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gdf15  (Proteintech)


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    Structured Review

    Proteintech gdf15
    The non-linear dose-response relationships between serum protein levels of <t>GDF15</t> and GFRAL and sarcopenia risk (A) Serum GDF15 concentrations with age across three sarcopenia status groups; (B) The non-linear dose-response relationship between serum protein levels of GDF15 and sarcopenia risk.; (C) Serum GFRAL concentrations with age across three sarcopenia status groups; (D) The non-linear dose-response relationship between serum protein levels of GFRAL and sarcopenia risk. Data are presented as fitted values with 95% confidence intervals (CIs). See also .
    Gdf15, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/27455+1+ap/GDF15+Antibody/pmc12964241-55-0-5
    Average 94 stars, based on 62 article reviews
    gdf15 - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Association between elevated expression of GDF15/GFRAL and sarcopenia risk"

    Article Title: Association between elevated expression of GDF15/GFRAL and sarcopenia risk

    Journal: iScience

    doi: 10.1016/j.isci.2026.115023

    The non-linear dose-response relationships between serum protein levels of GDF15 and GFRAL and sarcopenia risk (A) Serum GDF15 concentrations with age across three sarcopenia status groups; (B) The non-linear dose-response relationship between serum protein levels of GDF15 and sarcopenia risk.; (C) Serum GFRAL concentrations with age across three sarcopenia status groups; (D) The non-linear dose-response relationship between serum protein levels of GFRAL and sarcopenia risk. Data are presented as fitted values with 95% confidence intervals (CIs). See also .
    Figure Legend Snippet: The non-linear dose-response relationships between serum protein levels of GDF15 and GFRAL and sarcopenia risk (A) Serum GDF15 concentrations with age across three sarcopenia status groups; (B) The non-linear dose-response relationship between serum protein levels of GDF15 and sarcopenia risk.; (C) Serum GFRAL concentrations with age across three sarcopenia status groups; (D) The non-linear dose-response relationship between serum protein levels of GFRAL and sarcopenia risk. Data are presented as fitted values with 95% confidence intervals (CIs). See also .

    Techniques Used:

    Associations between serum protein levels of GDF15 and GFRAL and risks of sarcopenia and its phenotypes (A) Association of serum protein levels of GDF15 with risks of sarcopenia and its phenotypes; (B) Association of serum protein levels of GFRAL with risks of sarcopenia and its phenotypes. Model 0 was the crude model; Model 1 was adjusted for sex and age; Model 2 was further adjusted for Townsend deprivation index, educational attainment, smoking status, and alcohol consumption based on Model1. Abbreviations: CI, confidence interval. Data are presented as fitted values with 95% CIs. See also and , , and .
    Figure Legend Snippet: Associations between serum protein levels of GDF15 and GFRAL and risks of sarcopenia and its phenotypes (A) Association of serum protein levels of GDF15 with risks of sarcopenia and its phenotypes; (B) Association of serum protein levels of GFRAL with risks of sarcopenia and its phenotypes. Model 0 was the crude model; Model 1 was adjusted for sex and age; Model 2 was further adjusted for Townsend deprivation index, educational attainment, smoking status, and alcohol consumption based on Model1. Abbreviations: CI, confidence interval. Data are presented as fitted values with 95% CIs. See also and , , and .

    Techniques Used:

    The effects of elevated GDF15 and GFRAL levels on sarcopenia (A) UMAP visualization of 11 annotated cell types in skeletal muscles from two frail mice and three control mice; (B) volcano plot showing differentially expressed genes in M2 macrophages from non-frail and frail muscle; (C) pathways involving GDF15 in M2 macrophages; (D–E) significantly up-regulated pathways of fibrosis-related genes between non-frail and frail muscle; (F) immunohistochemical staining for GDF15, with positive signals visualized as brown DAB precipitate. Scale bars, 200 μm.
    Figure Legend Snippet: The effects of elevated GDF15 and GFRAL levels on sarcopenia (A) UMAP visualization of 11 annotated cell types in skeletal muscles from two frail mice and three control mice; (B) volcano plot showing differentially expressed genes in M2 macrophages from non-frail and frail muscle; (C) pathways involving GDF15 in M2 macrophages; (D–E) significantly up-regulated pathways of fibrosis-related genes between non-frail and frail muscle; (F) immunohistochemical staining for GDF15, with positive signals visualized as brown DAB precipitate. Scale bars, 200 μm.

