells. E: Vascular network formation from D was quantified. F: GDF15-blocking antibodies reverse the pro-angiogenic effects of CM. HUVEC cells were treated with CM from MP41-LX2 co-cultures in the absence and presence of the GDF15 blocking antibody (Ponsegromab,120ng/ml) and vascular network formation imaged. G : Quantification of endothelial cell network formation from F.
    Figure Legend Snippet: A: CellChat analysis of scRNA-Seq from human UM identifies endothelial cells as being a major target of secreted GDF15. B: Exogenous GDF15 and IL8 increase vascular network formation. HUVEC cells were plated on Matrigel and treated with basal media, IL-8 or GDF15 (both 1μg/ml for 0–24 hr). C: Scoring of endothelial network formation data from B. D: Conditioned media (CM) from UM-HSC co-cultures increases vascular network formation. HUVECs were plated onto Matrigel and treated with basal media or CM from MP41, UMM061 and MM28 cells grown in co-culture with LX2 cells. E: Vascular network formation from D was quantified. F: GDF15-blocking antibodies reverse the pro-angiogenic effects of CM. HUVEC cells were treated with CM from MP41-LX2 co-cultures in the absence and presence of the GDF15 blocking antibody (Ponsegromab,120ng/ml) and vascular network formation imaged. G : Quantification of endothelial cell network formation from F.

    Techniques Used: Co-Culture Assay, Blocking Assay

    A: IVIS imaging of mice with either shCRTL or shGDF15#2 MP41 cells at days 49 and 77, respectively. B: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 MP41 cells. C: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) MP41 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. D: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced MP41 cells (GDF15 shRNA#1 and shRNA#2). E: IVIS imaging of mice with either shCRTL or shGDF15#2 OMM1 cells at days 56 and 70, respectively. F: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 OMM1 cells. G: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) OMM1 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. H: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced OMM1 cells (GDF15 shRNA#1 and shRNA#2).
    Figure Legend Snippet: A: IVIS imaging of mice with either shCRTL or shGDF15#2 MP41 cells at days 49 and 77, respectively. B: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 MP41 cells. C: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) MP41 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. D: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced MP41 cells (GDF15 shRNA#1 and shRNA#2). E: IVIS imaging of mice with either shCRTL or shGDF15#2 OMM1 cells at days 56 and 70, respectively. F: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 OMM1 cells. G: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) OMM1 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. H: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced OMM1 cells (GDF15 shRNA#1 and shRNA#2).

    Techniques Used: Imaging, Injection, Staining, shRNA, Expressing

    A: H&E staining of livers from the eye to liver metastasis model, demonstrating fewer and smaller liver lesions following GDF15 shRNA silencing (shGDF15#1). B: Quantification of the size and number of liver metastases from A. C: IHC staining of liver metastases for fibronectin in MP41 tumors either expressing or with GDF15 silenced. D: Quantification of data from C. E: IHC staining of liver metastases from MP41 tumors for the ECM protein Collagen 1A1. F: Quantification of data from F. G: IHC staining of liver metastases for Ki67 in MP41 tumors either expressing or with GDF15 silenced. H: Quantification of data from G. I: IHC staining of liver metastases for the endothelial cell marker CD31 in MP41 tumors either expressing or with GDF15 silenced. J: Quantification of data from I.
    Figure Legend Snippet: A: H&E staining of livers from the eye to liver metastasis model, demonstrating fewer and smaller liver lesions following GDF15 shRNA silencing (shGDF15#1). B: Quantification of the size and number of liver metastases from A. C: IHC staining of liver metastases for fibronectin in MP41 tumors either expressing or with GDF15 silenced. D: Quantification of data from C. E: IHC staining of liver metastases from MP41 tumors for the ECM protein Collagen 1A1. F: Quantification of data from F. G: IHC staining of liver metastases for Ki67 in MP41 tumors either expressing or with GDF15 silenced. H: Quantification of data from G. I: IHC staining of liver metastases for the endothelial cell marker CD31 in MP41 tumors either expressing or with GDF15 silenced. J: Quantification of data from I.

