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Developmental Studies Hybridoma Bank anti-titin
Anti Titin, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 94/100, based on 101 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/9/anti-Titin/custom%409%2Ed10%4042569301
Average 94 stars, based on 101 article reviews

anti-titin - by Bioz Stars, 2026-10

94/100 stars

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Incubation:

Article Title: Human in vitro neuromuscular junction model to functionally dissect the pathogenic mechanism of anti-AChR autoantibody-positive myasthenia gravis
Article Snippet: .. Subsequently, the samples were incubated overnight with primary antibodies against class III beta-tubulin (1:200; Abcam, Cambridge, UK), HB9 (1:50; Santa Cruz, Dallas, TX, USA), SMI-32 (1:100; BioLegend, San Diego, CA, USA), vesicular glutamate transporter 1 (VGLUT1) (1:100; Abcam), sarcomeric α-actinin (1:100; Abcam), titin (1:200; Developmental Studies Hybridoma Bank, Iowa City, IA, USA), and C5b9 (1:500; BD Biosciences, Franklin Lakes, NJ, USA) in the blocking buffer. .. The samples were then stained with secondary antibodies conjugated to Alexa Fluor 647 or 488 (donkey anti-mouse or donkey anti-rabbit, 1:200; Thermo Fisher Scientific) in the blocking buffer for 1 hour.

Blocking Assay:

Marker:

Article Title: Muscle-fiber-inspired nanofibrillar microbundles induce myogenic differentiation in human adipose-derived stem cells
Article Snippet: .. For myogenic marker staining, samples were immunostained using anti-myosin (Invitrogen), anti-myogenin (DSHB, Iowa City, USA), or anti-titin (DSHB, Iowa City, USA) following the same procedure described infocal adhesion and ECM staining. ..

Staining:

Image Search Results

Concentration-dependent change in the humoral inflammatory response following incubation with Escherichia coli ( E. coli ) in the ex vivo whole blood model. a Absolute plasma concentrations of IL-6, IL-8, and MMP9 determined by enzyme-linked immunosorbent assay. b Normalized values and EC 50 curve fit by BuC=0% and 50 000 CFU/ml E. coli= 100%, respectively, for IL-6, IL-8, and MMP9 as indicated by EC 50 (%) on the respective Y-axis. BuC indicates buffer control after 60 min incubation; numbers on the X-axis indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation; LPS indicates lipopolysaccharide (LPS) 100 ng/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, comparing all shown concentrations of E. coli bacteria and 100 ng/ml LPS with BuC. P -values are indicated above the respective data points. ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Concentration-dependent change in the humoral inflammatory response following incubation with Escherichia coli ( E. coli ) in the ex vivo whole blood model. a Absolute plasma concentrations of IL-6, IL-8, and MMP9 determined by enzyme-linked immunosorbent assay. b Normalized values and EC 50 curve fit by BuC=0% and 50 000 CFU/ml E. coli= 100%, respectively, for IL-6, IL-8, and MMP9 as indicated by EC 50 (%) on the respective Y-axis. BuC indicates buffer control after 60 min incubation; numbers on the X-axis indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation; LPS indicates lipopolysaccharide (LPS) 100 ng/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, comparing all shown concentrations of E. coli bacteria and 100 ng/ml LPS with BuC. P -values are indicated above the respective data points. ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Concentration Assay, Incubation, Ex Vivo, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Bacteria

