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p2rx7  (Proteintech)
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Proteintech p2rx7
Fig. 2. <t>P2rx7</t> promoted the bone formation of MSCs. a The CFU-F in MSCs derived from the control and the P2rx7-/- MSCs. b Mineralized nodules formed by MSCs of the control and the P2rx7-/- mice were analyzed by alizarin red staining. c, d The expressions of osteogenesis marker genes in the control and the P2rx7-/- MSCs, as assessed by western blotting (c) and qPCR (d). e, f Transplants consisting of MSCs from control and P2rx7-/- mice mixed with HA/TCP were analyzed by H&E staining (e), and immunofluorescent staining of CD31 and ACAN (f), n = 5 per group. g Mineralized nodules formed by MSCs under osteogenic induction when exposed to 0, 40 nM or 100 nM BzATP were showed by alizarin red staining. h The expressions of osteogenic markers Runx2, ALP, and OCN in MSCs exposed to 0, 40 nM or 100 nM BzATP, as assessed by western blotting. i, j Transplants consisting of MSCs treated with 0, 40, 100 nM BzATP from control mice mixed with HA/TCP were analyzed by H&E staining (i), and immunofluorescent staining of CD31 and ACAN (j), n = 5 per group. Scale bar: e, f, i, j: 50 lm. e, i yellow, new bone; black, blood vessel; blue, new cartilage. Data was presented as mean ± SD. The data (a-d, g) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test (a, b, e, f) and one-way ANOVA (d, g, i, j). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Fig. 2. P2rx7 promoted the bone formation of MSCs. a The CFU-F in MSCs derived from the control and the P2rx7-/- MSCs. b Mineralized nodules formed by MSCs of the control and the P2rx7-/- mice were analyzed by alizarin red staining. c, d The expressions of osteogenesis marker genes in the control and the P2rx7-/- MSCs, as assessed by western blotting (c) and qPCR (d). e, f Transplants consisting of MSCs from control and P2rx7-/- mice mixed with HA/TCP were analyzed by H&E staining (e), and immunofluorescent staining of CD31 and ACAN (f), n = 5 per group. g Mineralized nodules formed by MSCs under osteogenic induction when exposed to 0, 40 nM or 100 nM BzATP were showed by alizarin red staining. h The expressions of osteogenic markers Runx2, ALP, and OCN in MSCs exposed to 0, 40 nM or 100 nM BzATP, as assessed by western blotting. i, j Transplants consisting of MSCs treated with 0, 40, 100 nM BzATP from control mice mixed with HA/TCP were analyzed by H&E staining (i), and immunofluorescent staining of CD31 and ACAN (j), n = 5 per group. Scale bar: e, f, i, j: 50 lm. e, i yellow, new bone; black, blood vessel; blue, new cartilage. Data was presented as mean ± SD. The data (a-d, g) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test (a, b, e, f) and one-way ANOVA (d, g, i, j). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of advanced research

Article Title: The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.