    Techniques Used: Muscles, Control, Immunohistochemical staining, Staining

    Related Articles

    other:


    Article Title: Lipoylation is dependent on the ferredoxin FDX1 and dispensable under hypoxia in human cells
    Article Snippet: GDF15 , 27455-1-AP , ProteinTech.

    Saline:

    Article Title: Exosomes Derived from Meningitic Escherichia coli-Infected Brain Microvascular Endothelial Cells Facilitate Astrocyte Activation.
    Article Snippet: Numerous studies have shown that exosomes play a regulatory role in a variety of biological processes as well as in disease development and progression.. However, exosome-mediated intercellular communication between brain microvascular endothelial cells (BMECs) and astrocytes during meningitic Escherichia coli (E. coli)–induced neuroinflammation remains largely unknown.. Here, by using in vivo and in vitro models, we demonstrate that exosomes derived from meningitic E. coli–infected BMECs can activate the inflammatory response of astrocytes.

    Incubation:

    Article Title: Exosomes Derived from Meningitic Escherichia coli-Infected Brain Microvascular Endothelial Cells Facilitate Astrocyte Activation.
    Article Snippet: Numerous studies have shown that exosomes play a regulatory role in a variety of biological processes as well as in disease development and progression.. However, exosome-mediated intercellular communication between brain microvascular endothelial cells (BMECs) and astrocytes during meningitic Escherichia coli (E. coli)–induced neuroinflammation remains largely unknown.. Here, by using in vivo and in vitro models, we demonstrate that exosomes derived from meningitic E. coli–infected BMECs can activate the inflammatory response of astrocytes.

    Membrane:

    Article Title: Exosomes Derived from Meningitic Escherichia coli-Infected Brain Microvascular Endothelial Cells Facilitate Astrocyte Activation.
    Article Snippet: Numerous studies have shown that exosomes play a regulatory role in a variety of biological processes as well as in disease development and progression.. However, exosome-mediated intercellular communication between brain microvascular endothelial cells (BMECs) and astrocytes during meningitic Escherichia coli (E. coli)–induced neuroinflammation remains largely unknown.. Here, by using in vivo and in vitro models, we demonstrate that exosomes derived from meningitic E. coli–infected BMECs can activate the inflammatory response of astrocytes.

    Western Blot:

    Article Title: Dual functions of SPOP and ERG dictate androgen therapy responses in prostate cancer
    Article Snippet: .. Antibodies used in immunoblotting and immunoprecipitation assays were: anti-SPOP dilution 1:1000 (ab81163, Abcam), anti-TRIM24, dilution 1:1000 (Sc-271266, Santa Cruz), anti-ß-ACTIN dilution 1:1000 (4967, Cell Signaling), anti-AR dilution 1:1000 (Sc-7305, Santa Cruz), anti-GADPH dilution 1:1000 (Sc-47724, Santa Cruz), anti-ERG dilution 1:1000 (Sc-271048, Santa Cruz), anti-α-Tubulin dilution 1:1000 (3873S, Cell Signaling), anti-ZMYND11 dilution 1:1000 (NBP2-20960, Novus Biologicals), anti-HA dilution 1:1000 (H3663, Sigma), anti-BRD2 dilution 1:1000 (A302-583A, Bethyl Labs), anti-NCOA3 dilution 1:1000 (2126, Cell Signaling), anti-DEK dilution 1:1000 (610948, BDBioscience), anti-p21 dilution 1:1000 (2947S, Cell Signaling), anti-c-MYC dilution 1:1000 (5605S, Cell Signaling), anti-HOXB13 dilution 1:1000 (Sc-28333, Santa Cruz), anti-PTEN dilution 1:1000 (9559, cell signaling), anti-p21 dilution 1:1000 (ab188224, Abcam), anti-HOXB13 dilution 1:1000 (NBP2-43655, Novus biologicals), anti-GDF-15 dilution 1:1000 (27455-1-AP, proteintech). .. For immunoblotting, cells were washed with PBS and subsequently lysed in RIPA buffer (Sigma) and sonicated.

