Review



anti fundc1 monoclonal antibody  (Cell Signaling Technology Inc)


Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 95
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc anti fundc1 monoclonal antibody
    Activation of Fn14 inhibits mitophagy in fibroblasts. A , primary fibroblasts were treated with rTWEAK (100 ng/mL) for 48 h. Cell samples were harvested after 48 h. Volcano plot showing the changes of fibroblast genes (fold change ≥ 2). B , KEGG enrichment analysis for differentially expressed genes in Control vs. rTWEAK-treated primary fibroblasts. C , Mitochondrial membrane potential was measured by JC-1 staining. D , the expression of Mfn1 , Opa1 , and Dnm1 mRNA in primary fibroblasts was detected by Real-time PCR ( n = 3). E-J , The protein levels of L-OPA1, MFN1, <t>FUNDC1,</t> PINK1, and LC3 were determined by Western blot analysis ( n = 3). K , Immunofluorescence and confocal microscopy show the colocalization of Mito Tracker (green) and LAMP1 (red) in rTWEAK-treated primary fibroblasts, scale bar = 50 μm. * P < 0.05 and ** P < 0.01
    Anti Fundc1 Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+fundc1/FUNDC1+Rabbit+mAb/pmc13013858-28-0-4
    Average 95 stars, based on 46 article reviews
    anti fundc1 monoclonal antibody - by Bioz Stars, 2026-10
    95/100 stars

    Images

    1) Product Images from "Fibroblast growth factor-inducible 14 accelerates pulmonary fibrosis by inducing fibroblast senescence in mice"

    Article Title: Fibroblast growth factor-inducible 14 accelerates pulmonary fibrosis by inducing fibroblast senescence in mice

    Journal: Cellular and Molecular Life Sciences: CMLS

    doi: 10.1007/s00018-026-06161-w

    Activation of Fn14 inhibits mitophagy in fibroblasts. A , primary fibroblasts were treated with rTWEAK (100 ng/mL) for 48 h. Cell samples were harvested after 48 h. Volcano plot showing the changes of fibroblast genes (fold change ≥ 2). B , KEGG enrichment analysis for differentially expressed genes in Control vs. rTWEAK-treated primary fibroblasts. C , Mitochondrial membrane potential was measured by JC-1 staining. D , the expression of Mfn1 , Opa1 , and Dnm1 mRNA in primary fibroblasts was detected by Real-time PCR ( n = 3). E-J , The protein levels of L-OPA1, MFN1, FUNDC1, PINK1, and LC3 were determined by Western blot analysis ( n = 3). K , Immunofluorescence and confocal microscopy show the colocalization of Mito Tracker (green) and LAMP1 (red) in rTWEAK-treated primary fibroblasts, scale bar = 50 μm. * P < 0.05 and ** P < 0.01
    Figure Legend Snippet: Activation of Fn14 inhibits mitophagy in fibroblasts. A , primary fibroblasts were treated with rTWEAK (100 ng/mL) for 48 h. Cell samples were harvested after 48 h. Volcano plot showing the changes of fibroblast genes (fold change ≥ 2). B , KEGG enrichment analysis for differentially expressed genes in Control vs. rTWEAK-treated primary fibroblasts. C , Mitochondrial membrane potential was measured by JC-1 staining. D , the expression of Mfn1 , Opa1 , and Dnm1 mRNA in primary fibroblasts was detected by Real-time PCR ( n = 3). E-J , The protein levels of L-OPA1, MFN1, FUNDC1, PINK1, and LC3 were determined by Western blot analysis ( n = 3). K , Immunofluorescence and confocal microscopy show the colocalization of Mito Tracker (green) and LAMP1 (red) in rTWEAK-treated primary fibroblasts, scale bar = 50 μm. * P < 0.05 and ** P < 0.01

    Techniques Used: Activation Assay, Control, Membrane, Staining, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Immunofluorescence, Confocal Microscopy

    Related Articles

    Incubation:

    Article Title: Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy
    Article Snippet: .. The membranes were incubated with anti-FUNDC1 (1:2,000; cat. no. 49240; CST Biological Reagents Co., Ltd.), anti-p-FUNDC1 (1:2,000; cat. no. AF0001; Affinity Biosciences), anti-PGAM5 (1:2,000; cat. no. ab244218; Abcam), anti-ULK1 (1:5,000; cat. no. 8054; Abcam), anti-OPA1 (1:2,000; cat. no. ab157457; Abcam), anti-DRP1 (1:2,000; cat. no. ab184247; Abcam), anti-FIS1 (1:2,000; cat. no. ab156865; Abcam), anti-LC3 II (1:2,000; cat. no. 43566; CST Biological Reagents Co., Ltd.), anti-LC3 I (1:2,000; cat. no. 12741; CST Biological Reagents Co., Ltd.), anti-P62 (1:2,000; cat. no. ab109012; Abcam) and anti-glyceraldehyde 3-phosphate dehydrogenase (GAPDH; 1:2,000; cat. no. K106389P; Beijing Solarbio Science & Technology Co., Ltd.) primary antibodies for 1 h at room temperature in a dark room. .. Then, the membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies (1:3,000; cat. no. SE134; Beijing Solarbio Science & Technology Co., Ltd.) at room temperature for 1-2 h and exposed to an ECL Substrate kit (Beijing Solarbio Science & Technology Co., Ltd.).

    Article Title: Activation of ULK1 to trigger FUNDC1-mediated mitophagy in heart failure: Effect of Ginsenoside Rg3 intervention.
    Article Snippet: Background: Although the development of therapies for heart failure (HF) continues apace, clinical outcomes are often far from ideal.. Unc51-like-kinase 1 (ULK1)-mediated mitophagy prevents pathological cardiac remodeling and heart failure (HF).. Molecularly ULK1-targeted agent to enhance mitophagy is scanty.

    Article Title: FUNDC1 deficiency aggravates endothelial senescence and retinal dysfunction.
    Article Snippet: Natural aging leads to various age-related changes that impair visual function and cause ocular diseases.. Endothelial cells, key components of blood vessels, play a crucial role in vascular aging and retinal degeneration.. However, the exact mechanisms by which endothelial cell aging promotes retinopathy are not fully understood.

    Article Title: METTL3-mediated m6A modification of FUNDC1/IP3R2 pathway facilitates cardiac hypertrophy in obesity hypertension.
    Article Snippet: .. Membranes were blocked with 5 % skimmed milk for 1 h at room temperature and then incubated overnight at 4 ◦C with anti-METTL3 (Abcam, ab195352), anti-FUNDC1 (CST, #49240), anti-IP3R2 (Santa, sc-398434), antiIGF2BP2 (Abcam, ab128175), anti-nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) (Abcam, ab263899), anti-caspase-1, processed fragment p10 (Caspase1/ p10) (Absin, abs155181), anti- GSDMD-N-terminal domain (GSDMD-N) (CST, #10137), anti-Calreticulin (Abcam, ab92516), anti-GAPDH (Abcam, ab8245) or anti-ubiquitin Polyclonal (Proteintech, 10201-2- AP). .. After three washes with TBST, membranes were incubated with HRP-labelled secondary antibody at 37 ◦C for 1 h. Membranes were then treated with ECL luminescent solution, protected from light in a dark room for 5 min and scanned and analysed using Tanon-5200.

    Article Title: Early Mitochondrial Defects in the 5xFAD mouse model of Alzheimer’s Disease
    Article Snippet: Resulting blots were incubated in Ponceau S staining solution (Tocris #5225) for 5 min to quantify total protein. .. The membranes were blocked in 5% non-fat dry milk for 1 hr at room temperature followed by overnight incubation with primary antibodies: anti-TFAM (1:3000, Abcam; ab131607), anti-Sirt3 (1:1000, Cell Signaling Technology; CST #5490), anti-MFN2 (1:1000, Cell Signaling Technology; CST #9482), anti-FIS1 (1:2000, Proteintech; 10956-1-AP), anti-MTP18 (1:1000, Abcam; ab198217), anti-DRP1 (1:1000, Abcam; ab184247), rabbit anti-LC3B (1:3000, Abcam; ab51520), rabbit anti-p62 (1:10,000, Abcam; ab109012), rabbit anti-OPTN1(1:1000, Cell Signaling Technology; CST #58981S), rabbit anti-PINK1 (1:500, Novus Biologicals; BC100-494), rabbit anti-Parkin (1:1000, Cell Signaling Technology; CST #32833S), anti-BECN1 (1:1000, Cell Signaling Technology; CST #3495S), anti-pMFF (1:1000, Cell Signaling Technology; CST #49281S), anti-MFF (1:1000, Cell Signaling Technology; CST #84580S), anti-FUNDC1 (1:1000, Cell Signaling Technology; CST #49240S), anti-MICU1 (1:1000, Cell Signaling Technology; CST #12524), anti-MCU (1:1000, Cell Signaling Technology; CST #14997) diluted in blocking buffer at 4°C with gentle mixing. .. The membranes were washed 3 times in 1X TBST (Tris-buffered saline with 0.1% Tween) buffer and then incubated with either goat anti-rabbit IgG HRP (1:10000, Jackson ImmunoResearch #111-035-144) or goat anti-mouse IgG HRP (1:5000, Abcam) conjugated secondary antibodies for 1 hr at 23 °C.