doi: 10.1016/j.jare.2025.06.026

Figure Lengend Snippet: Fig. 2. P2rx7 promoted the bone formation of MSCs. a The CFU-F in MSCs derived from the control and the P2rx7-/- MSCs. b Mineralized nodules formed by MSCs of the control and the P2rx7-/- mice were analyzed by alizarin red staining. c, d The expressions of osteogenesis marker genes in the control and the P2rx7-/- MSCs, as assessed by western blotting (c) and qPCR (d). e, f Transplants consisting of MSCs from control and P2rx7-/- mice mixed with HA/TCP were analyzed by H&E staining (e), and immunofluorescent staining of CD31 and ACAN (f), n = 5 per group. g Mineralized nodules formed by MSCs under osteogenic induction when exposed to 0, 40 nM or 100 nM BzATP were showed by alizarin red staining. h The expressions of osteogenic markers Runx2, ALP, and OCN in MSCs exposed to 0, 40 nM or 100 nM BzATP, as assessed by western blotting. i, j Transplants consisting of MSCs treated with 0, 40, 100 nM BzATP from control mice mixed with HA/TCP were analyzed by H&E staining (i), and immunofluorescent staining of CD31 and ACAN (j), n = 5 per group. Scale bar: e, f, i, j: 50 lm. e, i yellow, new bone; black, blood vessel; blue, new cartilage. Data was presented as mean ± SD. The data (a-d, g) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test (a, b, e, f) and one-way ANOVA (d, g, i, j). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The antibodies used in this study were as follows: Anti-mouse CD29 (#2473836), anti-mouse CD31 (#2373735), anti-mouse CD44 (#2255545) antibodies from eBioscience (San Diego, CA, USA); PE anti-mouse CD11b (#101207), APC anti-mouse CD90.2 (#105311) antibodies from BioLegend (San Diego, CA, USA); Anti-Col1a1 (ab255809; Abcam, Cambridge, MA, USA); Drp1 (#8570), Erk1/2 (#4370), p-Erk1/2 (#4695) from CST (Danvers, MA, USA); alkaline phosphatase (ALP, PA5-106391; Invitrogen, Carlsbad, CA, USA); Bmp-2 (sc-137087), CD90 (sc-53116), Cytoc (sc-13156), Ocn (sc-390877), P2rx7 (sc-514962) from Santa Cruz Biotechnology (Santa Cruz, CA, USA); Fis1 (10956–1-AP), p16 (10883–1-AP), p21 (10355–1-AP), P2rx7 (28207–1-AP), Mfn1 (13798–1-AP), Mfn2 (12186–1-AP), Opa1 (27733–1-AP), Runx2 (82636–2-RR) from ProteinTech (Cook, Illinois, USA); p-Drp1 (Ser616) (AF8470) from Affinity (Liyang, China); Hsp60 (AF0186) and Mouse IgG (A7028) from Beyotime (Shanghai, China); bActin (GB15001-100) from Servicebio (Wuhan, China).

Techniques: Derivative Assay, Control, Staining, Marker, Western Blot, Two Tailed Test

Fig. 3. P2rx7 controls mitochondrial dynamics in MSCs. a OCR, calculated basal respiration and ATP-linked respiration of the control and the P2rx7-/- MSCs. b ATP contents of the control and the P2rx7-/- MSCs. c ECAR, and calculated glycolysis, glycolytic capability and glycolytic reverse of the control and the P2rx7-/- MSCs. d TEM images of mitochondria (arrows) in the control and the P2rx7-/- MSCs (n = 20 per group). e DWM of the control and the P2rx7-/- MSCs was measured by JC-1 staining (polymer: red; monomer: green). f The expressions of genes Nd1 and mt-Cytb in the control and the P2rx7-/- MSCs that related to the mitochondrial mass in cells assessed by qPCR. g DWM of MSCs treated with different concentrations of BzATP was analyzed by JC-1 staining. Scale bar: d: 500 nm; e, g: 100 lm. Data was presented as mean ± SD. The data (a, b, e-g) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test (a-f) and one-way ANOVA (g). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of advanced research

Article Title: The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.