    Immunoprecipitation:

    Article Title: Dual functions of SPOP and ERG dictate androgen therapy responses in prostate cancer
    Article Snippet: .. Antibodies used in immunoblotting and immunoprecipitation assays were: anti-SPOP dilution 1:1000 (ab81163, Abcam), anti-TRIM24, dilution 1:1000 (Sc-271266, Santa Cruz), anti-ß-ACTIN dilution 1:1000 (4967, Cell Signaling), anti-AR dilution 1:1000 (Sc-7305, Santa Cruz), anti-GADPH dilution 1:1000 (Sc-47724, Santa Cruz), anti-ERG dilution 1:1000 (Sc-271048, Santa Cruz), anti-α-Tubulin dilution 1:1000 (3873S, Cell Signaling), anti-ZMYND11 dilution 1:1000 (NBP2-20960, Novus Biologicals), anti-HA dilution 1:1000 (H3663, Sigma), anti-BRD2 dilution 1:1000 (A302-583A, Bethyl Labs), anti-NCOA3 dilution 1:1000 (2126, Cell Signaling), anti-DEK dilution 1:1000 (610948, BDBioscience), anti-p21 dilution 1:1000 (2947S, Cell Signaling), anti-c-MYC dilution 1:1000 (5605S, Cell Signaling), anti-HOXB13 dilution 1:1000 (Sc-28333, Santa Cruz), anti-PTEN dilution 1:1000 (9559, cell signaling), anti-p21 dilution 1:1000 (ab188224, Abcam), anti-HOXB13 dilution 1:1000 (NBP2-43655, Novus biologicals), anti-GDF-15 dilution 1:1000 (27455-1-AP, proteintech). .. For immunoblotting, cells were washed with PBS and subsequently lysed in RIPA buffer (Sigma) and sonicated.



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    Image Search Results


    The non-linear dose-response relationships between serum protein levels of GDF15 and GFRAL and sarcopenia risk (A) Serum GDF15 concentrations with age across three sarcopenia status groups; (B) The non-linear dose-response relationship between serum protein levels of GDF15 and sarcopenia risk.; (C) Serum GFRAL concentrations with age across three sarcopenia status groups; (D) The non-linear dose-response relationship between serum protein levels of GFRAL and sarcopenia risk. Data are presented as fitted values with 95% confidence intervals (CIs). See also .

    Journal: iScience

    Article Title: Association between elevated expression of GDF15/GFRAL and sarcopenia risk

    doi: 10.1016/j.isci.2026.115023

    Figure Lengend Snippet: The non-linear dose-response relationships between serum protein levels of GDF15 and GFRAL and sarcopenia risk (A) Serum GDF15 concentrations with age across three sarcopenia status groups; (B) The non-linear dose-response relationship between serum protein levels of GDF15 and sarcopenia risk.; (C) Serum GFRAL concentrations with age across three sarcopenia status groups; (D) The non-linear dose-response relationship between serum protein levels of GFRAL and sarcopenia risk. Data are presented as fitted values with 95% confidence intervals (CIs). See also .

    Article Snippet: GDF15 (for immunohistochemical staining) , Proteintech , Cat No. 27455-1-AP.

    Techniques:

    Associations between serum protein levels of GDF15 and GFRAL and risks of sarcopenia and its phenotypes (A) Association of serum protein levels of GDF15 with risks of sarcopenia and its phenotypes; (B) Association of serum protein levels of GFRAL with risks of sarcopenia and its phenotypes. Model 0 was the crude model; Model 1 was adjusted for sex and age; Model 2 was further adjusted for Townsend deprivation index, educational attainment, smoking status, and alcohol consumption based on Model1. Abbreviations: CI, confidence interval. Data are presented as fitted values with 95% CIs. See also and , , and .

