PCNA Recombinant Rabbit Monoclonal Antibody [43A09]
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-
- 50μL
- ¥580
- 1-3个工作日
-
- 100μL
- ¥920
- 1-3个工作日
-
- 500μL
- ¥3800
- 1-3个工作日
Product Details | Host Species: Rabbit | Reactivity: Human, Mouse, Rat, Monkey | Molecular Wt: Predicted MW: 29 kDa | |||
| Clonality: Monoclonal | Isotype: IgG | Concentration: 1.144mg/ml | |||
| Other Names: Proliferating cell nuclear antigen; DNA polymerase delta auxiliary protein; ATLD2; cb16; Cyclin; Pcna/cyclin; PCNAR; PCNA | |||||
| Formulation: Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide. | |||||
| Purification: Affinity-chromatography | |||||
| Storage: Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20°C storage. | |||||
Applications | WB 1:1000-1:10000 | |||||
Immunogen | Gene Name: PCNA | Protein Name: Proliferating cell nuclear antigen | ||||
| Gene ID: | SwissPro: | ||||
Immunogen | Subcellular Location: Nucleus. | |||||
| Immunogen: Synthetic peptide within human PCNA. AA range: 88-137. | |||||
| Specificity: PCNA Monoclonal Antibody detects endogenous levels of PCNA protein. | |||||
| Product images | |
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Fig : Western blot analysis of PCNA on different lysates. Proteins were transferred to a NC membrane and blocked with 5% NF-Milk in TBST for 1 hour at room temperature. The primary antibody (AWA10303, 1/1000) was used in TBST at room temperature for 2 hours. Goat Anti-Rabit IgG - HRP Secondary Antibody (AWS0002) at 1:5,000 dilution was used for 1 hour at room temperature. Positive control:* Lane 1: HepG2 cell Lane 2: Hela cell Lane 3: Ramos cell Predicted molecular weight:29 kDa Observed molecular weight:34 kDa |
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Fig: Fluorescence immunohistochemical analysis of Rat-testis tissue (Formalin/PFA-fixed paraffin-embedded sections). with Rabbit anti-PCNA antibody (AWA10303) at 1/200 dilution. The immunostaining was performed with the TSA Immuno-staining Kit (ABIOWELL, AWI0691). The section was pre-treated using heat mediated antigen retrieval with Sodium citrate buffer (pH 6.0) for 20 minutes. The tissues were blocked in 3% H2O2 for 15 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (AWA10303) at 1/200 dilution for 2 hour at 37℃ or overnignt at 4℃. The detection was performed using an HRP conjugated compact polymer system followed by a separate fluorescent tyramide signal amplification system (Purple). DAPI (blue, AWC0291) was used as a nuclear counter stain. Image acquisition was performed with Slide Scanner. |
|
Fig : Western blot analysis of PCNA on different lysates. Proteins were transferred to a NC membrane and blocked with 5% NF-Milk in TBST for 1 hour at room temperature. The primary antibody (AWA10303, 1/4000) was used in TBST at room temperature for 2 hours. Goat Anti-Ribbit IgG - HRP Secondary Antibody (AWS0002) at 1:5,000 dilution was used for 1 hour at room temperature. Positive control: Lane 1: MCF-7 cell Lane 2: Jurkat cell Lane 3: Raji cell Lane 4: C2C12 cell Lane 5: COS7 cell Lane 6: SH-SY5Y cell Predicted molecular weight:29 kDa Observed molecular weight:34 kDa |
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Fig:Flow cytometric analysis of HELA cells labeling PCNA. Overlay histogram showing HELA cells stained with PCNA (green line). The cell were fixed in 4% paraformaldehyde for 30 minutes at 37 ℃, permeabilized with 0.02% Triton X-100 in PBS for 30 minutes,and then stained with the primary antibody(AWA10303, 1:50 ) for 30 min at 4°C. The secondary antibody used was an Alexa Fluor 488-conjugated Goat anti-Rabbit IgG Secondary antibody (AWS0005b) at 1/1000 dilution for 30 min at 4ºC. Unlabelled sample was used as a control (cells without incubation with primary antibody; red). |
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Fig : Immunohistochemical analysis of paraffin-embedded Mouse-testis tissue with Rabbit anti-PCNA antibody (AWA10303) at 1/200 dilution. The section was pre-treated using heat mediated antigen retrieval with Sodium citrate buffer (pH 6.0) for 20 minutes. The tissues were blocked in 3% H2O2 for 15 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (AWA10303) at 1/200 dilution for 2 hour at 37℃or overnignt at 4℃. The detection was performed using an HRP conjugated compact polymer system(ABIOWELL, AWI0629). DAB was used as the chromogen. Tissues were counterstained with hematoxylin and mounted with DPX. |