Diagnostic performance for the detection of bacteremia, analyzing the neutrophil phenotype by determining the median fluorescence intensity (MFI) and the cellular response capacity (CRC) in comparison with traditional markers of humoral inflammation (IL-6, IL-8, MMP9). a Comparison of receiver operating characteristic (ROC) at 10,000 CFU/ml Escherichia coli ( E. coli ) with the respective 95% confidence interval (CI) and P -value, and half-maximal effective concentration (EC 50 ) as a function of the E. coli concentration. b Detailed comparison of the EC 50 as a function of the E. coli concentration. c Exemplary comparison of EC 50 curve fit after normalization as indicated by EC 50 (%) on the respective Y-axis to BuC=100% and 50 000 CFU/ml E. coli =0% for the humoral marker IL-6 (the IL-6 values were multiplied by −1 before EC 50 calculation to facilitate comparability with the CRC) and the change in neutrophil phenotype represented by CD11b CRC. BuC indicates buffer control after 60 min incubation; numbers on the X-axis of c indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, evaluating the EC 50 of IL-8, MMP9, the MFI, and CRC of CD10, CD11b, and CD62L in comparison to the EC 50 of IL-6. P -values are indicated above the respective data points. ⁎ P <0.05. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Diagnostic performance for the detection of bacteremia, analyzing the neutrophil phenotype by determining the median fluorescence intensity (MFI) and the cellular response capacity (CRC) in comparison with traditional markers of humoral inflammation (IL-6, IL-8, MMP9). a Comparison of receiver operating characteristic (ROC) at 10,000 CFU/ml Escherichia coli ( E. coli ) with the respective 95% confidence interval (CI) and P -value, and half-maximal effective concentration (EC 50 ) as a function of the E. coli concentration. b Detailed comparison of the EC 50 as a function of the E. coli concentration. c Exemplary comparison of EC 50 curve fit after normalization as indicated by EC 50 (%) on the respective Y-axis to BuC=100% and 50 000 CFU/ml E. coli =0% for the humoral marker IL-6 (the IL-6 values were multiplied by −1 before EC 50 calculation to facilitate comparability with the CRC) and the change in neutrophil phenotype represented by CD11b CRC. BuC indicates buffer control after 60 min incubation; numbers on the X-axis of c indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, evaluating the EC 50 of IL-8, MMP9, the MFI, and CRC of CD10, CD11b, and CD62L in comparison to the EC 50 of IL-6. P -values are indicated above the respective data points. ⁎ P <0.05. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Techniques: Diagnostic Assay, Fluorescence, Comparison, Concentration Assay, Marker, Control, Incubation, Bacteria

Clinical specifications and parameters over all time points of the sepsis cohort. a Suspected infection cause of sepsis. b Distribution of the individual score points of the Sequential Organ Failure Assessment (SOFA) score. c Total SOFA score. d-h Traditional and humoral markers of inflammation: leukocytes and neutrophil-lymphocyte ratio ( d ), C-reactive protein (CRP) and procalcitonin (PCT) ( e ), interleukin-6 (IL-6) and interleukin-8 (IL-8) ( f ), serum amyloid A (SAA) and calprotectin ( g ), matrix metallopeptidase 9 (MMP9) and myeloperoxidase (MPO) ( h ). Values are shown as median and interquartile range. n =14. CNS. Central nervous system; HV. Healthy volunteers.

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Clinical specifications and parameters over all time points of the sepsis cohort. a Suspected infection cause of sepsis. b Distribution of the individual score points of the Sequential Organ Failure Assessment (SOFA) score. c Total SOFA score. d-h Traditional and humoral markers of inflammation: leukocytes and neutrophil-lymphocyte ratio ( d ), C-reactive protein (CRP) and procalcitonin (PCT) ( e ), interleukin-6 (IL-6) and interleukin-8 (IL-8) ( f ), serum amyloid A (SAA) and calprotectin ( g ), matrix metallopeptidase 9 (MMP9) and myeloperoxidase (MPO) ( h ). Values are shown as median and interquartile range. n =14. CNS. Central nervous system; HV. Healthy volunteers.

Techniques: Infection

$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.

Article Snippet: To induce cardiac-specific USP18 overexpression, male C57BL/6 J mice received a single tail vein injection of adeno-associated virus serotype 9 (AAV9)-cardiac troponin T (cTnT)-USP18 or control AAV9-negative control [60–80 μl, (5.0–6.5)×1013 viral genome/ml, Vigene Bioscience, China] under 1.5%–2% isoflurane anesthesia.