doi: 10.1016/j.jare.2025.06.026

Figure Lengend Snippet: Fig. 3. P2rx7 controls mitochondrial dynamics in MSCs. a OCR, calculated basal respiration and ATP-linked respiration of the control and the P2rx7-/- MSCs. b ATP contents of the control and the P2rx7-/- MSCs. c ECAR, and calculated glycolysis, glycolytic capability and glycolytic reverse of the control and the P2rx7-/- MSCs. d TEM images of mitochondria (arrows) in the control and the P2rx7-/- MSCs (n = 20 per group). e DWM of the control and the P2rx7-/- MSCs was measured by JC-1 staining (polymer: red; monomer: green). f The expressions of genes Nd1 and mt-Cytb in the control and the P2rx7-/- MSCs that related to the mitochondrial mass in cells assessed by qPCR. g DWM of MSCs treated with different concentrations of BzATP was analyzed by JC-1 staining. Scale bar: d: 500 nm; e, g: 100 lm. Data was presented as mean ± SD. The data (a, b, e-g) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test (a-f) and one-way ANOVA (g). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The antibodies used in this study were as follows: Anti-mouse CD29 (#2473836), anti-mouse CD31 (#2373735), anti-mouse CD44 (#2255545) antibodies from eBioscience (San Diego, CA, USA); PE anti-mouse CD11b (#101207), APC anti-mouse CD90.2 (#105311) antibodies from BioLegend (San Diego, CA, USA); Anti-Col1a1 (ab255809; Abcam, Cambridge, MA, USA); Drp1 (#8570), Erk1/2 (#4370), p-Erk1/2 (#4695) from CST (Danvers, MA, USA); alkaline phosphatase (ALP, PA5-106391; Invitrogen, Carlsbad, CA, USA); Bmp-2 (sc-137087), CD90 (sc-53116), Cytoc (sc-13156), Ocn (sc-390877), P2rx7 (sc-514962) from Santa Cruz Biotechnology (Santa Cruz, CA, USA); Fis1 (10956–1-AP), p16 (10883–1-AP), p21 (10355–1-AP), P2rx7 (28207–1-AP), Mfn1 (13798–1-AP), Mfn2 (12186–1-AP), Opa1 (27733–1-AP), Runx2 (82636–2-RR) from ProteinTech (Cook, Illinois, USA); p-Drp1 (Ser616) (AF8470) from Affinity (Liyang, China); Hsp60 (AF0186) and Mouse IgG (A7028) from Beyotime (Shanghai, China); bActin (GB15001-100) from Servicebio (Wuhan, China).

Techniques: Control, Staining, Polymer, Two Tailed Test

Fig. 4. P2rx7 regulated mitochondrial fusion through Mfn1. a The mitochondria (top) labeled by Mitotracker Red and mitochondrial morphology (bottom) based on Mitochondrial Analyzer after grey processing, analyzed by Airyscan confocal images in the control and P2rx7-/- MSCs. b The expression of genes associated with mitochondrial dynamics in the control and the P2rx7-/- MSCs as assessed by western blotting. c Representative micrographs visualizing P2rx7 (arrows) on the mitochondria. d Reprehensive Airyscan confocal images of mitochondrial morphology (Mitotracker Red, top) and mitochondrial morphology (bottom) based on Mitochondrial Analyzer after grey processing in the MSCs treated with 0, 40 nM and 100 nM BzATP. e The expression of genes associated with mitochondrial dynamics in the MSCs treated with 0, 40 nM and 100 nM BzATP as assessed by western blotting. f Western blotting analysis of mitochondrial (left) and cytosolic (right) fractions of the MSCs treated with 40 nM and 100 nM BzATP. g IHC staining of Mfn1 and Opa1 proteins in the control and the P2rx7-/- MSCs that were subcutaneously implanted into immunocompromised mice with HA/TCP (n = 5 per group). Scale bar: a, d:10 lm (top), 5 lm(bottom); g: 100 lm; h: 500 lm. Data was presented as mean ± SD. The data (a, b, d-f) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of advanced research

Article Title: The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.