    Techniques Used: Staining, shRNA, Immunohistochemistry, Expressing, Marker

    Related Articles

    Blocking Assay:

    Article Title: Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms.
    Article Snippet: .. To block SASP- associated cytokine signaling, mice were injected intraperitoneally 24 h before infection with: anti- IL6R (clone 15A7, MCE), 300 μg/mouse; anti- GDF15 (Ponsegromab, Taoshu), 200 μg/mouse; and anti- IGF1R (Ganitumab, Taoshu), 250 μg/mouse; and the natural IL- 1 receptor antagonistic protein IL1Ra (Raleukin, MCE), 500 μg/mouse. ..

    Article Title: Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms
    Article Snippet: .. To block SASP‐associated cytokine signaling, mice were injected intraperitoneally 24 h before infection with: anti‐IL6R (clone 15A7, MCE), 300 μg/mouse; anti‐GDF15 (Ponsegromab, Taoshu), 200 μg/mouse; and anti‐IGF1R (Ganitumab, Taoshu), 250 μg/mouse; and the natural IL‐1 receptor antagonistic protein IL1Ra (Raleukin, MCE), 500 μg/mouse. ..

    Injection:

    Article Title: Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms.
    Article Snippet: .. To block SASP- associated cytokine signaling, mice were injected intraperitoneally 24 h before infection with: anti- IL6R (clone 15A7, MCE), 300 μg/mouse; anti- GDF15 (Ponsegromab, Taoshu), 200 μg/mouse; and anti- IGF1R (Ganitumab, Taoshu), 250 μg/mouse; and the natural IL- 1 receptor antagonistic protein IL1Ra (Raleukin, MCE), 500 μg/mouse. ..

    Article Title: Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms
    Article Snippet: .. To block SASP‐associated cytokine signaling, mice were injected intraperitoneally 24 h before infection with: anti‐IL6R (clone 15A7, MCE), 300 μg/mouse; anti‐GDF15 (Ponsegromab, Taoshu), 200 μg/mouse; and anti‐IGF1R (Ganitumab, Taoshu), 250 μg/mouse; and the natural IL‐1 receptor antagonistic protein IL1Ra (Raleukin, MCE), 500 μg/mouse. ..

    Infection:

    Article Title: Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms.
    Article Snippet: .. To block SASP- associated cytokine signaling, mice were injected intraperitoneally 24 h before infection with: anti- IL6R (clone 15A7, MCE), 300 μg/mouse; anti- GDF15 (Ponsegromab, Taoshu), 200 μg/mouse; and anti- IGF1R (Ganitumab, Taoshu), 250 μg/mouse; and the natural IL- 1 receptor antagonistic protein IL1Ra (Raleukin, MCE), 500 μg/mouse. ..

    Article Title: Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms
    Article Snippet: .. To block SASP‐associated cytokine signaling, mice were injected intraperitoneally 24 h before infection with: anti‐IL6R (clone 15A7, MCE), 300 μg/mouse; anti‐GDF15 (Ponsegromab, Taoshu), 200 μg/mouse; and anti‐IGF1R (Ganitumab, Taoshu), 250 μg/mouse; and the natural IL‐1 receptor antagonistic protein IL1Ra (Raleukin, MCE), 500 μg/mouse. ..



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    Image Search Results


    The p38‐ATF3 axis mediates resveratrol‐induced GDF15 expression. (A) Volcano plot from RNA‐seq analysis of MEF cells treated with resveratrol (10 μM), highlighting Atf3 as a significantly upregulated transcript (A). ATF3 mRNA (B) and protein (C) expression in resveratrol‐treated MEF cells. Gdf15 mRNA levels in MEF cells transfected with control or Atf3 ‐targeting siRNA, followed by resveratrol treatment (D). KEGG pathway enrichment analysis of differentially expressed genes from RNA‐seq data (E). Gdf15 mRNA expression in MEF cells treated with a p38 inhibitor (SB203580, 10 μM) (F). Levels of ATF3, GDF15, p38, and p‐p38 proteins in HepG2 cells treated with resveratrol, a p38 inhibitor, or a combination of both (G). Data are mean ± SEM; * p < 0.05.