    Immunoprecipitation:

    Article Title: Activation of ULK1 to trigger FUNDC1-mediated mitophagy in heart failure: Effect of Ginsenoside Rg3 intervention.
    Article Snippet: Background: Although the development of therapies for heart failure (HF) continues apace, clinical outcomes are often far from ideal.. Unc51-like-kinase 1 (ULK1)-mediated mitophagy prevents pathological cardiac remodeling and heart failure (HF).. Molecularly ULK1-targeted agent to enhance mitophagy is scanty.

    Electrophoresis:

    Article Title: FUNDC1 deficiency aggravates endothelial senescence and retinal dysfunction.
    Article Snippet: Natural aging leads to various age-related changes that impair visual function and cause ocular diseases.. Endothelial cells, key components of blood vessels, play a crucial role in vascular aging and retinal degeneration.. However, the exact mechanisms by which endothelial cell aging promotes retinopathy are not fully understood.

    Western Blot:

    Article Title: FUNDC1 interacts with GPx4 to govern hepatic ferroptosis and fibrotic injury through a mitophagy-dependent manner.
    Article Snippet: .. Protein samples were subjected to immunoblotting using anti-GPx4, anti-FUNDC1 and anti-LC3B antibodies (1:1000, Cell Signaling Technology) [33]. ..

    Immunohistochemistry:

    Article Title: FUNDC1 drives cholangiocarcinoma progression via RAC1 interaction and ferroptosis suppression.
    Article Snippet: Cholangiocarcinoma (CCA) is a highly lethal epithelial malignancy that can arise at any site within the biliary tract.. Our findings revealed that FUN14 domain-containing protein 1 (FUNDC1) expression was significantly elevated in CCA samples compared to matched peritumoral tissues.. Survival analysis indicated that patients with high FUNDC1 expression had shorter overall survival.

    Blocking Assay:

    Article Title: Early Mitochondrial Defects in the 5xFAD mouse model of Alzheimer’s Disease
    Article Snippet: Resulting blots were incubated in Ponceau S staining solution (Tocris #5225) for 5 min to quantify total protein. .. The membranes were blocked in 5% non-fat dry milk for 1 hr at room temperature followed by overnight incubation with primary antibodies: anti-TFAM (1:3000, Abcam; ab131607), anti-Sirt3 (1:1000, Cell Signaling Technology; CST #5490), anti-MFN2 (1:1000, Cell Signaling Technology; CST #9482), anti-FIS1 (1:2000, Proteintech; 10956-1-AP), anti-MTP18 (1:1000, Abcam; ab198217), anti-DRP1 (1:1000, Abcam; ab184247), rabbit anti-LC3B (1:3000, Abcam; ab51520), rabbit anti-p62 (1:10,000, Abcam; ab109012), rabbit anti-OPTN1(1:1000, Cell Signaling Technology; CST #58981S), rabbit anti-PINK1 (1:500, Novus Biologicals; BC100-494), rabbit anti-Parkin (1:1000, Cell Signaling Technology; CST #32833S), anti-BECN1 (1:1000, Cell Signaling Technology; CST #3495S), anti-pMFF (1:1000, Cell Signaling Technology; CST #49281S), anti-MFF (1:1000, Cell Signaling Technology; CST #84580S), anti-FUNDC1 (1:1000, Cell Signaling Technology; CST #49240S), anti-MICU1 (1:1000, Cell Signaling Technology; CST #12524), anti-MCU (1:1000, Cell Signaling Technology; CST #14997) diluted in blocking buffer at 4°C with gentle mixing. .. The membranes were washed 3 times in 1X TBST (Tris-buffered saline with 0.1% Tween) buffer and then incubated with either goat anti-rabbit IgG HRP (1:10000, Jackson ImmunoResearch #111-035-144) or goat anti-mouse IgG HRP (1:5000, Abcam) conjugated secondary antibodies for 1 hr at 23 °C.