doi: 10.1016/j.jare.2025.06.026

Figure Lengend Snippet: Fig. 4. P2rx7 regulated mitochondrial fusion through Mfn1. a The mitochondria (top) labeled by Mitotracker Red and mitochondrial morphology (bottom) based on Mitochondrial Analyzer after grey processing, analyzed by Airyscan confocal images in the control and P2rx7-/- MSCs. b The expression of genes associated with mitochondrial dynamics in the control and the P2rx7-/- MSCs as assessed by western blotting. c Representative micrographs visualizing P2rx7 (arrows) on the mitochondria. d Reprehensive Airyscan confocal images of mitochondrial morphology (Mitotracker Red, top) and mitochondrial morphology (bottom) based on Mitochondrial Analyzer after grey processing in the MSCs treated with 0, 40 nM and 100 nM BzATP. e The expression of genes associated with mitochondrial dynamics in the MSCs treated with 0, 40 nM and 100 nM BzATP as assessed by western blotting. f Western blotting analysis of mitochondrial (left) and cytosolic (right) fractions of the MSCs treated with 40 nM and 100 nM BzATP. g IHC staining of Mfn1 and Opa1 proteins in the control and the P2rx7-/- MSCs that were subcutaneously implanted into immunocompromised mice with HA/TCP (n = 5 per group). Scale bar: a, d:10 lm (top), 5 lm(bottom); g: 100 lm; h: 500 lm. Data was presented as mean ± SD. The data (a, b, d-f) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The antibodies used in this study were as follows: Anti-mouse CD29 (#2473836), anti-mouse CD31 (#2373735), anti-mouse CD44 (#2255545) antibodies from eBioscience (San Diego, CA, USA); PE anti-mouse CD11b (#101207), APC anti-mouse CD90.2 (#105311) antibodies from BioLegend (San Diego, CA, USA); Anti-Col1a1 (ab255809; Abcam, Cambridge, MA, USA); Drp1 (#8570), Erk1/2 (#4370), p-Erk1/2 (#4695) from CST (Danvers, MA, USA); alkaline phosphatase (ALP, PA5-106391; Invitrogen, Carlsbad, CA, USA); Bmp-2 (sc-137087), CD90 (sc-53116), Cytoc (sc-13156), Ocn (sc-390877), P2rx7 (sc-514962) from Santa Cruz Biotechnology (Santa Cruz, CA, USA); Fis1 (10956–1-AP), p16 (10883–1-AP), p21 (10355–1-AP), P2rx7 (28207–1-AP), Mfn1 (13798–1-AP), Mfn2 (12186–1-AP), Opa1 (27733–1-AP), Runx2 (82636–2-RR) from ProteinTech (Cook, Illinois, USA); p-Drp1 (Ser616) (AF8470) from Affinity (Liyang, China); Hsp60 (AF0186) and Mouse IgG (A7028) from Beyotime (Shanghai, China); bActin (GB15001-100) from Servicebio (Wuhan, China).

Techniques: Labeling, Control, Expressing, Western Blot, Immunohistochemistry, Two Tailed Test

Fig. 5. P2rx7 enhanced the sensitivity of ERK pathway to promote mitochondrial fusion. a Top 10 significantly enrichment of downregulated DEGs between control and P2rx7-/- MSCs analyzed by KEGG. b Expressions of Erk1/2 and p-Erk1/2 protein in the distal femurs were analyzed by IHC staining (n = 5 per group). c The phosphorylation level and the total expression level of Erk1/2 in the control and the P2rx7-/- MSCs before and after the activated by bFGF, as assessed by western blotting. d The phosphorylation level and the total expression level of Erk1/2 in MSCs treated with different concentrations of BzATP before and after the activated by 10 lM bFGF for 1 h, as assessed by western blotting. e Expressions of genes associated with mitochondrial dynamics in the Widetype (WT) and the P2rx7-/- MSCs treated with bFGF as assessed by western blotting. f Expressions of genes associated with mitochondrial dynamics in MSCs treated with siNC, siMfn1 and BzATP as assessed by western blotting. g DWM of the Widetype (WT) and the P2rx7-/-MSCs treated with BzATP and bFGF was analyzed by JC-1 staining. h ALP activity (top) and mineralized nodules (bottom) under osteogenic induction of human MSCs when exposed to 100 nM BzATP in the presence and absence of U0126. i The expression of osteogenesis marker genes in MSCs exposed with BzATP, in the presence and absence of 10 lM U0126. Scale bar: b: 100 lm; d: 50 lm; h: 500 lm. Data was presented as mean ± SD. The data (c-i) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test (b) and one-way ANOVA (g, h).