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Fig: Fluorescence immunohistochemical analysis of Mouse-brain tissue (Formalin/PFA-fixed paraffin-embedded sections). with Rabbit anti-PCNA antibody (AWA10303) at 1/200 dilution. The immunostaining was performed with the TSA Immuno-staining Kit (ABIOWELL, AWI0691). The section was pre-treated using heat mediated antigen retrieval with Sodium citrate buffer (pH 6.0) for 20 minutes. The tissues were blocked in 3% H2O2 for 15 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (AWA10303) at 1/200 dilution for 2 hour at 37℃ or overnignt at 4℃. The detection was performed using an HRP conjugated compact polymer system followed by a separate fluorescent tyramide signal amplification system (Purple). DAPI (blue, AWC0291) was used as a nuclear counter stain. Image acquisition was performed with Slide Scanner. |
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Overlay histogram showing Hep3B cells stained with PCNA (green line). The cells were fixed, permeabilized and stained with the primary antibody(AWA10303, 1µg/1x106 cells) for 30 min at 4°C. The secondary antibody used was an Alexa Fluor 488-conjugated Goat anti-Rabbit IgG Secondary antibody (AWS0005) at 1/500 dilution for 30 min at 4ºC. Unlabelled sample was used as a control (cells without incubation with primary antibody; red). |
引用文献 (2)
HighlightsWhat are the main findings?Salvia miltiorrhizaBunge regulates mESC differentiation into cardiomyocytes in a stage-dependent manner.The pro-cardiogenic activity ofSalvia miltiorrhizaBunge is mainly mediated by suppression of canonical Wnt/β-catenin signaling, with tanshinone IIA identified as a key active constituent.What are the implications of the main findings?Salvia miltiorrhizaBunge and tanshinone IIA as natural small-molecule regulators to enhance stem cell-derived cardiomyocyte generation.Precise temporal modulation of Wnt/β-catenin signaling is critical for optimizing pluripotent stem cell cardiac differentiation strategies.Salvia miltiorrhizaBunge has been used traditionally for cardiovascular disorders, but its specific roles in stem cell cardiac differentiation remain unclear. In this study, we examined whetherSalvia miltiorrhizaBunge (SM) promotes cardiomyocyte differentiation from mouse embryonic stem cells (mESCs) and defined its underlying mechanism. To dynamically monitor cardiac differentiation, we established aTnnt2-H2B-mCherry reporter mESC line that retained normal pluripotency and differentiation capacity. Using an embryoid body-based differentiation system, we found that SM exerted a distinct temporal effect on lineage progression: treatment during the early differentiation window inhibited pluripotency maintenance, proliferation, and mesodermal development, whereas administration during the cardiac precursor stage markedly enhanced cardiomyocyte formation, as indicated by increased beating embryoid bodies and upregulation ofIsl1,Nkx2.5,Tnnt2,Myh6, andMyl7. Mechanistically, transcriptomic and protein analyses showed that SM suppressed canonical Wnt/β-catenin signaling, including downregulation ofDvl2,β-catenin,Axin2,c-Myc, andCyclin D1, while Wnt activation WAY262611 partially reversed these effects. Further compound screening identified tanshinone IIA (Tan IIA) as the principal active constituent of SM, which largely recapitulated the pro-cardiogenic and Wnt-inhibitory effects of the crude extract. Together, these findings identify SM and Tan IIA as stage-dependent regulators of mESC fate and support their potential utility in natural product-based strategies for improving stem cell-derived cardiomyocyte generation.
Cisplatin stands as a highly effective chemotherapeutic agent for ovarian cancer (OC); yet, the development of resistance to it poses a significant clinical challenge. In this study, we utilized prior RNA-sequencing and immunoprecipitation-mass spectrometry (IP-MS) data to identify downstream genes and interacting proteins altered following ESM1 knockdown, and further confirmed the impact of these changes on ferroptosis and cisplatin resistance in OC cells through electron microscopy and various molecular biology experiments. Additionally, public databases, tissue microarrays, and multiplex immunofluorescence staining were employed to assess the prognostic value of genes like ESM1 for OC patients. The results demonstrate that HSPB1 acts as a pivotal gene in ESM1-mediated cisplatin and ferroptosis resistance. Mechanistically, ESM1 binds to ERBB2 to promote HSPB1 transcription, thereby activating the FAK/SRC and NF-κB pathways, which ultimately inhibits ferroptosis and enhances cisplatin resistance in OC. Collectively, these findings elucidate a regulatory mechanism by which ESM1 drives cisplatin and ferroptosis resistance via the ERBB2/FAK/SRC/HSPB1/NF-κB axis in ovarian cancer.
-
-
- 50μL
- ¥580
- 1-3个工作日
-
- 100μL
- ¥920
- 1-3个工作日
-
- 500μL
- ¥3800
- 1-3个工作日
-
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