    Journal: iScience

    Article Title: Association between elevated expression of GDF15/GFRAL and sarcopenia risk

    doi: 10.1016/j.isci.2026.115023

    Figure Lengend Snippet: Associations between serum protein levels of GDF15 and GFRAL and risks of sarcopenia and its phenotypes (A) Association of serum protein levels of GDF15 with risks of sarcopenia and its phenotypes; (B) Association of serum protein levels of GFRAL with risks of sarcopenia and its phenotypes. Model 0 was the crude model; Model 1 was adjusted for sex and age; Model 2 was further adjusted for Townsend deprivation index, educational attainment, smoking status, and alcohol consumption based on Model1. Abbreviations: CI, confidence interval. Data are presented as fitted values with 95% CIs. See also and , , and .

    Article Snippet: GDF15 (for immunohistochemical staining) , Proteintech , Cat No. 27455-1-AP.

    Techniques:

    The effects of elevated GDF15 and GFRAL levels on sarcopenia (A) UMAP visualization of 11 annotated cell types in skeletal muscles from two frail mice and three control mice; (B) volcano plot showing differentially expressed genes in M2 macrophages from non-frail and frail muscle; (C) pathways involving GDF15 in M2 macrophages; (D–E) significantly up-regulated pathways of fibrosis-related genes between non-frail and frail muscle; (F) immunohistochemical staining for GDF15, with positive signals visualized as brown DAB precipitate. Scale bars, 200 μm.

    Journal: iScience

    Article Title: Association between elevated expression of GDF15/GFRAL and sarcopenia risk

    doi: 10.1016/j.isci.2026.115023

    Figure Lengend Snippet: The effects of elevated GDF15 and GFRAL levels on sarcopenia (A) UMAP visualization of 11 annotated cell types in skeletal muscles from two frail mice and three control mice; (B) volcano plot showing differentially expressed genes in M2 macrophages from non-frail and frail muscle; (C) pathways involving GDF15 in M2 macrophages; (D–E) significantly up-regulated pathways of fibrosis-related genes between non-frail and frail muscle; (F) immunohistochemical staining for GDF15, with positive signals visualized as brown DAB precipitate. Scale bars, 200 μm.

    Article Snippet: GDF15 (for immunohistochemical staining) , Proteintech , Cat No. 27455-1-AP.

    Techniques: Muscles, Control, Immunohistochemical staining, Staining

    GDF15 preserves mitochondrial homeostasis in LPS-stimulated macrophages through dual regulation of SMAD7 and PKM2 pathways. (A) HIF-1α and SMAD7 expression in RAW264.7 macrophages across conditions: Untreated, LPS, LPS with rAAV8-mGdf15 overexpression (LPS+GDF15), and LPS with GDF15 knockdown (si-GDF15). β-actin: loading control.(HIF-1α suppression and SMAD7 induction by GDF15.) (B) Cytosolic and nuclear PKM2 protein levels. Lamin B1 (nuclear) and α-tubulin (cytosolic) markers validate fractionation efficiency. Study groups and individual replicates are identified in the figure key.(PKM2 subcellular redistribution modulated by GDF15.) (C) Immunofluorescence of PKM2 (red) and nuclei (DAPI, blue). Arrows indicate nuclear PKM2 accumulation. Scale bar: 15 μm.(Nuclear PKM2 enrichment upon LPS challenge mitigated by GDF15 and exacerbated by GDF15 knockdown.).

    Journal: Frontiers in Immunology

    Article Title: GDF15 orchestrates mitochondrial-immune crosstalk via SMAD7-HIF-1α-PKM2 cascade to attenuate septic liver injury

    doi: 10.3389/fimmu.2025.1712741

    Figure Lengend Snippet: GDF15 preserves mitochondrial homeostasis in LPS-stimulated macrophages through dual regulation of SMAD7 and PKM2 pathways. (A) HIF-1α and SMAD7 expression in RAW264.7 macrophages across conditions: Untreated, LPS, LPS with rAAV8-mGdf15 overexpression (LPS+GDF15), and LPS with GDF15 knockdown (si-GDF15). β-actin: loading control.(HIF-1α suppression and SMAD7 induction by GDF15.) (B) Cytosolic and nuclear PKM2 protein levels. Lamin B1 (nuclear) and α-tubulin (cytosolic) markers validate fractionation efficiency. Study groups and individual replicates are identified in the figure key.(PKM2 subcellular redistribution modulated by GDF15.) (C) Immunofluorescence of PKM2 (red) and nuclei (DAPI, blue). Arrows indicate nuclear PKM2 accumulation. Scale bar: 15 μm.(Nuclear PKM2 enrichment upon LPS challenge mitigated by GDF15 and exacerbated by GDF15 knockdown.).

