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Bio-Rad goat anti mouse igg
Goat Anti Mouse Igg, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 96/100, based on 3744 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse/Goat+anti+Mouse+IgG/pmc13004575-85-30-34
Average 96 stars, based on 3744 article reviews

goat anti mouse igg - by Bioz Stars, 2026-11

96/100 stars

Images

Blood/Plasma/Serum Samples:

Article Title: A viral-vectored multipathogen vaccine platform based on replication-competent vaccinia virus and adeno-associated virus.
Article Snippet: The 96-well microplates (Costar EIA/RIA polystyrene plates, Corning Inc., Corning, New York, NY, USA) were coated with 200–400 ng/ml of each antigen overnight at 4°C and then blocked with PBS containing 1% BSA. .. Tail blood samples were serially diluted, then added to the wells and incubated at room temperature for 1 h. After washing, HRP-conjugated goat anti-mouse IgG (H+L) antibodies (Bio-Rad, Tokyo, Japan) were added to the wells. ..

Incubation:

Article Title: Oligopeptide-binding protein A is a potential target for combating Salmonella infection
Article Snippet: .. The plates were washed with PBS-T and incubated with horseradish peroxidase–conjugated goat anti-mouse IgG for 1 h at room temperature and washed with PBS-T. Tetramethylbenzidine peroxidase substrate was added to the wells, and the plates were incubated for 2 min. Absorbance was measured at 450 nm using an iMark microplate reader (Bio-Rad Laboratories). .. Lyophilized heat-killed cells as antigens for ELISA were as follows: S. Enteritidis (RIMD1933006), S. Typhimurium (RIMD1985055), S. Infantis (RIMD1905012), S. Thompson (RIMD1982025), S . Schwarzengrund (RIMD3178001) provided by the RIMD-PMRU through the Pathogenic Bacteria program in the National BioResource Project of MEXT.

Article Title: Interleukin‐35 Ameliorates Obesity‐Associated Impairment of Endothelium‐Dependent Vasodilation via the STAT3‐MAPK/ERK‐eNOS Signaling Axis
Article Snippet: .. Following incubation with HRP‐conjugated goat anti‐rabbit IgG and goat anti‐mouse IgG secondary antibodies (both 1:5000), protein bands were analyzed using Image Lab 6.0 software (BioRad, USA). ..

Article Title: The effect of lignocellulosic biomass pretreatment by-products on the fermentation activity of Saccharomyces cerevisiae yeast, measured using indices of toxic stress.
Article Snippet: The LF PVDF membranes with transferred proteins were blocked using 2% Bovine Serum Albumin and incubated with the primary antibody (HSP 70 Ms mAb to HSP70 ab 2787 or HSP 104 Rb pAb to HSP 104 ab 2924, Abcam, Cambridge, UK). .. Then, after washing the membranes with TBST (1xTBS, 0.5 ml L− 1 Tween20), they were incubated with the secondary antibody (Goat Anti-Mouse IgG (H + L)- HRP Conjugate Cat# 170-6516 or Goat Anti-Rabbit IgG (H + L)- HRP ConjugateCat# 170- 6515, Bio-Rad, Hercules, California, USA). .. For digital imaging of the obtained results, Clarity Western ECL Substrate (Bio-Rad, Hercules, California, USA) was applied to the membranes and the chemiluminescently labeled HSP proteins were read on a Chemi-Doc MT Imager, Bio-Rad.

Article Title: EEF1G promotes cancer-associated fibroblast activation and drives lung cancer metastasis
Article Snippet: The membrane was blocked with 5% non-fat milk (Carl Roth, L 301.2) at room temperature for 1 h and then incubated overnight at 4 °C with the primary antibody against the target protein (dilution per manufacturer's instructions; Abcam, ab124994 for EEF1G; anti-CD81 [ab79559]; anti-CD63 [ab315108]; anti-calnexin antibody [ab22595]; antiSTAT3 [phospho Y705] antibody [ab76315]; anti-STAT3 [ab68153]; anti-JAK2 antibody [ab108596]; anti-JAK2 [phospho Y1007 + Y1008] antibody [ab32101]; anti-beta actin [ab8226]; anti-TAK1 [phospho S439] [ab109404]; TAK1 antibody [AF7616]; phospho-NF-κB p65 antibody [AF2006]; and NF-κB p65 [BF8005]). .. Goat anti-rabbit IgG (H+L) HRP-conjugated secondary antibody (Bio-Rad, 170-6515) or goat anti-mouse IgG (H+L) HRP-conjugated secondary antibody (Bio-Rad, 170-6516) was used and incubated at room temperature for 2 h. After removing the secondary antibody, the membrane was washed three times with TBST buffer (Tris-buffered saline with 0.1% Tween 20; Sigma–Aldrich, P1379), with each wash lasting 10 min. .. Protein expression AR TIC LE IN PR ES S was detected using an ECL chemiluminescent imager (GE Healthcare, 28906836), and semiquantitative analysis was conducted using Amersham Imager 680 software (GE Healthcare).