    Gentle:

    Article Title: Early Mitochondrial Defects in the 5xFAD mouse model of Alzheimer’s Disease
    Article Snippet: Resulting blots were incubated in Ponceau S staining solution (Tocris #5225) for 5 min to quantify total protein. .. The membranes were blocked in 5% non-fat dry milk for 1 hr at room temperature followed by overnight incubation with primary antibodies: anti-TFAM (1:3000, Abcam; ab131607), anti-Sirt3 (1:1000, Cell Signaling Technology; CST #5490), anti-MFN2 (1:1000, Cell Signaling Technology; CST #9482), anti-FIS1 (1:2000, Proteintech; 10956-1-AP), anti-MTP18 (1:1000, Abcam; ab198217), anti-DRP1 (1:1000, Abcam; ab184247), rabbit anti-LC3B (1:3000, Abcam; ab51520), rabbit anti-p62 (1:10,000, Abcam; ab109012), rabbit anti-OPTN1(1:1000, Cell Signaling Technology; CST #58981S), rabbit anti-PINK1 (1:500, Novus Biologicals; BC100-494), rabbit anti-Parkin (1:1000, Cell Signaling Technology; CST #32833S), anti-BECN1 (1:1000, Cell Signaling Technology; CST #3495S), anti-pMFF (1:1000, Cell Signaling Technology; CST #49281S), anti-MFF (1:1000, Cell Signaling Technology; CST #84580S), anti-FUNDC1 (1:1000, Cell Signaling Technology; CST #49240S), anti-MICU1 (1:1000, Cell Signaling Technology; CST #12524), anti-MCU (1:1000, Cell Signaling Technology; CST #14997) diluted in blocking buffer at 4°C with gentle mixing. .. The membranes were washed 3 times in 1X TBST (Tris-buffered saline with 0.1% Tween) buffer and then incubated with either goat anti-rabbit IgG HRP (1:10000, Jackson ImmunoResearch #111-035-144) or goat anti-mouse IgG HRP (1:5000, Abcam) conjugated secondary antibodies for 1 hr at 23 °C.