    Article Snippet: Proteins (30 μg/lane) were separated on 10% SDS-PAGE gels, transferred to PVDF membranes (Millipore, IPVH00010), and probed with the following primary antibodies: rabbit anti-mouse UQCRC1 (Proteintech, Cat. No. 21705-1-AP, 1:1000), rabbit anti-mouse GDF15 (Proteintech, Cat. No. 27455-1-AP, 1:1000), rabbit anti-mouse HIF-1α (Proteintech, Cat. No. 20960-1-AP, 1:1000), rabbit anti-mouse SMAD7 (Proteintech, Cat. No. 725840-1-AP, 1:1000), mouse anti-mouse PKM2 (Proteintech, Cat. No. 60268-1-Ig, 1:1000), rabbit anti-mouse H3 (Proteintech, Cat. No. 17168-1-AP, 1:5000) and mouse anti-mouse β-actin (Proteintech, Cat. No. 66009-1-Ig, 1:5000).

    Techniques: Expressing, Over Expression, Knockdown, Control, Fractionation, Immunofluorescence

    HIF-1α and PKM2 are critical effectors of GDF15-driven mitochondrial protection and anti-inflammatory responses. (A) HIF-1α inhibition by BAY 87-2243 (5 μM, 24 h). β-actin: loading control.(Pharmacological HIF-1α blockade.) (B) PKM2 inhibition by Shikonin (2 μM, 24 h). β-actin: loading control.(PKM2 activity suppression.) (C) UQCRC1 recovery in LPS-injured macrophages treated with: GDF15 overexpression, HIF-1α inhibitor (BAY), or PKM2 inhibitor (Shikonin). β-actin: loading control.(Mitochondrial complex III rescue via HIF-1α/PKM2 inhibition mirrors GDF15 effects.) (D) Inflammatory (TNF-α, IL-6) and metabolic (lactate) markers in cell supernatant (n = 5). Study groups and individual replicates are identified in the figure key. ***p < 0.001.(HIF-1α/PKM2 targeting replicates GDF15-mediated anti-inflammatory and metabolic homeostasis.) (E) UQCRC1 expression under GDF15 loss-of-function: si-GDF15 alone vs. combined with BAY 87–2243 or Shikonin. β-actin: loading control. Study groups and individual replicates are identified in the figure key.(Mitochondrial rescue in GDF15-deficient macrophages requires HIF-1α/PKM2 inhibition.) (F) Supernatant cytokines and lactate in si-GDF15 macrophages with/without inhibitors (n = 5). ***p < 0.001. (Inflammation reversal in GDF15-knockdown macrophages depends on HIF-1α/PKM2 blockade.).

    Journal: Frontiers in Immunology

    Article Title: GDF15 orchestrates mitochondrial-immune crosstalk via SMAD7-HIF-1α-PKM2 cascade to attenuate septic liver injury

    doi: 10.3389/fimmu.2025.1712741

    Figure Lengend Snippet: HIF-1α and PKM2 are critical effectors of GDF15-driven mitochondrial protection and anti-inflammatory responses. (A) HIF-1α inhibition by BAY 87-2243 (5 μM, 24 h). β-actin: loading control.(Pharmacological HIF-1α blockade.) (B) PKM2 inhibition by Shikonin (2 μM, 24 h). β-actin: loading control.(PKM2 activity suppression.) (C) UQCRC1 recovery in LPS-injured macrophages treated with: GDF15 overexpression, HIF-1α inhibitor (BAY), or PKM2 inhibitor (Shikonin). β-actin: loading control.(Mitochondrial complex III rescue via HIF-1α/PKM2 inhibition mirrors GDF15 effects.) (D) Inflammatory (TNF-α, IL-6) and metabolic (lactate) markers in cell supernatant (n = 5). Study groups and individual replicates are identified in the figure key. ***p < 0.001.(HIF-1α/PKM2 targeting replicates GDF15-mediated anti-inflammatory and metabolic homeostasis.) (E) UQCRC1 expression under GDF15 loss-of-function: si-GDF15 alone vs. combined with BAY 87–2243 or Shikonin. β-actin: loading control. Study groups and individual replicates are identified in the figure key.(Mitochondrial rescue in GDF15-deficient macrophages requires HIF-1α/PKM2 inhibition.) (F) Supernatant cytokines and lactate in si-GDF15 macrophages with/without inhibitors (n = 5). ***p < 0.001. (Inflammation reversal in GDF15-knockdown macrophages depends on HIF-1α/PKM2 blockade.).