Software:

Control:

Article Title: The pyrin inflammasome senses OCTN2-mediated uptake of extracellular ʟ-carnitine from muscle injury or ingestion.
Article Snippet: In brief ʟ-Carnitine is a nonproteinogenic amino acid highly abundant in myocytes, and both excess ingestion of myocytes and myocyte necrosis are associated with systemic inflammation.. Here, we find that the pyrin inflammasome senses extracellular ʟ-carnitine through the highaffinity carnitine transporter OCTN2 (SLC22A5) and this leads to IL1β-mediated inflammation.. Our findings position OCTN2 as a potential target to reduce inflammation from exogenous or endogenous sources of extracellular ʟ-carnitine.

Recombinant:

other:

Article Title: Modified tumor uptake and biodistribution of nanoparticles coated with small extracellular vesicle membranes derived from distinct tumor cell lines
Article Snippet: Membranes were then probed with primary antibodies diluted 1:1000 in blocking buffer overnight at 4 °C: mouse monoclonal CD63 (sc-5275, Santa Cruz), mouse monoclonal CD81 (sc-166029 and sc-23962, Santa Cruz), rat monoclonal CD9 (sc-18869, Santa Cruz), rat monoclonal CD47 (16-0471-81, eBioscience, Invitrogen).

Membrane:

Saline:

Image Search Results

USP18 expression is induced by cardiac I/R injury. a Gene Ontology (GO) enrichment analysis of the RNA-seq data in I/R and control hearts at 24 h postsurgery ( n =3). b Heatmap displaying differentially expressed ubiquitination-associated genes in I/R and control hearts at 24 h postsurgery ( n =3). c Protein levels of USP18 in donor heart tissue and patients with ischemic heart disease (IHD) ( n =4). d Immunofluorescence staining of USP18 and α-actin in donor heart tissue and patients with IHD ( n =3). Scale bar=35 μm (left) and 50 μm (right). e Protein levels of USP18 in heart tissue post-IR ( n =4). f Immunofluorescence staining of USP18 and WGA in heart tissue 24 h after I/R injury ( n =5). Scale bar=50 μm. g Protein expression of USP18 in primary neonatal rat cardiomyocytes (NRVMs) after H/R challenge ( n =4). h Immunofluorescence staining of USP18 in cardiomyocytes after H/R challenge. Scale bar=50 μm. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WGA. Wheat germ agglutinin; DAPI. 4′,6-diamidino-2-phenylindole; H/R. Hypoxia/reoxygenation; RNA-seq. RNA sequencing; MAPK. Mitogen-activated protein kinase; GABA. γ-aminobutyric acid.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 expression is induced by cardiac I/R injury. a Gene Ontology (GO) enrichment analysis of the RNA-seq data in I/R and control hearts at 24 h postsurgery ( n =3). b Heatmap displaying differentially expressed ubiquitination-associated genes in I/R and control hearts at 24 h postsurgery ( n =3). c Protein levels of USP18 in donor heart tissue and patients with ischemic heart disease (IHD) ( n =4). d Immunofluorescence staining of USP18 and α-actin in donor heart tissue and patients with IHD ( n =3). Scale bar=35 μm (left) and 50 μm (right). e Protein levels of USP18 in heart tissue post-IR ( n =4). f Immunofluorescence staining of USP18 and WGA in heart tissue 24 h after I/R injury ( n =5). Scale bar=50 μm. g Protein expression of USP18 in primary neonatal rat cardiomyocytes (NRVMs) after H/R challenge ( n =4). h Immunofluorescence staining of USP18 in cardiomyocytes after H/R challenge. Scale bar=50 μm. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WGA. Wheat germ agglutinin; DAPI. 4′,6-diamidino-2-phenylindole; H/R. Hypoxia/reoxygenation; RNA-seq. RNA sequencing; MAPK. Mitogen-activated protein kinase; GABA. γ-aminobutyric acid.