    Journal: Food Science & Nutrition

    Article Title: Resveratrol Attenuates Obesity by Inducing GDF15 Expression via the p38‐ ATF3 Signaling Pathway

    doi: 10.1002/fsn3.72052

    Figure Lengend Snippet: The p38‐ATF3 axis mediates resveratrol‐induced GDF15 expression. (A) Volcano plot from RNA‐seq analysis of MEF cells treated with resveratrol (10 μM), highlighting Atf3 as a significantly upregulated transcript (A). ATF3 mRNA (B) and protein (C) expression in resveratrol‐treated MEF cells. Gdf15 mRNA levels in MEF cells transfected with control or Atf3 ‐targeting siRNA, followed by resveratrol treatment (D). KEGG pathway enrichment analysis of differentially expressed genes from RNA‐seq data (E). Gdf15 mRNA expression in MEF cells treated with a p38 inhibitor (SB203580, 10 μM) (F). Levels of ATF3, GDF15, p38, and p‐p38 proteins in HepG2 cells treated with resveratrol, a p38 inhibitor, or a combination of both (G). Data are mean ± SEM; * p < 0.05.

    Article Snippet: Equal amounts of protein were separated by SDS‐PAGE, transferred to PVDF membranes, and probed with specific primary antibodies against GDF15 (Abclonal, A0185), ATF3 (Abclonal, A1852), P38MAPK (Abclonal, A4771), Phospho‐P38MAPK (Abclonal, AP1372), phospho‐ERK (CST, 4370), total ERK (CST, 4695), GAPDH (CST, 5174 T) and beta‐actin (ACTB) (Abclonal, AC026).

    Techniques: Expressing, RNA Sequencing, Transfection, Control

    Tissue induction of ATF3 and GDF15 by resveratrol in vivo. (A, B) Relative mRNA expression of Atf3 (A) and Gdf15 (B) in liver, kidney, and colon tissues from resveratrol‐treated mice. (C–E) Representative Western blots and quantification of GDF15 protein expression in kidney (C), liver (D), and colon (E) tissues. Data are mean ± SEM; * p < 0.05.

    Journal: Food Science & Nutrition

    Article Title: Resveratrol Attenuates Obesity by Inducing GDF15 Expression via the p38‐ ATF3 Signaling Pathway

    doi: 10.1002/fsn3.72052

    Figure Lengend Snippet: Tissue induction of ATF3 and GDF15 by resveratrol in vivo. (A, B) Relative mRNA expression of Atf3 (A) and Gdf15 (B) in liver, kidney, and colon tissues from resveratrol‐treated mice. (C–E) Representative Western blots and quantification of GDF15 protein expression in kidney (C), liver (D), and colon (E) tissues. Data are mean ± SEM; * p < 0.05.

    Article Snippet: Equal amounts of protein were separated by SDS‐PAGE, transferred to PVDF membranes, and probed with specific primary antibodies against GDF15 (Abclonal, A0185), ATF3 (Abclonal, A1852), P38MAPK (Abclonal, A4771), Phospho‐P38MAPK (Abclonal, AP1372), phospho‐ERK (CST, 4370), total ERK (CST, 4695), GAPDH (CST, 5174 T) and beta‐actin (ACTB) (Abclonal, AC026).

    Techniques: In Vivo, Expressing, Western Blot

    Proposed model for resveratrol‐induced body weight reduction via the GDF15 pathway. Schematic illustration summarizing the proposed mechanism: Resveratrol activates the p38 MAPK signaling pathway, leading to upregulation of ATF3. This transcription factor then promotes GDF15 expression and secretion in peripheral tissues. The elevated circulating GDF15 acts on the brain, potentially through activation of the ERK pathway in the hypothalamus, resulting in reduced food intake and subsequent protection against diet‐induced obesity.

    Journal: Food Science & Nutrition

    Article Title: Resveratrol Attenuates Obesity by Inducing GDF15 Expression via the p38‐ ATF3 Signaling Pathway

    doi: 10.1002/fsn3.72052

    Figure Lengend Snippet: Proposed model for resveratrol‐induced body weight reduction via the GDF15 pathway. Schematic illustration summarizing the proposed mechanism: Resveratrol activates the p38 MAPK signaling pathway, leading to upregulation of ATF3. This transcription factor then promotes GDF15 expression and secretion in peripheral tissues. The elevated circulating GDF15 acts on the brain, potentially through activation of the ERK pathway in the hypothalamus, resulting in reduced food intake and subsequent protection against diet‐induced obesity.