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

$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

Evaluation of the drug combinations for anti-proliferative effects on different CRC cell lines. The response of drug combinations was further evaluated for antagonistic, additive, and synergistic responses on CRC cell proliferation. The combination effects were calculated as a ratio of the observed response divided by the predicted response based on the Bliss independence model. <xref ref-type=

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: Evaluation of the drug combinations for anti-proliferative effects on different CRC cell lines. The response of drug combinations was further evaluated for antagonistic, additive, and synergistic responses on CRC cell proliferation. The combination effects were calculated as a ratio of the observed response divided by the predicted response based on the Bliss independence model. ⁵² Panel A shows that 9-cis-RA + Sulindac and Piroxicam, Liarozole + Piroxicam, and ATRA + Sulindac have additive effects in HT29 cells. Panel B shows that 9-cis-RA + Sulindac and Piroxicam, Liarozole + Piroxicam, and ATRA + Sulindac have synergistic effects in HCT116 cells. Panel C shows that Talarozole + Sulindac have synergistic effects in SW480 cells. The synergistic response is < 1, additive ~1, and antagonistic > 1.

Article Snippet: Drug sources are as follows: Sulindac, Piroxicam, and Talarozole (Sigma-Aldrich, St Louis, MO), 9-cis retinoic acid (Santa Cruz Biotechnology, Dallas, TX), Liarozole (R&D Chemical, Gonzales, LA), and all-trans retinoic acid (Stem Cell Technologies, Vancouver, BC).

Techniques:

Drug combination effects on stem cells and neuroendocrine cells. The effects of retinoids and anti-WNT agents on ALDH + stem cells were evaluated based on the ALDEFLUOR assay. The results showed that treatment with the 9-cis RA + Sulindac drug combination substantially decreased the population of ALDH + cells in HCT116 cells (Panel B), but not in HT29 (Panel A) or SW480 (Panel C) cells. Notably, this decrease was seen in HCT116 cells at both time points (24 and 48 h). Neuroendocrine cells (NECs). The effects of retinoids and anti-WNT agents on NEC differentiation were evaluated using western blot analysis for expression of differentiation markers in HCT116 CRC cells (Panels D–F) and SW480 cells (Panels G–I). The results show that drug combinations increase NEC differentiation in HCT116 and SW480 CRC cells. GLP2R = glucagon-like protein two receptors, SSTR1 = somatostatin receptor 1, CHGA = chromogranin A, NSE = neuron-specific enolase. The experiments were done in triplicate, and the error bars represent ± the SEM. * p < 0.05.

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: Drug combination effects on stem cells and neuroendocrine cells. The effects of retinoids and anti-WNT agents on ALDH + stem cells were evaluated based on the ALDEFLUOR assay. The results showed that treatment with the 9-cis RA + Sulindac drug combination substantially decreased the population of ALDH + cells in HCT116 cells (Panel B), but not in HT29 (Panel A) or SW480 (Panel C) cells. Notably, this decrease was seen in HCT116 cells at both time points (24 and 48 h). Neuroendocrine cells (NECs). The effects of retinoids and anti-WNT agents on NEC differentiation were evaluated using western blot analysis for expression of differentiation markers in HCT116 CRC cells (Panels D–F) and SW480 cells (Panels G–I). The results show that drug combinations increase NEC differentiation in HCT116 and SW480 CRC cells. GLP2R = glucagon-like protein two receptors, SSTR1 = somatostatin receptor 1, CHGA = chromogranin A, NSE = neuron-specific enolase. The experiments were done in triplicate, and the error bars represent ± the SEM. * p < 0.05.

Techniques: Western Blot, Analysis, Expressing

The effect of drug combinations on changes in gene expression in CRC cells. We conducted NanoString Profiling of HCT116 and SW480 cells treated with 9-cis-RA and Liarozole in combination with Sulindac to study the effects of drug combinations on gene expression. The heat maps (Panels A & B) show that drug combination treatments involving an RA agent (9-cis RA or Liarozole) in combination with an anti-WNT agent (Sulindac) lead to dramatic differences in gene expression compared to treatment with single agents. Sulindac treatment leads to the downregulation of a substantial number of genes in HCT116 cells (Panel C) and SW480 cells (Panel D). This down-regulation is characterized by changes in the expression of various WNT target genes. Changes in the expression of genes with WNT-regulatory elements (WREs) in HCT116 (Panels A and C) and SW480 (Panels B and D) cells indicate that Sulindac targets WNT signaling. Genes with WNT-regulatory elements show up- or down-regulation of expression (>2X-fold) in response to Sulindac treatment in HCT116 (Panel C) and SW480 (Panel D) CRC cells. In HCT116 cells, decreased expression of the notable WNT target genes MET , MYC , AXIN2 , BMP4 , RNF43 , and TCF3 are shown (Panel E). While in SW480 cells, the expression of the WNT target genes AXIN2 , BMP4 , RNF43 , and CCND1 had decreased (Panel F).