Journal: Journal of advanced research

Article Title: The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.

doi: 10.1016/j.jare.2025.06.026

Figure Lengend Snippet: Fig. 5. P2rx7 enhanced the sensitivity of ERK pathway to promote mitochondrial fusion. a Top 10 significantly enrichment of downregulated DEGs between control and P2rx7-/- MSCs analyzed by KEGG. b Expressions of Erk1/2 and p-Erk1/2 protein in the distal femurs were analyzed by IHC staining (n = 5 per group). c The phosphorylation level and the total expression level of Erk1/2 in the control and the P2rx7-/- MSCs before and after the activated by bFGF, as assessed by western blotting. d The phosphorylation level and the total expression level of Erk1/2 in MSCs treated with different concentrations of BzATP before and after the activated by 10 lM bFGF for 1 h, as assessed by western blotting. e Expressions of genes associated with mitochondrial dynamics in the Widetype (WT) and the P2rx7-/- MSCs treated with bFGF as assessed by western blotting. f Expressions of genes associated with mitochondrial dynamics in MSCs treated with siNC, siMfn1 and BzATP as assessed by western blotting. g DWM of the Widetype (WT) and the P2rx7-/-MSCs treated with BzATP and bFGF was analyzed by JC-1 staining. h ALP activity (top) and mineralized nodules (bottom) under osteogenic induction of human MSCs when exposed to 100 nM BzATP in the presence and absence of U0126. i The expression of osteogenesis marker genes in MSCs exposed with BzATP, in the presence and absence of 10 lM U0126. Scale bar: b: 100 lm; d: 50 lm; h: 500 lm. Data was presented as mean ± SD. The data (c-i) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two-tailed Student’s t test (b) and one-way ANOVA (g, h).

Article Snippet: The antibodies used in this study were as follows: Anti-mouse CD29 (#2473836), anti-mouse CD31 (#2373735), anti-mouse CD44 (#2255545) antibodies from eBioscience (San Diego, CA, USA); PE anti-mouse CD11b (#101207), APC anti-mouse CD90.2 (#105311) antibodies from BioLegend (San Diego, CA, USA); Anti-Col1a1 (ab255809; Abcam, Cambridge, MA, USA); Drp1 (#8570), Erk1/2 (#4370), p-Erk1/2 (#4695) from CST (Danvers, MA, USA); alkaline phosphatase (ALP, PA5-106391; Invitrogen, Carlsbad, CA, USA); Bmp-2 (sc-137087), CD90 (sc-53116), Cytoc (sc-13156), Ocn (sc-390877), P2rx7 (sc-514962) from Santa Cruz Biotechnology (Santa Cruz, CA, USA); Fis1 (10956–1-AP), p16 (10883–1-AP), p21 (10355–1-AP), P2rx7 (28207–1-AP), Mfn1 (13798–1-AP), Mfn2 (12186–1-AP), Opa1 (27733–1-AP), Runx2 (82636–2-RR) from ProteinTech (Cook, Illinois, USA); p-Drp1 (Ser616) (AF8470) from Affinity (Liyang, China); Hsp60 (AF0186) and Mouse IgG (A7028) from Beyotime (Shanghai, China); bActin (GB15001-100) from Servicebio (Wuhan, China).