    Article Snippet: Equal amounts of protein were separated by SDS‐PAGE, transferred to PVDF membranes, and probed with specific primary antibodies against GDF15 (Abclonal, A0185), ATF3 (Abclonal, A1852), P38MAPK (Abclonal, A4771), Phospho‐P38MAPK (Abclonal, AP1372), phospho‐ERK (CST, 4370), total ERK (CST, 4695), GAPDH (CST, 5174 T) and beta‐actin (ACTB) (Abclonal, AC026).

    Techniques: Expressing, Activation Assay

    A: UMAP of 6 individual clinical UM “and healthy” scRNA-seq datasets. Data shows major cell types identified and then GDF15 expression in the UM cells (malignant cells) B: Violin plots showing expression of GDF15 in a scRNA-Seq analysis of human Class 1 and Class 2 UM. C: Western Blot showing the expression of BAP1, PRAME and GDF15 in a panel of UM cell lines. D: Silencing of BAP1 is associated with increased expression of GDF15 in Mel202 and 92.1 UM cells. BAP1 was silenced using siRNA and resulting lysates probed for expression of BAP1 and GDF15. E: ChIP-Seq analysis of Mel202 cells expressing BAP1 or silenced for BAP1 demonstrates an increase in H3K27ac at the GDF15 promoter following BAP1 knockdown. F: Analysis of GDF15 secretion by ELISA assay demonstrates that co-culture of UM cells with HSCs is associated with increased GDF15 expression, even in UM cell lines with high basal expression of GDF15. Cell lines derived from primary or metastatic specimens are indicated.

    Journal: Cancer research

    Article Title: GDF15 Reprograms the Microenvironment to Drive Liver Metastasis of Uveal Melanoma

    doi: 10.1158/0008-5472.CAN-25-0536

    Figure Lengend Snippet: A: UMAP of 6 individual clinical UM “and healthy” scRNA-seq datasets. Data shows major cell types identified and then GDF15 expression in the UM cells (malignant cells) B: Violin plots showing expression of GDF15 in a scRNA-Seq analysis of human Class 1 and Class 2 UM. C: Western Blot showing the expression of BAP1, PRAME and GDF15 in a panel of UM cell lines. D: Silencing of BAP1 is associated with increased expression of GDF15 in Mel202 and 92.1 UM cells. BAP1 was silenced using siRNA and resulting lysates probed for expression of BAP1 and GDF15. E: ChIP-Seq analysis of Mel202 cells expressing BAP1 or silenced for BAP1 demonstrates an increase in H3K27ac at the GDF15 promoter following BAP1 knockdown. F: Analysis of GDF15 secretion by ELISA assay demonstrates that co-culture of UM cells with HSCs is associated with increased GDF15 expression, even in UM cell lines with high basal expression of GDF15. Cell lines derived from primary or metastatic specimens are indicated.

    Article Snippet: The effectiveness of blocking GDF15 on tube formation was assessed using an anti-GDF15 blocking antibody (ponsegromab: 120ng/ml, #HY-P99241, MedChemExpress, NJ, USA).

    Techniques: Expressing, Western Blot, ChIP-sequencing, Knockdown, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Derivative Assay

    A: RNA-seq analysis of HSCs (LX2) treated with GDF15 (1μg/ml, 24 hr) identifies increased expression of genes encoding multiple ECM proteins ( COL7A1 ), and molecules involved in angiogenesis ( VCAM1, ANGPLT4, PDGFB, FLT1 ). B: Pathway analysis identifies GDF15 to increase expression of genes involved in inflammatory signaling ( TNFA, IFNγ, IL6 ), angiogenesis (hypoxia, angiogenesis) and metabolism. C: Human primary HSCs (HHStec) were stimulated with either GDF15 (1μg/ml) or SPP1 (osteopontin, (1μg/ml)) for 24 hr and Western Blotting used to determine expression of IL-8 and phospho-STAT3. D: HSC (HHStec cells) were grown in monoculture, MP41 cells were grown in monoculture, HSC+MP41 cells were grown in co-culture, HSCs were treated with conditioned media (CM) from MP41 cells or GDF15 (1μg/ml) for 24 hr before probing for the expression of COL1A1 and PDGFRB by Western Blot. E: Immunofluorescence staining of COL1A1 in HSCs (HHStec) cells treated with basal media or conditioned media from MP41 or UMM061 cells. F: CellChat analysis of human UM samples identifies HSC-derived collagens as being a potential outgoing signal to multiple immune subtypes and UM cells.