    Similar Products

    fundc1  (ABclonal Biotechnology)
    95
    ABclonal Biotechnology fundc1
    Fundc1, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+fundc1/FUNDC1+Rabbit+pAb/pm42708506-211-9-17
    Average 95 stars, based on 1 article reviews
    fundc1 - by Bioz Stars, 2026-10
    95/100 stars
    		  Buy from Supplier
    anti fundc1  (ABclonal Biotechnology)
    95
    ABclonal Biotechnology anti fundc1
    Anti Fundc1, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+fundc1/FUNDC1+Rabbit+pAb/pmc13453718-82-83-85
    Average 95 stars, based on 1 article reviews
    anti fundc1 - by Bioz Stars, 2026-10
    95/100 stars
    		  Buy from Supplier
    anti fundc1  (Aviva Systems)
    92
    Aviva Systems anti fundc1
    Anti Fundc1, supplied by Aviva Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+fundc1/FUNDC1+antibody+-+N-terminal+region+(ARP53280_P050)/bio_rxiv__64898__2026__03__20__711686-322-38-39
    Average 92 stars, based on 1 article reviews
    anti fundc1 - by Bioz Stars, 2026-10
    92/100 stars
    		  Buy from Supplier
    fundc1  (Proteintech)
    96
    Proteintech fundc1
    (A) GO analysis revealed that cardiomyocytes under HHCY conditions were mainly enriched in mitochondrial processes, mitochondrial function, and inner mitochondrial membrane signaling pathways. (B) GSEA of AP39-intervened samples that showed significant enrichment and upregulation of the mitophagy pathway. (C) Cystoscope analysis the top 5 ranked genes were SQSTM1, PINK1, HIF1α, <t>FUNDC1,</t> and TBK1. Expression of FUNDC1, LC3A/B in SD rats induced by HHCY (D) and H9c2 cardiomyocytes (E) in each group. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; $p < 0.05 vs. HHCY + AP39, $$$p < 0.005 vs. HHCY + AP39); (F) Expression of P53,P16 in H9c2 cardiomyocytes in each group after siRNA interference. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY; $$$p < 0.005 vs. HHCY + AP39); (G) Observation of changes in Mitophagy formation in each group under transmission electron microscopy. Expression of MFN1, MFN2, Drp1 in SD rats induced by HHCY (H) and H9c2 cardiomyocytes (I) in each group. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; ***p < 0.005 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; ###p < 0.005 vs. HHCY; $p < 0.05 vs. HHCY + AP39, $$p < 0.01 vs. HHCY + AP39, $$$p < 0.005 vs. HHCY + AP39); (J) Co-localization of FUNDC1 and LC3B in cardiomyocytes in each group under fluorescence microscopy. (K) Mitochondrial membrane potential changes after siRNA interference. (Red fluorescence indicates high mitochondrial membrane potential; green fluorescence indicates low mitochondrial membrane potential). Gene Ontology: GO; high homocysteine: HHCY; Gene Set Enrichment Analysis: GSEA.
    Fundc1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+fundc1/LC3+Antibody/pmc13006662-62-49-50
    Average 96 stars, based on 1 article reviews
    fundc1 - by Bioz Stars, 2026-10
    96/100 stars
    		  Buy from Supplier
    anti fundc1 monoclonal antibody  (Cell Signaling Technology Inc)
    95
    Cell Signaling Technology Inc anti fundc1 monoclonal antibody
    Activation of Fn14 inhibits mitophagy in fibroblasts. A , primary fibroblasts were treated with rTWEAK (100 ng/mL) for 48 h. Cell samples were harvested after 48 h. Volcano plot showing the changes of fibroblast genes (fold change ≥ 2). B , KEGG enrichment analysis for differentially expressed genes in Control vs. rTWEAK-treated primary fibroblasts. C , Mitochondrial membrane potential was measured by JC-1 staining. D , the expression of Mfn1 , Opa1 , and Dnm1 mRNA in primary fibroblasts was detected by Real-time PCR ( n = 3). E-J , The protein levels of L-OPA1, MFN1, <t>FUNDC1,</t> PINK1, and LC3 were determined by Western blot analysis ( n = 3). K , Immunofluorescence and confocal microscopy show the colocalization of Mito Tracker (green) and LAMP1 (red) in rTWEAK-treated primary fibroblasts, scale bar = 50 μm. * P < 0.05 and ** P < 0.01
    Anti Fundc1 Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+fundc1/FUNDC1+Rabbit+mAb/pmc13013858-28-0-4
    Average 95 stars, based on 1 article reviews
    anti fundc1 monoclonal antibody - by Bioz Stars, 2026-10
    95/100 stars
    		  Buy from Supplier
    fundc1  (Cell Signaling Technology Inc)
    95
    Cell Signaling Technology Inc fundc1
    Activation of Fn14 inhibits mitophagy in fibroblasts. A , primary fibroblasts were treated with rTWEAK (100 ng/mL) for 48 h. Cell samples were harvested after 48 h. Volcano plot showing the changes of fibroblast genes (fold change ≥ 2). B , KEGG enrichment analysis for differentially expressed genes in Control vs. rTWEAK-treated primary fibroblasts. C , Mitochondrial membrane potential was measured by JC-1 staining. D , the expression of Mfn1 , Opa1 , and Dnm1 mRNA in primary fibroblasts was detected by Real-time PCR ( n = 3). E-J , The protein levels of L-OPA1, MFN1, <t>FUNDC1,</t> PINK1, and LC3 were determined by Western blot analysis ( n = 3). K , Immunofluorescence and confocal microscopy show the colocalization of Mito Tracker (green) and LAMP1 (red) in rTWEAK-treated primary fibroblasts, scale bar = 50 μm. * P < 0.05 and ** P < 0.01
    Fundc1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+fundc1/FUNDC1+Rabbit+mAb/pmc12959280-86-35-36
    Average 95 stars, based on 1 article reviews
    fundc1 - by Bioz Stars, 2026-10
    95/100 stars
    		  Buy from Supplier

