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Proteintech pgc1α
Pgc1α, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 831 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgc1%CE%B1/PGC1a+Antibody/pm41897550-42-65-72
Average 96 stars, based on 831 article reviews
pgc1α - by Bioz Stars, 2026-09
96/100 stars

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Related Articles

Western Blot:

Article Title: Melatonin Ameliorates decaBDE-Induced Autism-Relevant Behaviors Through Promoting SIRT1/SIRT3/FOXO3a-Dependent Mitochondrial Quality Control.
Article Snippet: Decabromodiphenyl ether (deca-BDE or BDE-209, 98%, CAS#1163-19-5) was obtained from J & K Chemical Technology (Beijing, China); sodium valproate (VPA, powder, 98%, CAS#1069-66-5) and melatonin (MT, powder, ≥98%, CAS#73-31-4) were from SigmaAldrich Trading Co., Ltd. (Shanghai, China); Sirt1/Sir2 inhibitor Selisistat (EX527, 99.85%, CAS#49843-98-3) was from MedChemExpress (Shanghai, China). .. Primary antibodies used for Western blotting were as follows: GAPDH (60004-1-Ig) and PSD95 (20665-1-AP) were from Proteintech (Wuhan, China); SNAP25 (sc-73044), cytochrome c (sc-13156), caspase-3 (sc-56053), COX4 (sc-517553), DRP1 (sc-271583), FIS1 (sc-376447), MFN2 (sc-100560), OPA1 (sc-393296), NRF1 (sc-28379), TFAM (sc-166965), SOD2 (sc-133134), PINK1 (sc-517353), and PRKN (sc-32282) were from Santa Cruz (Dallas, TX, USA); Acetylated-Lysine Antibody (#9441, CST, Danvers, MA, USA); SIRT1 (13161-1-AP), SIRT3 (10099-1-AP), PGC1α (66369-1-Ig), and FOXO3a (66428-1-Ig) were from Proteintech (Wuhan, China). .. Ten-week-old Sprague-Dawley rats (weighing 280 g ± 30 g) were obtained from Changsheng Biotechnology (Liaoning, China, license number: SYXK 2019-0007).

Article Title: Melatonin Ameliorates decaBDE-Induced Autism-Relevant Behaviors Through Promoting SIRT1/SIRT3/FOXO3a-Dependent Mitochondrial Quality Control
Article Snippet: Decabromodiphenyl ether (deca-BDE or BDE-209, 98%, CAS#1163-19-5) was obtained from J & K Chemical Technology (Beijing, China); sodium valproate (VPA, powder, 98%, CAS#1069-66-5) and melatonin (MT, powder, ≥98%, CAS#73-31-4) were from Sigma-Aldrich Trading Co., Ltd. (Shanghai, China); Sirt1/Sir2 inhibitor Selisistat (EX527, 99.85%, CAS#49843-98-3) was from MedChemExpress (Shanghai, China). .. Primary antibodies used for Western blotting were as follows: GAPDH (60004-1-Ig) and PSD95 (20665-1-AP) were from Proteintech (Wuhan, China); SNAP25 (sc-73044), cytochrome c (sc-13156), caspase-3 (sc-56053), COX4 (sc-517553), DRP1 (sc-271583), FIS1 (sc-376447), MFN2 (sc-100560), OPA1 (sc-393296), NRF1 (sc-28379), TFAM (sc-166965), SOD2 (sc-133134), PINK1 (sc-517353), and PRKN (sc-32282) were from Santa Cruz (Dallas, TX, USA); Acetylated-Lysine Antibody (#9441, CST, Danvers, MA, USA); SIRT1 (13161-1-AP), SIRT3 (10099-1-AP), PGC1α (66369-1-Ig), and FOXO3a (66428-1-Ig) were from Proteintech (Wuhan, China). .. Ten-week-old Sprague-Dawley rats (weighing 280 g ± 30 g) were obtained from Changsheng Biotechnology (Liaoning, China, license number: SYXK 2019-0007).

other:

Article Title: Hyperglycemia in combination with excess fat intake promotes renal pyroptosis and fibrosis through Gα 12 -dependent endoplasmic reticulum stress
Article Snippet: Sigma-Aldrich (St. Louis, MO, USA) provided the β-actin antibody (A5441), while PGC1α (66369-1-Ig) was procured from Proteintech (Rosemont, IL, USA).