Article Snippet: To establish a cardiac-specific USP18 knockout mice model (USP18-cKO), USP18 flox/flox mice (C57BL/6 J; Shanghai Model Organisms, NM-cKO-215042) were bred with α-MHC-MerCreMer mice (C57BL/6 J; Jackson Laboratory, stock No. 024992).

Techniques: Expressing, RNA Sequencing, Control, Ubiquitin Proteomics, Immunofluorescence, Staining

$USP18 deficiency mitigates mitochondrial dysfunction, acute cardiac I/R injury, and cardiac remodeling in vivo. a 2,3,5-triphenyltetrazolium chloride (TTC) staining of heart tissue 24 h post-I/R in WT and I/R groups ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA ( n =6) and mitochondrial complexes I and II–III activity ( n =5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001. c Representative electron micros c opy images of heart sections 24 h post-I/R; quantitative analysis of the mitochondrial volume density and percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss ⁎⁎⁎ P <0.001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001, ns non-significant. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricle (LV) fibrotic area in WT mice and USP18-cKO mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎ P <0.01. f Representative B-mode and M-mode echocardiographic images of LV from WT mice or USP18-cKO mice 4 weeks after I/R injury. g Cardiac function of WT mice and USP18-cKO mice after I/R injury at the indicated time points ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . WT, ns non-significant. USP18 . Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; USP18-cKO. Ubiquitin-specific protease 18 conditional knockout; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.$

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 deficiency mitigates mitochondrial dysfunction, acute cardiac I/R injury, and cardiac remodeling in vivo. a 2,3,5-triphenyltetrazolium chloride (TTC) staining of heart tissue 24 h post-I/R in WT and I/R groups ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA ( n =6) and mitochondrial complexes I and II–III activity ( n =5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001. c Representative electron micros c opy images of heart sections 24 h post-I/R; quantitative analysis of the mitochondrial volume density and percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss ⁎⁎⁎ P <0.001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001, ns non-significant. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricle (LV) fibrotic area in WT mice and USP18-cKO mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎ P <0.01. f Representative B-mode and M-mode echocardiographic images of LV from WT mice or USP18-cKO mice 4 weeks after I/R injury. g Cardiac function of WT mice and USP18-cKO mice after I/R injury at the indicated time points ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . WT, ns non-significant. USP18 . Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; USP18-cKO. Ubiquitin-specific protease 18 conditional knockout; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.

Techniques: In Vivo, Staining, Activity Assay, Ubiquitin Proteomics, Knock-Out

$Overexpression of USP18 in the heart exacerbates mitochondrial dysfunction, acute cardiac injury, and cardiac remodeling following I/R in mice. a TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA levels ( n= 6) and mitochondrial complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. c Representative electron microscopy images of heart sections 24 h post-I/R. Quantitative analysis of mitochondrial volume density and the percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss. ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎ P <0.05, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricl e (LV) fibrotic area in AAV9-USP18-transfected mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. f Representative B-mode and M-mode echocardiographic images of LV from AAV9-USP18-transfected mice 4 weeks after I/R injury. g Cardiac function of AAV9-USP18-transfected mice after I/R injury at the indicated time points ( n= 6). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . AAV9-NC, ns non-significant. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.$

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Overexpression of USP18 in the heart exacerbates mitochondrial dysfunction, acute cardiac injury, and cardiac remodeling following I/R in mice. a TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA levels ( n= 6) and mitochondrial complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. c Representative electron microscopy images of heart sections 24 h post-I/R. Quantitative analysis of mitochondrial volume density and the percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss. ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎ P <0.05, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricl e (LV) fibrotic area in AAV9-USP18-transfected mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. f Representative B-mode and M-mode echocardiographic images of LV from AAV9-USP18-transfected mice 4 weeks after I/R injury. g Cardiac function of AAV9-USP18-transfected mice after I/R injury at the indicated time points ( n= 6). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . AAV9-NC, ns non-significant. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.