    Image Search Results


    (A) GO analysis revealed that cardiomyocytes under HHCY conditions were mainly enriched in mitochondrial processes, mitochondrial function, and inner mitochondrial membrane signaling pathways. (B) GSEA of AP39-intervened samples that showed significant enrichment and upregulation of the mitophagy pathway. (C) Cystoscope analysis the top 5 ranked genes were SQSTM1, PINK1, HIF1α, FUNDC1, and TBK1. Expression of FUNDC1, LC3A/B in SD rats induced by HHCY (D) and H9c2 cardiomyocytes (E) in each group. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; $p < 0.05 vs. HHCY + AP39, $$$p < 0.005 vs. HHCY + AP39); (F) Expression of P53,P16 in H9c2 cardiomyocytes in each group after siRNA interference. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY; $$$p < 0.005 vs. HHCY + AP39); (G) Observation of changes in Mitophagy formation in each group under transmission electron microscopy. Expression of MFN1, MFN2, Drp1 in SD rats induced by HHCY (H) and H9c2 cardiomyocytes (I) in each group. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; ***p < 0.005 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; ###p < 0.005 vs. HHCY; $p < 0.05 vs. HHCY + AP39, $$p < 0.01 vs. HHCY + AP39, $$$p < 0.005 vs. HHCY + AP39); (J) Co-localization of FUNDC1 and LC3B in cardiomyocytes in each group under fluorescence microscopy. (K) Mitochondrial membrane potential changes after siRNA interference. (Red fluorescence indicates high mitochondrial membrane potential; green fluorescence indicates low mitochondrial membrane potential). Gene Ontology: GO; high homocysteine: HHCY; Gene Set Enrichment Analysis: GSEA.

    Journal: Frontiers in Pharmacology

    Article Title: AP39 alleviates HHCY-induced myocardial remodeling by regulating FUNDC1-mediated mitochondrial dynamics via S-sulfhydration of NEDD8/CUL4B

    doi: 10.3389/fphar.2026.1729145

    Figure Lengend Snippet: (A) GO analysis revealed that cardiomyocytes under HHCY conditions were mainly enriched in mitochondrial processes, mitochondrial function, and inner mitochondrial membrane signaling pathways. (B) GSEA of AP39-intervened samples that showed significant enrichment and upregulation of the mitophagy pathway. (C) Cystoscope analysis the top 5 ranked genes were SQSTM1, PINK1, HIF1α, FUNDC1, and TBK1. Expression of FUNDC1, LC3A/B in SD rats induced by HHCY (D) and H9c2 cardiomyocytes (E) in each group. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; $p < 0.05 vs. HHCY + AP39, $$$p < 0.005 vs. HHCY + AP39); (F) Expression of P53,P16 in H9c2 cardiomyocytes in each group after siRNA interference. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY; $$$p < 0.005 vs. HHCY + AP39); (G) Observation of changes in Mitophagy formation in each group under transmission electron microscopy. Expression of MFN1, MFN2, Drp1 in SD rats induced by HHCY (H) and H9c2 cardiomyocytes (I) in each group. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; ***p < 0.005 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; ###p < 0.005 vs. HHCY; $p < 0.05 vs. HHCY + AP39, $$p < 0.01 vs. HHCY + AP39, $$$p < 0.005 vs. HHCY + AP39); (J) Co-localization of FUNDC1 and LC3B in cardiomyocytes in each group under fluorescence microscopy. (K) Mitochondrial membrane potential changes after siRNA interference. (Red fluorescence indicates high mitochondrial membrane potential; green fluorescence indicates low mitochondrial membrane potential). Gene Ontology: GO; high homocysteine: HHCY; Gene Set Enrichment Analysis: GSEA.

    Article Snippet: All primary antibodies used for Western blotting (WB) and immunofluorescence (IF) were purchased from the corresponding commercial suppliers, and their detailed information is listed as follows: GAPDH (Proteintech, USA; 10494-1-AP; WB 1:8000), α-smooth muscle actin (α-SMA) (Proteintech, USA; 14395-1-AP; WB 1:4000), Collagen type III (Proteintech, USA; 22734-1-AP; WB 1:800), FUNDC1 (Proteintech, China; AWA51295 ; IF 1:100, WB 1:1000), LC3B (Proteintech, USA; 14600-1-AP; IF 1:500, WB 1:4000), MFN1 (Proteintech, USA; 13798-1-AP; WB 1:5000), MFN2 (Proteintech, USA; 12186-1-AP; WB 1:20000), DRP1 (Proteintech, USA; 12957-1-AP; WB 1:5000), P53 (Proteintech, USA; 10442-1-AP; WB 1:20000), P16 (Proteintech, USA; 10883-1-AP; WB 1:3000), NEDD8 (Abways, China; AWA11003 ; WB 1:1000), and CUL4B (Abways, China; AWA48229 ; WB 1:1000).