Techniques: Control, Immunohistochemistry, Phospho-proteomics, Expressing, Western Blot, Staining, Activity Assay, Marker, Two Tailed Test

Fig. 6. Bone metabolism and regeneration could be promoted by DCA treatment. a, b Increased mineralized nodules (a) and ALP activity (b) under osteogenic induction of the P2rx7-/- MSCs treated with PBS (Control) and 5 lM DCA. c, d Expressions of osteogenesis marker genes in the P2rx7-/- MSCs treated with Control and 5 lM DCA, as assessed by western blotting (c) and qPCR analysis (d). e, f Cross-sectional lCT images of the trabecular bone (e) and H&E staining of distal femurs (f) of 4-month-old P2rx7-/- mice treated with and without DCA, n = 5 per group. g, h Mouse mandibles of the Control and the BzATP group after 4 weeks of healing were presented as lCT images (g) and statistical analysis (g right, BV/TV in lCT images; h right, percent of area of bone tissue according to Masson staining), H&E staining (h, top) and Masson staining (h, bottom), n = 5 per group. Black arrow: new bone. i Expressions of Mfn1 and Opa1 proteins in the area of defect after 4-week healing were analyzed by IHC staining (n = 5 per group). Scale bar: f, h: 500 lm; i: 100 lm. Data was presented as mean ± SD. The data (a-d) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two- tailed Student’s t test.

Journal: Journal of advanced research

Article Title: The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.

doi: 10.1016/j.jare.2025.06.026

Figure Lengend Snippet: Fig. 6. Bone metabolism and regeneration could be promoted by DCA treatment. a, b Increased mineralized nodules (a) and ALP activity (b) under osteogenic induction of the P2rx7-/- MSCs treated with PBS (Control) and 5 lM DCA. c, d Expressions of osteogenesis marker genes in the P2rx7-/- MSCs treated with Control and 5 lM DCA, as assessed by western blotting (c) and qPCR analysis (d). e, f Cross-sectional lCT images of the trabecular bone (e) and H&E staining of distal femurs (f) of 4-month-old P2rx7-/- mice treated with and without DCA, n = 5 per group. g, h Mouse mandibles of the Control and the BzATP group after 4 weeks of healing were presented as lCT images (g) and statistical analysis (g right, BV/TV in lCT images; h right, percent of area of bone tissue according to Masson staining), H&E staining (h, top) and Masson staining (h, bottom), n = 5 per group. Black arrow: new bone. i Expressions of Mfn1 and Opa1 proteins in the area of defect after 4-week healing were analyzed by IHC staining (n = 5 per group). Scale bar: f, h: 500 lm; i: 100 lm. Data was presented as mean ± SD. The data (a-d) are representative of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs con by two- tailed Student’s t test.

Article Snippet: The antibodies used in this study were as follows: Anti-mouse CD29 (#2473836), anti-mouse CD31 (#2373735), anti-mouse CD44 (#2255545) antibodies from eBioscience (San Diego, CA, USA); PE anti-mouse CD11b (#101207), APC anti-mouse CD90.2 (#105311) antibodies from BioLegend (San Diego, CA, USA); Anti-Col1a1 (ab255809; Abcam, Cambridge, MA, USA); Drp1 (#8570), Erk1/2 (#4370), p-Erk1/2 (#4695) from CST (Danvers, MA, USA); alkaline phosphatase (ALP, PA5-106391; Invitrogen, Carlsbad, CA, USA); Bmp-2 (sc-137087), CD90 (sc-53116), Cytoc (sc-13156), Ocn (sc-390877), P2rx7 (sc-514962) from Santa Cruz Biotechnology (Santa Cruz, CA, USA); Fis1 (10956–1-AP), p16 (10883–1-AP), p21 (10355–1-AP), P2rx7 (28207–1-AP), Mfn1 (13798–1-AP), Mfn2 (12186–1-AP), Opa1 (27733–1-AP), Runx2 (82636–2-RR) from ProteinTech (Cook, Illinois, USA); p-Drp1 (Ser616) (AF8470) from Affinity (Liyang, China); Hsp60 (AF0186) and Mouse IgG (A7028) from Beyotime (Shanghai, China); bActin (GB15001-100) from Servicebio (Wuhan, China).

Techniques: Activity Assay, Control, Marker, Western Blot, Staining, Immunohistochemistry, Two Tailed Test