Techniques: Over Expression, Staining, Activity Assay, Electron Microscopy, Transfection, Ubiquitin Proteomics, Negative Control, Virus

Effects of USP18 on H/R-induced injury to NRVMs. a-d NRVMs were transfected with USP18 siRNA and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( a and b ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( c and d ). e-h NRVMs were infected with Ad-USP18 and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( e and f ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( g and h ). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. US P 18. Ubiquitin-specific protease 18; H/R. Hypoxia/reoxygenation; NC. Negative control; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; NRVMs. Neonatal rat ventricular cardiomyocytes; ATP. Adenosine triphosphate; OCR. Oxygen consumption rate.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Effects of USP18 on H/R-induced injury to NRVMs. a-d NRVMs were transfected with USP18 siRNA and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( a and b ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( c and d ). e-h NRVMs were infected with Ad-USP18 and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( e and f ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( g and h ). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. US P 18. Ubiquitin-specific protease 18; H/R. Hypoxia/reoxygenation; NC. Negative control; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; NRVMs. Neonatal rat ventricular cardiomyocytes; ATP. Adenosine triphosphate; OCR. Oxygen consumption rate.

Techniques: Transfection, Confocal Microscopy, Infection, Ubiquitin Proteomics, Negative Control

USP18 aggravates cardiac I/R injury through regulation of mitochondria and inhibition of mitophagy. a Electron microscopy image showing mitophagy in USP18-cKO mouse hearts ( n= 5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. b Protein levels of PINK1, Parkin, ubiquitinated proteins (Ub), P62, and LC3II in mitochondria from heart tissue in USP18-cKO and WT mice 24 h after I/R injury ( n =4). c Electron microscopy image showing mitophagy in USP18-overexpres (OV) mouse hearts ( n =5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. d Protein levels of PINK1, Parkin, Ub, P62, and LC3II proteins in mitochondria from the heart tissue of USP18-OV mice 24 h after I/R injury ( n =4). Color shift in mitophagy dye (red) and lysosomal dye (green) in NRVMs showing mitophagy in NRVMs with USP18 siRNA transfection ( e ) or Ad-USP18 infection ( f ) and the quantitative mitophagy index in each group ( n= 5). Scale bar=9 μm. Protein levels of PINK1, Parkin, Ub, P62, and LC3II in mitochondria from NRVMs transfected with USP18 siRNA ( g ) or infected with Ad-USP18 ( h ). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001 ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; KO. Knockout; P62. Sequestosome 1; LC3. Microtubule-associated protein 1 light chain 3; VDAC. Voltage-dependent anion channel.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 aggravates cardiac I/R injury through regulation of mitochondria and inhibition of mitophagy. a Electron microscopy image showing mitophagy in USP18-cKO mouse hearts ( n= 5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. b Protein levels of PINK1, Parkin, ubiquitinated proteins (Ub), P62, and LC3II in mitochondria from heart tissue in USP18-cKO and WT mice 24 h after I/R injury ( n =4). c Electron microscopy image showing mitophagy in USP18-overexpres (OV) mouse hearts ( n =5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. d Protein levels of PINK1, Parkin, Ub, P62, and LC3II proteins in mitochondria from the heart tissue of USP18-OV mice 24 h after I/R injury ( n =4). Color shift in mitophagy dye (red) and lysosomal dye (green) in NRVMs showing mitophagy in NRVMs with USP18 siRNA transfection ( e ) or Ad-USP18 infection ( f ) and the quantitative mitophagy index in each group ( n= 5). Scale bar=9 μm. Protein levels of PINK1, Parkin, Ub, P62, and LC3II in mitochondria from NRVMs transfected with USP18 siRNA ( g ) or infected with Ad-USP18 ( h ). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001 ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; KO. Knockout; P62. Sequestosome 1; LC3. Microtubule-associated protein 1 light chain 3; VDAC. Voltage-dependent anion channel.