    Journal: Cancer research

    Article Title: GDF15 Reprograms the Microenvironment to Drive Liver Metastasis of Uveal Melanoma

    doi: 10.1158/0008-5472.CAN-25-0536

    Figure Lengend Snippet: A: RNA-seq analysis of HSCs (LX2) treated with GDF15 (1μg/ml, 24 hr) identifies increased expression of genes encoding multiple ECM proteins ( COL7A1 ), and molecules involved in angiogenesis ( VCAM1, ANGPLT4, PDGFB, FLT1 ). B: Pathway analysis identifies GDF15 to increase expression of genes involved in inflammatory signaling ( TNFA, IFNγ, IL6 ), angiogenesis (hypoxia, angiogenesis) and metabolism. C: Human primary HSCs (HHStec) were stimulated with either GDF15 (1μg/ml) or SPP1 (osteopontin, (1μg/ml)) for 24 hr and Western Blotting used to determine expression of IL-8 and phospho-STAT3. D: HSC (HHStec cells) were grown in monoculture, MP41 cells were grown in monoculture, HSC+MP41 cells were grown in co-culture, HSCs were treated with conditioned media (CM) from MP41 cells or GDF15 (1μg/ml) for 24 hr before probing for the expression of COL1A1 and PDGFRB by Western Blot. E: Immunofluorescence staining of COL1A1 in HSCs (HHStec) cells treated with basal media or conditioned media from MP41 or UMM061 cells. F: CellChat analysis of human UM samples identifies HSC-derived collagens as being a potential outgoing signal to multiple immune subtypes and UM cells.

    Article Snippet: The effectiveness of blocking GDF15 on tube formation was assessed using an anti-GDF15 blocking antibody (ponsegromab: 120ng/ml, #HY-P99241, MedChemExpress, NJ, USA).

    Techniques: Expressing, RNA Sequencing, Western Blot, Co-Culture Assay, Immunofluorescence, Staining, Derivative Assay

    A: CellChat analysis of scRNA-Seq from human UM identifies endothelial cells as being a major target of secreted GDF15. B: Exogenous GDF15 and IL8 increase vascular network formation. HUVEC cells were plated on Matrigel and treated with basal media, IL-8 or GDF15 (both 1μg/ml for 0–24 hr). C: Scoring of endothelial network formation data from B. D: Conditioned media (CM) from UM-HSC co-cultures increases vascular network formation. HUVECs were plated onto Matrigel and treated with basal media or CM from MP41, UMM061 and MM28 cells grown in co-culture with LX2 cells. E: Vascular network formation from D was quantified. F: GDF15-blocking antibodies reverse the pro-angiogenic effects of CM. HUVEC cells were treated with CM from MP41-LX2 co-cultures in the absence and presence of the GDF15 blocking antibody (Ponsegromab,120ng/ml) and vascular network formation imaged. G : Quantification of endothelial cell network formation from F.

    Journal: Cancer research

    Article Title: GDF15 Reprograms the Microenvironment to Drive Liver Metastasis of Uveal Melanoma

    doi: 10.1158/0008-5472.CAN-25-0536

    Figure Lengend Snippet: A: CellChat analysis of scRNA-Seq from human UM identifies endothelial cells as being a major target of secreted GDF15. B: Exogenous GDF15 and IL8 increase vascular network formation. HUVEC cells were plated on Matrigel and treated with basal media, IL-8 or GDF15 (both 1μg/ml for 0–24 hr). C: Scoring of endothelial network formation data from B. D: Conditioned media (CM) from UM-HSC co-cultures increases vascular network formation. HUVECs were plated onto Matrigel and treated with basal media or CM from MP41, UMM061 and MM28 cells grown in co-culture with LX2 cells. E: Vascular network formation from D was quantified. F: GDF15-blocking antibodies reverse the pro-angiogenic effects of CM. HUVEC cells were treated with CM from MP41-LX2 co-cultures in the absence and presence of the GDF15 blocking antibody (Ponsegromab,120ng/ml) and vascular network formation imaged. G : Quantification of endothelial cell network formation from F.

