anti mmp9 picoband antibody  (Boster Bio)

Journal: BioMed Research International

Article Title: Curcumin Administered in Combination with Glu-GNPs Induces Radiosensitivity in Transplanted Tumor MDA-MB-231-luc Cells in Nude Mice

doi: 10.1155/2021/9262453

Figure Lengend Snippet: The protein expressions of MMP9 and HIF-1 α in tumor tissue samples by immunohistochemistry. (a) Representative images of MMP9 and (b) HIF-1 α IHC staining (magnification, ×200). Tumor tissue was immunostained using DAB (brown) and hematoxylin (blue) for nuclear counterstaining. Arrows indicate the nuclear expression of MMP9 or HIF-1 α in breast cancer cells (scale bars, 100 μ m). (c) The semiquantitative scoring analysis of MMP9 and (d) HIF-1 α protein expression in tumor tissue. IHC: immunohistochemistry; MMP9: matrix metalloprotein-9; HIF-1 α : hypoxia-inducible factor-1 α .

Article Snippet: MMP9 (cat. no. PB9669) and goat anti-rabbit and goat anti-mouse secondary antibodies were obtained from Boster Biological Technology Ltd.

Techniques: Immunohistochemistry, Staining, Expressing

Journal: Annals of Translational Medicine

Article Title: The mechanisms of celastrol in treating papillary thyroid carcinoma based on network pharmacology and experiment verification

doi: 10.21037/atm-21-1854

Figure Lengend Snippet: Molecular docking data indicated that the binding capacity of celastrol with PTC was significant in the key targets of MMP9 (A), JUN (B), ICAM1 (C), and VCAM1 (D). PTC, papillary thyroid carcinoma.

Article Snippet: The primary antibodies used for the western blot were MMP9 (BOSTER, PB9669; 1:1,000), JUN (BOSTER, BM4168; 1:1,000), ICAM1 (BOSTER, PB9018; 1:1,000), VCAM1 (BOSTER, A01199; 1:1,000) and GAPDH (Cell Signaling Technology, 5174; 1:40,000).

Techniques: Binding Assay

Journal: Annals of Translational Medicine

Article Title: The mechanisms of celastrol in treating papillary thyroid carcinoma based on network pharmacology and experiment verification

doi: 10.21037/atm-21-1854

Figure Lengend Snippet: The differentially expressed of four core proteins in BCPAP cell line after 24 hrs of celastrol treatment. (A) qRT-PCR was used to detect the MMP9, JUN, ICAM1, VCAM1 expression with or without celastrol treatment. (B) Western blotting analyses of MMP9, JUN, ICAM1, VCAM1 expression with or without celastrol treatment. **, P

Article Snippet: The primary antibodies used for the western blot were MMP9 (BOSTER, PB9669; 1:1,000), JUN (BOSTER, BM4168; 1:1,000), ICAM1 (BOSTER, PB9018; 1:1,000), VCAM1 (BOSTER, A01199; 1:1,000) and GAPDH (Cell Signaling Technology, 5174; 1:40,000).

Techniques: Quantitative RT-PCR, Expressing, Western Blot

Journal: Respiratory Research

Article Title: TRB3 mediates vascular remodeling by activating the MAPK signaling pathway in hypoxic pulmonary hypertension

doi: 10.1186/s12931-021-01908-4

Figure Lengend Snippet: Inhibitors of ERK, JNK, and p38 MAPK reversed the effect of TRB3 overexpression on PASMC biological behavior. A The CCK-8 assay was used to evaluated the proliferation of TRB3-overexpressing cells after treating with U0126, SP600125, and SB203580. B – D Western blot analysis of PCNA expression in TRB3 overexpressing cells incubated with U0126, SP600125, or SB203580 for 12 h. E Cell apoptosis induced by U0126, SP600125 and SB203580 in TRB3-overexpressing cells was evaluated using flow cytometry, and the percentage of early apoptotic (Annexin V+/PI−) and late apoptotic (Annexin V+ /PI+) cells was analyzed. F – H Western blot analysis of the protein expression of PARP, BAX, and Bcl2 in TRB3-overexpressing cells incubated with U0126, SP600125, and SB203580 for 12 h. I Crystal violet staining is presented at × 200 magnification for the Transwell assay and the migrated cells were counted and analyzed. J – L Western blot analysis of MMP9 expression in TRB3-overexpressing cells incubated with U0126, SP600125, and SB203580 for 12 h. Data represent the mean ± SEM (n = 4). *P

Article Snippet: Polyclonal antibodies against PCNA, BAX, caspase 3, PARP, HRP-conjugated β-actin, and Survivin were purchased from Proteintech (USA); anti-Bcl2 antibody was obtained from Boster (China); anti-MMP9 antibody was obtained from Affinity (USA); anti-p38/p-p38 MAPK, anti-JNK/p-JNK, anti-ERK/p-ERK, and normal rabbit IgG antibodies were acquired from Cell Signaling Technology (USA); normal mouse IgG was obtained from Santa Cruz Biotechnology (USA).