Techniques: Inhibition, Electron Microscopy, Transfection, Infection, Ubiquitin Proteomics, Knock-Out

$Parkin knockdown counteracts the protection of USP18 deficiency in vivo. USP18-cKO mice were infected with AAV9-shParkin and subjected to I/R surgery. a Parkin protein levels in mouse hearts infected with AAV9-shParkin ( n= 4). b TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. c Serum levels of cTnI, CK-MB, and LDH in AAV9-shParkin-infected mice 4 h after I/R surgery ( n= 5). d DNA fragmentation and cleaved caspase-3 activity in heart tissue from AAV9-shParkin-infected mice 24 h after I/R injury ( n= 6). e Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). f Mitochondrial DNA ( n= 6) and complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. g Representative electron microscopy images of heart sections 24 h post-I/R. The mitochondrial volume density and percent of mitochondria with cristae loss were measured in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). h Protein levels of P62, ubiquitinated proteins (Ub), and LC3II in mitochondria from heart tissue 24 h after I/R injury ( n= 4). i H&E staining and quantitative statistical analysis of cell size ( n= 5) in USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. Scale bar=1 μm (top) and 50 μm (bottom). j Heart weight-to-tibia length ratio (HW/TL) ( n= 6) in each group. k Representative B-mode and M-mode echocardiographic images of the left ventricle from USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. l Cardiac function of USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; cTnI. Cardiac Troponin I; CK-MB. Creatine kinase-MB isoenzyme; LDH. Lactate dehydrogenase; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening; HR. Heart rate.$

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Parkin knockdown counteracts the protection of USP18 deficiency in vivo. USP18-cKO mice were infected with AAV9-shParkin and subjected to I/R surgery. a Parkin protein levels in mouse hearts infected with AAV9-shParkin ( n= 4). b TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. c Serum levels of cTnI, CK-MB, and LDH in AAV9-shParkin-infected mice 4 h after I/R surgery ( n= 5). d DNA fragmentation and cleaved caspase-3 activity in heart tissue from AAV9-shParkin-infected mice 24 h after I/R injury ( n= 6). e Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). f Mitochondrial DNA ( n= 6) and complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. g Representative electron microscopy images of heart sections 24 h post-I/R. The mitochondrial volume density and percent of mitochondria with cristae loss were measured in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). h Protein levels of P62, ubiquitinated proteins (Ub), and LC3II in mitochondria from heart tissue 24 h after I/R injury ( n= 4). i H&E staining and quantitative statistical analysis of cell size ( n= 5) in USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. Scale bar=1 μm (top) and 50 μm (bottom). j Heart weight-to-tibia length ratio (HW/TL) ( n= 6) in each group. k Representative B-mode and M-mode echocardiographic images of the left ventricle from USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. l Cardiac function of USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; cTnI. Cardiac Troponin I; CK-MB. Creatine kinase-MB isoenzyme; LDH. Lactate dehydrogenase; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening; HR. Heart rate.

Techniques: Knockdown, In Vivo, Infection, Staining, Activity Assay, Electron Microscopy, Ubiquitin Proteomics, Negative Control, Virus