    Article Snippet: The effectiveness of blocking GDF15 on tube formation was assessed using an anti-GDF15 blocking antibody (ponsegromab: 120ng/ml, #HY-P99241, MedChemExpress, NJ, USA).

    Techniques: Co-Culture Assay, Blocking Assay

    A: IVIS imaging of mice with either shCRTL or shGDF15#2 MP41 cells at days 49 and 77, respectively. B: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 MP41 cells. C: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) MP41 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. D: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced MP41 cells (GDF15 shRNA#1 and shRNA#2). E: IVIS imaging of mice with either shCRTL or shGDF15#2 OMM1 cells at days 56 and 70, respectively. F: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 OMM1 cells. G: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) OMM1 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. H: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced OMM1 cells (GDF15 shRNA#1 and shRNA#2).

    Journal: Cancer research

    Article Title: GDF15 Reprograms the Microenvironment to Drive Liver Metastasis of Uveal Melanoma

    doi: 10.1158/0008-5472.CAN-25-0536

    Figure Lengend Snippet: A: IVIS imaging of mice with either shCRTL or shGDF15#2 MP41 cells at days 49 and 77, respectively. B: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 MP41 cells. C: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) MP41 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. D: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced MP41 cells (GDF15 shRNA#1 and shRNA#2). E: IVIS imaging of mice with either shCRTL or shGDF15#2 OMM1 cells at days 56 and 70, respectively. F: Metastasis-free survival of mice following tail vein injection of either shCRTL or shGDF15#2 OMM1 cells. G: H&E staining of livers following tail vein injection of shCRTL or GDF15 silenced (GDF15 shRNA#2) OMM1 UM cells. Livers were collected after 7 weeks (shCRTL) or 11 weeks (shGDF15). Scale Bar = 6 mm. H: Quantification of liver metastases following tail vein injection of GDF15-expressing or silenced OMM1 cells (GDF15 shRNA#1 and shRNA#2).

    Article Snippet: The effectiveness of blocking GDF15 on tube formation was assessed using an anti-GDF15 blocking antibody (ponsegromab: 120ng/ml, #HY-P99241, MedChemExpress, NJ, USA).

    Techniques: Imaging, Injection, Staining, shRNA, Expressing

    A: H&E staining of livers from the eye to liver metastasis model, demonstrating fewer and smaller liver lesions following GDF15 shRNA silencing (shGDF15#1). B: Quantification of the size and number of liver metastases from A. C: IHC staining of liver metastases for fibronectin in MP41 tumors either expressing or with GDF15 silenced. D: Quantification of data from C. E: IHC staining of liver metastases from MP41 tumors for the ECM protein Collagen 1A1. F: Quantification of data from F. G: IHC staining of liver metastases for Ki67 in MP41 tumors either expressing or with GDF15 silenced. H: Quantification of data from G. I: IHC staining of liver metastases for the endothelial cell marker CD31 in MP41 tumors either expressing or with GDF15 silenced. J: Quantification of data from I.

    Journal: Cancer research

    Article Title: GDF15 Reprograms the Microenvironment to Drive Liver Metastasis of Uveal Melanoma

    doi: 10.1158/0008-5472.CAN-25-0536

    Figure Lengend Snippet: A: H&E staining of livers from the eye to liver metastasis model, demonstrating fewer and smaller liver lesions following GDF15 shRNA silencing (shGDF15#1). B: Quantification of the size and number of liver metastases from A. C: IHC staining of liver metastases for fibronectin in MP41 tumors either expressing or with GDF15 silenced. D: Quantification of data from C. E: IHC staining of liver metastases from MP41 tumors for the ECM protein Collagen 1A1. F: Quantification of data from F. G: IHC staining of liver metastases for Ki67 in MP41 tumors either expressing or with GDF15 silenced. H: Quantification of data from G. I: IHC staining of liver metastases for the endothelial cell marker CD31 in MP41 tumors either expressing or with GDF15 silenced. J: Quantification of data from I.

    Article Snippet: The effectiveness of blocking GDF15 on tube formation was assessed using an anti-GDF15 blocking antibody (ponsegromab: 120ng/ml, #HY-P99241, MedChemExpress, NJ, USA).

    Techniques: Staining, shRNA, Immunohistochemistry, Expressing, Marker