Blocking Assay:

Article Title: SERCA2 dysfunction stimulates inflammation and causes pulmonary vascular remodeling by downregulating PPARγ/PGC1α/Nrf2.
Article Snippet: Our prior research has demonstrated that dysfunction of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) is a common causal factor in the development of pulmonary vascular remodeling, as it accelerates cell proliferation and migration in pulmonary artery smooth muscle cells (PASMCs).. Inflammation is known to play a critical role in pulmonary vascular remodeling.. However, the contribution of SERCA2 dysfunction to inflammation within the pulmonary vasculature has not been previously reported.

Incubation:

Article Title: SERCA2 dysfunction stimulates inflammation and causes pulmonary vascular remodeling by downregulating PPARγ/PGC1α/Nrf2.
Article Snippet: Our prior research has demonstrated that dysfunction of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) is a common causal factor in the development of pulmonary vascular remodeling, as it accelerates cell proliferation and migration in pulmonary artery smooth muscle cells (PASMCs).. Inflammation is known to play a critical role in pulmonary vascular remodeling.. However, the contribution of SERCA2 dysfunction to inflammation within the pulmonary vasculature has not been previously reported.

Article Title: Short-chain acyl-CoA dehydrogenase initiates mtDNA demethylation and leakage to fuel antitumor immunity in colorectal cancer.
Article Snippet: .. The membranes were washed with TBST and incubated overnight at 4 °C with primary antibodies, including ACADS (#AP75024, Abcepta, Jiangsu, China), DNMT1 (#NB10056519AF594, NOVUS), cGAS (Cat#31659, Cell Signaling Technology), p-STING (#PA5-105674, Invitrogen), STING (#A3575, ABclonal), p-TBK1 (#AP1026, ABclonal), TBK1 (#AF8103, Beyotime), p-IRF3 (#4947, Cell Signaling Technology), IRF3 (#4302, Cell Signaling Technology), BAX (#A0207, ABclonal), VDAC1 (#A19707, ABclonal), VDAC3 (#55260-1-AP, Proteintech), HSP60 (#AF0186, Beyotime), PHB1 (#10787-1-AP, Proteintech), Lamin B1 (#ab16048, Abcam), HA (#51064-2-AP, Proteintech), TFAM (#A13552, ABclonal), NRF1 (#12482-1-AP, Proteintech), PGC1α (#66369-1-Ig, Proteintech), Twinkle (#18793-1-AP, Proteintech), POLG (#AP14948B, Abcepta), and β-actin (#66009-1-Ig, Proteintech). .. Following incubation with primary antibody, the membranes were washed 3 times with TBST and then hybridized with the corresponding secondary antibody at room temperature for 2 h. In certain instances, the membrane was subjected to washing with primary and secondary antibody removal solution (#P0025, Beyotime), followed by reincubation with either the indicated antibody or a loading control β-actin antibody, along with the corresponding secondary antibodies.

Article Title: Short-chain acyl-CoA dehydrogenase initiates mtDNA demethylation and leakage to fuel antitumor immunity in colorectal cancer
Article Snippet: .. The membranes were washed with TBST and incubated overnight at 4 °C with primary antibodies, including ACADS (#AP75024, Abcepta, Jiangsu, China), DNMT1 (#NB100-56519AF594, NOVUS), cGAS (Cat#31659, Cell Signaling Technology), p-STING (#PA5-105674, Invitrogen), STING (#A3575, ABclonal), p-TBK1 (#AP1026, ABclonal), TBK1 (#AF8103, Beyotime), p-IRF3 (#4947, Cell Signaling Technology), IRF3 (#4302, Cell Signaling Technology), BAX (#A0207, ABclonal), VDAC1 (#A19707, ABclonal), VDAC3 (#55260-1-AP, Proteintech), HSP60 (#AF0186, Beyotime), PHB1 (#10787-1-AP, Proteintech), Lamin B1 (#ab16048, Abcam), HA (#51064-2-AP, Proteintech), TFAM (#A13552, ABclonal), NRF1 (#12482-1-AP, Proteintech), PGC1α (#66369-1-Ig, Proteintech), Twinkle (#18793-1-AP, Proteintech), POLG (#AP14948B, Abcepta), and β-actin (#66009-1-Ig, Proteintech). .. Following incubation with primary antibody, the membranes were washed 3 times with TBST and then hybridized with the corresponding secondary antibody at room temperature for 2 h. In certain instances, the membrane was subjected to washing with primary and secondary antibody removal solution (#P0025, Beyotime), followed by reincubation with either the indicated antibody or a loading control β-actin antibody, along with the corresponding secondary antibodies.