USP18 inhibits mitophagy degradation and facilitates cardiac I/R injury through deubiquitinating and upregulating PTEN-L. a The protein levels of PTEN-L and PTEN in USP18-cKO mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎⁎ P <0.0001, ns non-significant. b The protein levels of PTEN-L and PTEN in AAV9-USP18-infected mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. c Co-IP of USP18 and PTEN-L in NRVMs (left); NRVMs were transfected with HA-PTEN-L and Flag-USP18 (middle); Co-IP of Flag-USP18 and HA-PTEN-L in NRVMs (right). d Endogenous Co-IP of USP18 and PTEN-L in NRVMs subjected to H/R injury. e Endogenous Co-IP of USP18 and PTEN-L in hearts subjected to I/R injury. f PTEN-L ubiquitination (Ub) levels assessed by CO-IP in NRVMs subjected to H/R injury (top) and hearts subjected to I/R injury (bottom). g NRVMs were transfected with Ad-USP18 or USP18 siRNA or HA-PTEN-L and Myc-Ub and treated with MG132. Co-IP of Myc-Ub and HA-PTEN-L. h Schematic representations of t h e domains of PTEN-L involved in binding to USP18. Full-length PTEN-L or truncated PTEN-L was coexpressed with USP18 in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. i Schematic representations of USP18 residues involved in binding to PTEN-L. Full-length USP18 or USP18 truncations were coexpressed with PTEN-L in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. j Ub assay of PTEN-L in HEK293T cells cotransfected with Myc-USP18, Myc-USP18-mut, and Flag-PTEN-L and treated with 10 μmol/L MG132. k, l NRVMs were transfected with scRNA or USP18 siRNA ( k ), infected with Ad-NC or Ad-USP18 ( l ), and then treated with cycloheximide (CHX, 10 μmol/L) for the indicated time periods. Representative immunoblot analysis of PTEN-L protein levels in each group. ⁎⁎⁎⁎ P <0.0001 vs . scRNA or Ad-NC. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; H/R. Hypoxia-reoxygenation; PTEN. Phosphatase and tensin homolog; PTEN-L. Phosphatase and tensin homolog-long; AAV9. Adeno-associated virus serotype 9; NC. Negative control.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 inhibits mitophagy degradation and facilitates cardiac I/R injury through deubiquitinating and upregulating PTEN-L. a The protein levels of PTEN-L and PTEN in USP18-cKO mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎⁎ P <0.0001, ns non-significant. b The protein levels of PTEN-L and PTEN in AAV9-USP18-infected mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. c Co-IP of USP18 and PTEN-L in NRVMs (left); NRVMs were transfected with HA-PTEN-L and Flag-USP18 (middle); Co-IP of Flag-USP18 and HA-PTEN-L in NRVMs (right). d Endogenous Co-IP of USP18 and PTEN-L in NRVMs subjected to H/R injury. e Endogenous Co-IP of USP18 and PTEN-L in hearts subjected to I/R injury. f PTEN-L ubiquitination (Ub) levels assessed by CO-IP in NRVMs subjected to H/R injury (top) and hearts subjected to I/R injury (bottom). g NRVMs were transfected with Ad-USP18 or USP18 siRNA or HA-PTEN-L and Myc-Ub and treated with MG132. Co-IP of Myc-Ub and HA-PTEN-L. h Schematic representations of t h e domains of PTEN-L involved in binding to USP18. Full-length PTEN-L or truncated PTEN-L was coexpressed with USP18 in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. i Schematic representations of USP18 residues involved in binding to PTEN-L. Full-length USP18 or USP18 truncations were coexpressed with PTEN-L in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. j Ub assay of PTEN-L in HEK293T cells cotransfected with Myc-USP18, Myc-USP18-mut, and Flag-PTEN-L and treated with 10 μmol/L MG132. k, l NRVMs were transfected with scRNA or USP18 siRNA ( k ), infected with Ad-NC or Ad-USP18 ( l ), and then treated with cycloheximide (CHX, 10 μmol/L) for the indicated time periods. Representative immunoblot analysis of PTEN-L protein levels in each group. ⁎⁎⁎⁎ P <0.0001 vs . scRNA or Ad-NC. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; H/R. Hypoxia-reoxygenation; PTEN. Phosphatase and tensin homolog; PTEN-L. Phosphatase and tensin homolog-long; AAV9. Adeno-associated virus serotype 9; NC. Negative control.

Techniques: Infection, Co-Immunoprecipitation Assay, Transfection, Ubiquitin Proteomics, Binding Assay, Immunoprecipitation, Western Blot, Virus, Negative Control

Summary of the key findings in this paper. Cardiac I/R injury upregulates USP18 in both mouse and human hearts. USP18 interacts with PTEN-L, inhibiting Parkin phosphorylation and mitochondrial translocation, thereby suppressing mitophagy and exacerbating mitochondrial dysfunction and myocardial injury. PTEN-L additionally promotes cardiac damage via a paracrine mechanism. Genetic or pharmacological targeting of the USP18-PTEN-L axis restores mitophagy and protects against I/R-induced cardiac injury, representing a potential therapeutic strategy. I/R. Ischemia/reperfusion; PTEN-L. Phosphatase and tensin homolog-long; USP18. Ubiquitin-specific protease 18; Ub. Ubiquitination.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Summary of the key findings in this paper. Cardiac I/R injury upregulates USP18 in both mouse and human hearts. USP18 interacts with PTEN-L, inhibiting Parkin phosphorylation and mitochondrial translocation, thereby suppressing mitophagy and exacerbating mitochondrial dysfunction and myocardial injury. PTEN-L additionally promotes cardiac damage via a paracrine mechanism. Genetic or pharmacological targeting of the USP18-PTEN-L axis restores mitophagy and protects against I/R-induced cardiac injury, representing a potential therapeutic strategy. I/R. Ischemia/reperfusion; PTEN-L. Phosphatase and tensin homolog-long; USP18. Ubiquitin-specific protease 18; Ub. Ubiquitination.

Techniques: Phospho-proteomics, Translocation Assay, Ubiquitin Proteomics

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