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: The effect of drug combinations on changes in gene expression in CRC cells. We conducted NanoString Profiling of HCT116 and SW480 cells treated with 9-cis-RA and Liarozole in combination with Sulindac to study the effects of drug combinations on gene expression. The heat maps (Panels A & B) show that drug combination treatments involving an RA agent (9-cis RA or Liarozole) in combination with an anti-WNT agent (Sulindac) lead to dramatic differences in gene expression compared to treatment with single agents. Sulindac treatment leads to the downregulation of a substantial number of genes in HCT116 cells (Panel C) and SW480 cells (Panel D). This down-regulation is characterized by changes in the expression of various WNT target genes. Changes in the expression of genes with WNT-regulatory elements (WREs) in HCT116 (Panels A and C) and SW480 (Panels B and D) cells indicate that Sulindac targets WNT signaling. Genes with WNT-regulatory elements show up- or down-regulation of expression (>2X-fold) in response to Sulindac treatment in HCT116 (Panel C) and SW480 (Panel D) CRC cells. In HCT116 cells, decreased expression of the notable WNT target genes MET , MYC , AXIN2 , BMP4 , RNF43 , and TCF3 are shown (Panel E). While in SW480 cells, the expression of the WNT target genes AXIN2 , BMP4 , RNF43 , and CCND1 had decreased (Panel F).

Techniques: Gene Expression, Profiling, Expressing

Analysis of Sulindac’s ability to sensitize CRC cells to the effect of retinoids based on gene expression. Further NanoString expression profiling was done on HCT116 and SW480 cells treated with 9-cis-RA or Liarozole in combination with Sulindac. The effect of RA agents on CRC cells . The Venn diagrams (Panel A) show that changes in the expression ( p < 0.05) of the same genes in both cell lines (HCT116 and SW480) occurred with 9-cis-RA treatment ( n = 38 genes) and Liarozole treatment ( n = 45 genes). The Venn diagrams (Panel B) also show that changes in the expression ( p < 0.05) of the same genes occur with both RA agents (9-cis-RA and Liarozole) in HCT116 ( n = 49 genes) and SW480 cells ( n = 65 genes). These results indicate that a common set of genes is targeted by both of the RA agents (9-cis-RA and Liarozole) in CRC cells. Indeed, 19 of the same genes changed in expression (7 upregulated and 12 down-regulated) with both RA agent treatments and in both CRC cell lines (Panel C). The effect of Sulindac on responses to RA agents . In both HCT116 (Panels D and E) and SW480 (Panels F and G) cells, one set of genes is down-regulated, and another set is up-regulated ( p < 0.05) by retinoid agents after Sulindac treatment. Additional analyses to illustrate the change in the expression of the specific genes are presented in waterfall plots (Figure S3) and in lists of the top 10 genes upregulated (Table S3) and downregulated (Table S4) by RA agents after Sulindac treatment. Interestingly, many of the same genes are upregulated or downregulated by Liarozole and 9-cis RA in both cell lines. Overall, these results indicate that Sulindac sensitizes HCT116 and SW480 CRC cells to the effect of retinoids on gene expression.