Techniques: Over Expression, CCK-8 Assay, Western Blot, Expressing, Incubation, Flow Cytometry, Staining, Transwell Assay

Journal: Respiratory Research

Article Title: TRB3 mediates vascular remodeling by activating the MAPK signaling pathway in hypoxic pulmonary hypertension

doi: 10.1186/s12931-021-01908-4

Figure Lengend Snippet: TRB3 knockdown reversed and prevented the progression of hypoxia -induced PH. A The right ventricular systolic pressure(RVSP) was measured by a 1.2-Fr pressure catheter (GuGeShengWu, Wuhan, China) inserted via the right jugular vein and positioned in the right ventricle. B The values of RVSP were obtained using the ADInstruments Powerlab data acquisition system. C Right ventricular hypertrophy was evaluated by the ratio of the RV/(LV + S). The right ventricle (RV) was peeled off from the left ventricle (LV) and the septum (S), and the dry weight of the two components was measured. D Systemic blood pressure was measured by a 1.2-Fr pressure catheter inserted via the left carotid artery. E Lung tissue sections were stained for hematoxylin–eosin (HE) (magnification, × 200) and α-SMA (magnification, × 400). F Pulmonary vascular remodeling was evaluated by the percentage of medial wall thickness of distal pulmonary vessels, which was expressed using the following equation: [(external diameter − internal diameter)/external diameter]. G The whole pulmonary artery of each rat from different groups was extracted, and TRB3 protein expression in each group was measured by western blot analysis. H and I PCNA protein expression in pulmonary arteries was examined by immunohistochemical staining and western blot analysis. J MMP9 protein expression in pulmonary arteries was examined by western blot analysis. K The phosphorylated forms of ERK, JNK, and p38 MAPK in pulmonary arteries in each group were evaluated by western blot analysis. Data represent the mean ± SEM (n = 4). *P

Article Snippet: Polyclonal antibodies against PCNA, BAX, caspase 3, PARP, HRP-conjugated β-actin, and Survivin were purchased from Proteintech (USA); anti-Bcl2 antibody was obtained from Boster (China); anti-MMP9 antibody was obtained from Affinity (USA); anti-p38/p-p38 MAPK, anti-JNK/p-JNK, anti-ERK/p-ERK, and normal rabbit IgG antibodies were acquired from Cell Signaling Technology (USA); normal mouse IgG was obtained from Santa Cruz Biotechnology (USA).

Techniques: Staining, Expressing, Western Blot, Immunohistochemistry

Journal: Respiratory Research

Article Title: TRB3 mediates vascular remodeling by activating the MAPK signaling pathway in hypoxic pulmonary hypertension

doi: 10.1186/s12931-021-01908-4

Figure Lengend Snippet: Effect of TRB3 knockdown on proliferation, migration, and apoptosis of hypoxic PASMCs. PASMCs were transfected with lentiviral vectors encoding short hairpin RNAs targeting against rat TRB3(si-TRB3) or negative control(si-NC) for further analysis. A CCK-8 assays were performed to test cell viability after TRB3 knockdown in hypoxic PASMCs. B The EdU proliferation assay was used to measure cell proliferation. All images are × 400 magnification. C EdU‐positive cells were analyzed. D and E The expression of PCNA and Survivin was examined by western blot, and the gray value was quantified by ImageJ software. F Cell apoptosis was evaluated by Hoechst 33342 staining, and the percentage of apoptosis was quantified. G Crystal violet staining of PASMCs is presented at × 200 magnification for the Transwell assay, and the migrated cells were counted manually. H Apoptosis-related protein expression was evaluated and quantification of the analysis is shown. I The expression of MMP9 was evaluated. Data represent the mean ± SEM (n = 4). *P

Article Snippet: Polyclonal antibodies against PCNA, BAX, caspase 3, PARP, HRP-conjugated β-actin, and Survivin were purchased from Proteintech (USA); anti-Bcl2 antibody was obtained from Boster (China); anti-MMP9 antibody was obtained from Affinity (USA); anti-p38/p-p38 MAPK, anti-JNK/p-JNK, anti-ERK/p-ERK, and normal rabbit IgG antibodies were acquired from Cell Signaling Technology (USA); normal mouse IgG was obtained from Santa Cruz Biotechnology (USA).

Techniques: Migration, Transfection, CCK-8 Assay, Proliferation Assay, Expressing, Western Blot, Software, Staining, Transwell Assay

Journal: Scientific Reports

Article Title: TGF-β1 promotes scar fibroblasts proliferation and transdifferentiation via up-regulating MicroRNA-21

doi: 10.1038/srep32231

Figure Lengend Snippet: TGF-β1 induced-expressions and activities of MMP2 and MMP9 in human keloid fibroblasts was attenuated by miR-21 inhibition. ( A ) The protein expressions of MMP9 and MMP2 were determined by western blot. The protein quantification histogram was shown. β-actin was used as a loading control. ( B ) The mRNA expressions of MMP9 and MMP2 were determined by real-time PCR. ( C ) The activities of MMP9 and MMP2 were detected by gelatin zymography assay. Each result represents at least three independent experiments. Data represents the mean ± SD (n = 3). **P

Article Snippet: Rabbit anti- E-cadherin (1:400), anti-MMP2 (1:400), anti-MMP9 (1:400) were obtained from Boster (Wuhan, China).

Techniques: Inhibition, Western Blot, Real-time Polymerase Chain Reaction, Zymography Assay