    Techniques: Membrane, Protein-Protein interactions, Expressing, Control, Transmission Assay, Electron Microscopy, Fluorescence, Microscopy

    (A) Co-Immunoprecipitation (Co-IP) analysis showing the binding of FUNDC1 to DRP1 in cardiomyocytes of each group; (B) Expression of P53, P16 in H9c2 cardiomyocytes in each group after siRNA interference. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; $p < 0.05 vs. HHCY + AP39); (C) Detection of cellular senescence in heart tissues of each group (upper panel) and in cardiomyocytes of each group (lower panel) by β-galactosidase assay.

    Journal: Frontiers in Pharmacology

    Article Title: AP39 alleviates HHCY-induced myocardial remodeling by regulating FUNDC1-mediated mitochondrial dynamics via S-sulfhydration of NEDD8/CUL4B

    doi: 10.3389/fphar.2026.1729145

    Figure Lengend Snippet: (A) Co-Immunoprecipitation (Co-IP) analysis showing the binding of FUNDC1 to DRP1 in cardiomyocytes of each group; (B) Expression of P53, P16 in H9c2 cardiomyocytes in each group after siRNA interference. (*p < 0.05 vs. Control; **p < 0.01 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY; $p < 0.05 vs. HHCY + AP39); (C) Detection of cellular senescence in heart tissues of each group (upper panel) and in cardiomyocytes of each group (lower panel) by β-galactosidase assay.

    Article Snippet: All primary antibodies used for Western blotting (WB) and immunofluorescence (IF) were purchased from the corresponding commercial suppliers, and their detailed information is listed as follows: GAPDH (Proteintech, USA; 10494-1-AP; WB 1:8000), α-smooth muscle actin (α-SMA) (Proteintech, USA; 14395-1-AP; WB 1:4000), Collagen type III (Proteintech, USA; 22734-1-AP; WB 1:800), FUNDC1 (Proteintech, China; AWA51295 ; IF 1:100, WB 1:1000), LC3B (Proteintech, USA; 14600-1-AP; IF 1:500, WB 1:4000), MFN1 (Proteintech, USA; 13798-1-AP; WB 1:5000), MFN2 (Proteintech, USA; 12186-1-AP; WB 1:20000), DRP1 (Proteintech, USA; 12957-1-AP; WB 1:5000), P53 (Proteintech, USA; 10442-1-AP; WB 1:20000), P16 (Proteintech, USA; 10883-1-AP; WB 1:3000), NEDD8 (Abways, China; AWA11003 ; WB 1:1000), and CUL4B (Abways, China; AWA48229 ; WB 1:1000).

    Techniques: Immunoprecipitation, Co-Immunoprecipitation Assay, Binding Assay, Expressing, Control

    (A) KEGG analysis revealed that cardiomyocytes under HHCY conditions were mainly enriched in ubiquitination pathway. (B) Heatmap showing differentially expressed CULLIN family genes in HHCY hearts. P value is shown. (C) Expression of NEDD8, Cul4b in SD rats induced by HHCY in each group. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY); (D) Co-Immunoprecipitation (Co-IP) analysis showing the binding of FUNDC1 to Cul4b in cardiomyocytes of each group; (E–G) Expression of Cul4b, FUNDC1, P53, P16 in H9c2 cardiomyocytes in each group. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY); (H) Co-immunoprecipitation (Co - IP) and ubiquitination assays were performed to assess FUNDC1 ubiquitination in Control, HHCY, and HHCY + AP39 groups. (I,J) Expression of FUNDC1, NEDD8, CUL48in H9c2 cardiomyocytes in each group. (K) Expression of NEDD8, CUL48, S-NEDD8, S-CUL4B in H9c2 cardiomyocytes in each group. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY; $p < 0.05 vs. HHCY + AP39).

    Journal: Frontiers in Pharmacology

    Article Title: AP39 alleviates HHCY-induced myocardial remodeling by regulating FUNDC1-mediated mitochondrial dynamics via S-sulfhydration of NEDD8/CUL4B