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: Analysis of Sulindac’s ability to sensitize CRC cells to the effect of retinoids based on gene expression. Further NanoString expression profiling was done on HCT116 and SW480 cells treated with 9-cis-RA or Liarozole in combination with Sulindac. The effect of RA agents on CRC cells . The Venn diagrams (Panel A) show that changes in the expression ( p < 0.05) of the same genes in both cell lines (HCT116 and SW480) occurred with 9-cis-RA treatment ( n = 38 genes) and Liarozole treatment ( n = 45 genes). The Venn diagrams (Panel B) also show that changes in the expression ( p < 0.05) of the same genes occur with both RA agents (9-cis-RA and Liarozole) in HCT116 ( n = 49 genes) and SW480 cells ( n = 65 genes). These results indicate that a common set of genes is targeted by both of the RA agents (9-cis-RA and Liarozole) in CRC cells. Indeed, 19 of the same genes changed in expression (7 upregulated and 12 down-regulated) with both RA agent treatments and in both CRC cell lines (Panel C). The effect of Sulindac on responses to RA agents . In both HCT116 (Panels D and E) and SW480 (Panels F and G) cells, one set of genes is down-regulated, and another set is up-regulated ( p < 0.05) by retinoid agents after Sulindac treatment. Additional analyses to illustrate the change in the expression of the specific genes are presented in waterfall plots (Figure S3) and in lists of the top 10 genes upregulated (Table S3) and downregulated (Table S4) by RA agents after Sulindac treatment. Interestingly, many of the same genes are upregulated or downregulated by Liarozole and 9-cis RA in both cell lines. Overall, these results indicate that Sulindac sensitizes HCT116 and SW480 CRC cells to the effect of retinoids on gene expression.

Techniques: Analysis, Gene Expression, Expressing, Profiling

The two sets of retinoid-response genes (down-regulated vs. up-regulated) have different functional classifications. <xref ref-type=

* " width="100%" height="100%">

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: The two sets of retinoid-response genes (down-regulated vs. up-regulated) have different functional classifications. *

Techniques: Functional Assay, Transduction, Tissue, Cell Differentiation

Measuring drug responses using organoid cultures of human CRC cells. The effect of therapeutic manipulation of WNT and RA signaling was evaluated in human patient-derived colon cancer organoids. Drug-response experiments were conducted using a CRC organoid model from the ATCC (HCM-CSHL-0257-C18). Treatment concentrations were chosen based on the effective IC50 doses as indicated: 9-cis-RA (90 µM), Sulindac (322.5, 430, 537.5 µM), and Liarozole (90 µM). Panels A & B show representative microscopy staining from cell viability analysis using CYTO 3D Live/Dead Assay Kit. Scale bars equal 50 µM. Each panel contains four rows of images. Brightfield shows the overall cell morphology under normal light. AO (acridine orange): green fluorescence indicating live cells. PI (propidium iodide): red fluorescence marks dead cells. Merged: A combination of AO and PI channels showing both live and dead cells simultaneously.Panels C and D give the quantification for cell death based on the PI (dead cells)/AO (live cells) ratio. The cells were treated with various concentrations of 9-cis-RA, Liarozole, Sulindac alone, or combinations of both compounds. The control represents untreated cells. Increasing ratios indicate higher proportions of dead cells than live cells, with combination treatments showing the most pronounced effects. This experiment was done in triplicate, and the error bars represent ± the SEM. Overall, treating CRC organoid cultures with anti-WNT & RA drug combinations causes a substantial increase in cell death compared to individual agents alone.

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: Measuring drug responses using organoid cultures of human CRC cells. The effect of therapeutic manipulation of WNT and RA signaling was evaluated in human patient-derived colon cancer organoids. Drug-response experiments were conducted using a CRC organoid model from the ATCC (HCM-CSHL-0257-C18). Treatment concentrations were chosen based on the effective IC50 doses as indicated: 9-cis-RA (90 µM), Sulindac (322.5, 430, 537.5 µM), and Liarozole (90 µM). Panels A & B show representative microscopy staining from cell viability analysis using CYTO 3D Live/Dead Assay Kit. Scale bars equal 50 µM. Each panel contains four rows of images. Brightfield shows the overall cell morphology under normal light. AO (acridine orange): green fluorescence indicating live cells. PI (propidium iodide): red fluorescence marks dead cells. Merged: A combination of AO and PI channels showing both live and dead cells simultaneously.Panels C and D give the quantification for cell death based on the PI (dead cells)/AO (live cells) ratio. The cells were treated with various concentrations of 9-cis-RA, Liarozole, Sulindac alone, or combinations of both compounds. The control represents untreated cells. Increasing ratios indicate higher proportions of dead cells than live cells, with combination treatments showing the most pronounced effects. This experiment was done in triplicate, and the error bars represent ± the SEM. Overall, treating CRC organoid cultures with anti-WNT & RA drug combinations causes a substantial increase in cell death compared to individual agents alone.