    Article Snippet: Proteins (30 μg/lane) were separated on 10% SDS-PAGE gels, transferred to PVDF membranes (Millipore, IPVH00010), and probed with the following primary antibodies: rabbit anti-mouse UQCRC1 (Proteintech, Cat. No. 21705-1-AP, 1:1000), rabbit anti-mouse GDF15 (Proteintech, Cat. No. 27455-1-AP, 1:1000), rabbit anti-mouse HIF-1α (Proteintech, Cat. No. 20960-1-AP, 1:1000), rabbit anti-mouse SMAD7 (Proteintech, Cat. No. 725840-1-AP, 1:1000), mouse anti-mouse PKM2 (Proteintech, Cat. No. 60268-1-Ig, 1:1000), rabbit anti-mouse H3 (Proteintech, Cat. No. 17168-1-AP, 1:5000) and mouse anti-mouse β-actin (Proteintech, Cat. No. 66009-1-Ig, 1:5000).

    Techniques: Inhibition, Control, Activity Assay, Over Expression, Expressing, Knockdown

    SMAD7 activation suppresses HIF-1α to mediate GDF15-dependent mitochondrial protection in LPS-challenged macrophages. (A) Pharmacological SMAD7 activation by Asiaticoside (20 μM, 48 h). β-actin: loading control. (B) HIF-1α expression under LPS challenge: LPS alone, LPS + AVV-GDF15, or LPS + SMAD7 activation (Asiaticoside). β-actin: loading control. (C) HIF-1α modulation across conditions: LPS, LPS + si-GDF15, LPS + Asiaticoside, or LPS + si-GDF15 + Asiaticoside. β-actin: loading control.

    Journal: Frontiers in Immunology

    Article Title: GDF15 orchestrates mitochondrial-immune crosstalk via SMAD7-HIF-1α-PKM2 cascade to attenuate septic liver injury

    doi: 10.3389/fimmu.2025.1712741

    Figure Lengend Snippet: SMAD7 activation suppresses HIF-1α to mediate GDF15-dependent mitochondrial protection in LPS-challenged macrophages. (A) Pharmacological SMAD7 activation by Asiaticoside (20 μM, 48 h). β-actin: loading control. (B) HIF-1α expression under LPS challenge: LPS alone, LPS + AVV-GDF15, or LPS + SMAD7 activation (Asiaticoside). β-actin: loading control. (C) HIF-1α modulation across conditions: LPS, LPS + si-GDF15, LPS + Asiaticoside, or LPS + si-GDF15 + Asiaticoside. β-actin: loading control.

    Article Snippet: Proteins (30 μg/lane) were separated on 10% SDS-PAGE gels, transferred to PVDF membranes (Millipore, IPVH00010), and probed with the following primary antibodies: rabbit anti-mouse UQCRC1 (Proteintech, Cat. No. 21705-1-AP, 1:1000), rabbit anti-mouse GDF15 (Proteintech, Cat. No. 27455-1-AP, 1:1000), rabbit anti-mouse HIF-1α (Proteintech, Cat. No. 20960-1-AP, 1:1000), rabbit anti-mouse SMAD7 (Proteintech, Cat. No. 725840-1-AP, 1:1000), mouse anti-mouse PKM2 (Proteintech, Cat. No. 60268-1-Ig, 1:1000), rabbit anti-mouse H3 (Proteintech, Cat. No. 17168-1-AP, 1:5000) and mouse anti-mouse β-actin (Proteintech, Cat. No. 66009-1-Ig, 1:5000).

    Techniques: Activation Assay, Control, Expressing