    doi: 10.3389/fphar.2026.1729145

    Figure Lengend Snippet: (A) KEGG analysis revealed that cardiomyocytes under HHCY conditions were mainly enriched in ubiquitination pathway. (B) Heatmap showing differentially expressed CULLIN family genes in HHCY hearts. P value is shown. (C) Expression of NEDD8, Cul4b in SD rats induced by HHCY in each group. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY); (D) Co-Immunoprecipitation (Co-IP) analysis showing the binding of FUNDC1 to Cul4b in cardiomyocytes of each group; (E–G) Expression of Cul4b, FUNDC1, P53, P16 in H9c2 cardiomyocytes in each group. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY; ##p < 0.01 vs. HHCY); (H) Co-immunoprecipitation (Co - IP) and ubiquitination assays were performed to assess FUNDC1 ubiquitination in Control, HHCY, and HHCY + AP39 groups. (I,J) Expression of FUNDC1, NEDD8, CUL48in H9c2 cardiomyocytes in each group. (K) Expression of NEDD8, CUL48, S-NEDD8, S-CUL4B in H9c2 cardiomyocytes in each group. (*p < 0.05 vs. Control; #p < 0.05 vs. HHCY; $p < 0.05 vs. HHCY + AP39).

    Article Snippet: All primary antibodies used for Western blotting (WB) and immunofluorescence (IF) were purchased from the corresponding commercial suppliers, and their detailed information is listed as follows: GAPDH (Proteintech, USA; 10494-1-AP; WB 1:8000), α-smooth muscle actin (α-SMA) (Proteintech, USA; 14395-1-AP; WB 1:4000), Collagen type III (Proteintech, USA; 22734-1-AP; WB 1:800), FUNDC1 (Proteintech, China; AWA51295 ; IF 1:100, WB 1:1000), LC3B (Proteintech, USA; 14600-1-AP; IF 1:500, WB 1:4000), MFN1 (Proteintech, USA; 13798-1-AP; WB 1:5000), MFN2 (Proteintech, USA; 12186-1-AP; WB 1:20000), DRP1 (Proteintech, USA; 12957-1-AP; WB 1:5000), P53 (Proteintech, USA; 10442-1-AP; WB 1:20000), P16 (Proteintech, USA; 10883-1-AP; WB 1:3000), NEDD8 (Abways, China; AWA11003 ; WB 1:1000), and CUL4B (Abways, China; AWA48229 ; WB 1:1000).

    Techniques: Ubiquitin Proteomics, Expressing, Control, Immunoprecipitation, Co-Immunoprecipitation Assay, Binding Assay

    Activation of Fn14 inhibits mitophagy in fibroblasts. A , primary fibroblasts were treated with rTWEAK (100 ng/mL) for 48 h. Cell samples were harvested after 48 h. Volcano plot showing the changes of fibroblast genes (fold change ≥ 2). B , KEGG enrichment analysis for differentially expressed genes in Control vs. rTWEAK-treated primary fibroblasts. C , Mitochondrial membrane potential was measured by JC-1 staining. D , the expression of Mfn1 , Opa1 , and Dnm1 mRNA in primary fibroblasts was detected by Real-time PCR ( n = 3). E-J , The protein levels of L-OPA1, MFN1, FUNDC1, PINK1, and LC3 were determined by Western blot analysis ( n = 3). K , Immunofluorescence and confocal microscopy show the colocalization of Mito Tracker (green) and LAMP1 (red) in rTWEAK-treated primary fibroblasts, scale bar = 50 μm. * P < 0.05 and ** P < 0.01

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Fibroblast growth factor-inducible 14 accelerates pulmonary fibrosis by inducing fibroblast senescence in mice

    doi: 10.1007/s00018-026-06161-w

    Figure Lengend Snippet: Activation of Fn14 inhibits mitophagy in fibroblasts. A , primary fibroblasts were treated with rTWEAK (100 ng/mL) for 48 h. Cell samples were harvested after 48 h. Volcano plot showing the changes of fibroblast genes (fold change ≥ 2). B , KEGG enrichment analysis for differentially expressed genes in Control vs. rTWEAK-treated primary fibroblasts. C , Mitochondrial membrane potential was measured by JC-1 staining. D , the expression of Mfn1 , Opa1 , and Dnm1 mRNA in primary fibroblasts was detected by Real-time PCR ( n = 3). E-J , The protein levels of L-OPA1, MFN1, FUNDC1, PINK1, and LC3 were determined by Western blot analysis ( n = 3). K , Immunofluorescence and confocal microscopy show the colocalization of Mito Tracker (green) and LAMP1 (red) in rTWEAK-treated primary fibroblasts, scale bar = 50 μm. * P < 0.05 and ** P < 0.01

    Article Snippet: Anti-FUNDC1 monoclonal antibody , CST , 49,240 , 1: 2000.

    Techniques: Activation Assay, Control, Membrane, Staining, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Immunofluorescence, Confocal Microscopy