Techniques: Derivative Assay, Organoids, Microscopy, Staining, Analysis, Live Dead Assay, Brightfield, Morphology, Fluorescence, Control

Drug combination responses in a human CRC PDX (CTG-2359) mouse model. Drug safety . Drug toxicity was initially evaluated for tolerability (Panel A), and during drug treatments for efficacy. Different colored lines indicate various treatment conditions, including control and combination treatments. Body weights remained mostly stable with no weight loss greater than 10%. This reveals that the drug treatments were reasonably well tolerated. Efficacy analysis . Panel B shows the time course results on tumor volume changes in the efficacy study over 28 d. The treatment groups included a placebo control and various Sulindac, Liarozole, and 9-cis RA combinations. The tumor volumes were measured in cubic millimeters and plotted against time (days). The error bars represent ± the SEM. All the treatment groups showed progressive tumor growth, with the combinations of Sulindac + Liarozole + 9-cis RA demonstrating the lowest tumor volume trajectory. The placebo group exhibited the highest tumor growth rate, reaching approximately 2000 mm 3 by day 25. Measurements were taken at 5-day intervals after treatment initiation at day 0. Panel C. The waterfall plot shows the percent decreased in tumor growth for all treatment groups. The corresponding values for anti-tumor activity are provided in Table 3 below.

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: Drug combination responses in a human CRC PDX (CTG-2359) mouse model. Drug safety . Drug toxicity was initially evaluated for tolerability (Panel A), and during drug treatments for efficacy. Different colored lines indicate various treatment conditions, including control and combination treatments. Body weights remained mostly stable with no weight loss greater than 10%. This reveals that the drug treatments were reasonably well tolerated. Efficacy analysis . Panel B shows the time course results on tumor volume changes in the efficacy study over 28 d. The treatment groups included a placebo control and various Sulindac, Liarozole, and 9-cis RA combinations. The tumor volumes were measured in cubic millimeters and plotted against time (days). The error bars represent ± the SEM. All the treatment groups showed progressive tumor growth, with the combinations of Sulindac + Liarozole + 9-cis RA demonstrating the lowest tumor volume trajectory. The placebo group exhibited the highest tumor growth rate, reaching approximately 2000 mm 3 by day 25. Measurements were taken at 5-day intervals after treatment initiation at day 0. Panel C. The waterfall plot shows the percent decreased in tumor growth for all treatment groups. The corresponding values for anti-tumor activity are provided in Table 3 below.

Techniques: Toxicity, Control, Analysis, Activity Assay

Anti-tumor activity for human CRC PDX (CTG-2359) mouse model.

Journal: Cancer Biology & Therapy

Article Title: Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology

doi: 10.1080/15384047.2026.2732738

Figure Lengend Snippet: Anti-tumor activity for human CRC PDX (CTG-2359) mouse model.

Techniques: Activity Assay, Control

Journal: eLife

Article Title: Bidirectional redistribution of actomyosin drives epithelial invagination in ascidian siphon tube morphogenesis

doi: 10.7554/eLife.108588

Figure Lengend Snippet:

Article Snippet: Software, algorithm , Imaris , Oxford Instruments , RRID: SCR_007370 , Version 9.0.1.

Techniques: Cell-Signaling, Recombinant, Plasmid Preparation, TUNEL Assay, Cloning, Sequencing, Software

In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia marker α-SMA (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.

Journal: Materials Today Bio

Article Title: Human iPSC-EV-loaded nanofiber stent coatings accelerate vascular repair by enhancing EGFR/HIF-1α signaling and suppressing ROCK1-mediated remodeling

doi: 10.1016/j.mtbio.2026.103564

Figure Lengend Snippet: In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia marker α-SMA (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.

Article Snippet: Proliferation and remodeling markers: PCNA (1:1000, ab29, Abcam), IL-6 (1:1000, A0286, ABclonal), TGF-β1 (1:1000, A2124, ABclonal), MMP-2 (1:1000, A6247, ABclonal), and MMP-9 (1:1000, A2095, ABclonal).

Techniques: In Vivo, Inhibition, Disruption, Staining, Expressing, Marker

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