Article Title: PSPC1-SMAD3 axis regulates iron-induced beiging of adipocytes in white adipose tissue.
Article Snippet: Protein in each sample (20–50μg) was separated by SDSPAGE and transferred to PVDF membrane (Millipore, China). .. The membranes were blocked with 5% milk powder in Tris-buffered saline with 0.1% Tween 20 (TBST) at room temperature for 1h, followed by incubation overnight at 4 °C with the following AR TIC LE IN PR ES S primary antibody: anti-UCP1 (Abcam, ab234430), anti FTH1 (Abclone, A19544), anti phospho-SMAD3 (Ser423/425) (CST, #9520), anti SMAD3(CST, #9523), anti phospho-SMAD2 (Ser465/467), anti SMAD2 (ZENBIO, 382472), anti FABP4 (Proteintech, 12802-1-AP), anti PSPC1 (Proteintech, 16714-1-AP), anti HSP90(Proteintech, 60318-1-Ig), antiβ-Actin (Abclone, AC026), anti PGC1α (Proteintech, 66369-1-Ig). .. The membranes were incubated with the secondary antibody (Proteintech, # SA00001-1, SA00001-2) for 1 h at room temperature after three washes with TBST.

Article Title: PSPC1-SMAD3 axis regulates iron-induced beiging of adipocytes in white adipose tissue
Article Snippet: PAGE and transferred to PVDF membrane (Millipore, China). .. The membranes were blocked with 5% milk powder in Tris-buffered saline with 0.1% Tween 20 (TBST) at room temperature for 1 h, followed by incubation overnight at 4 °C with the following primary antibody: anti-UCP1 (Abcam, ab234430), anti FTH1 (Abclone, A19544), anti phospho-SMAD3 (Ser423/425) (CST, #9520), anti SMAD3(CST, #9523), anti phospho-SMAD2 (Ser465/467), anti SMAD2 (ZENBIO, 382472), anti FABP4 (Proteintech, 12802-1-AP), anti PSPC1 (Proteintech, 16714-1-AP), anti HSP90(Proteintech, 60318-1-Ig), antiβ-Actin (Abclone, AC026), anti PGC1α (Proteintech, 66369-1-Ig). .. The membranes were incubated with the secondary antibody (Proteintech, # SA00001-1, SA00001-2) for 1 h at room temperature after three washes with TBST.

Saline:

Article Title: PSPC1-SMAD3 axis regulates iron-induced beiging of adipocytes in white adipose tissue.
Article Snippet: Protein in each sample (20–50μg) was separated by SDSPAGE and transferred to PVDF membrane (Millipore, China). .. The membranes were blocked with 5% milk powder in Tris-buffered saline with 0.1% Tween 20 (TBST) at room temperature for 1h, followed by incubation overnight at 4 °C with the following AR TIC LE IN PR ES S primary antibody: anti-UCP1 (Abcam, ab234430), anti FTH1 (Abclone, A19544), anti phospho-SMAD3 (Ser423/425) (CST, #9520), anti SMAD3(CST, #9523), anti phospho-SMAD2 (Ser465/467), anti SMAD2 (ZENBIO, 382472), anti FABP4 (Proteintech, 12802-1-AP), anti PSPC1 (Proteintech, 16714-1-AP), anti HSP90(Proteintech, 60318-1-Ig), antiβ-Actin (Abclone, AC026), anti PGC1α (Proteintech, 66369-1-Ig). .. The membranes were incubated with the secondary antibody (Proteintech, # SA00001-1, SA00001-2) for 1 h at room temperature after three washes with TBST.

Article Title: PSPC1-SMAD3 axis regulates iron-induced beiging of adipocytes in white adipose tissue
Article Snippet: PAGE and transferred to PVDF membrane (Millipore, China). .. The membranes were blocked with 5% milk powder in Tris-buffered saline with 0.1% Tween 20 (TBST) at room temperature for 1 h, followed by incubation overnight at 4 °C with the following primary antibody: anti-UCP1 (Abcam, ab234430), anti FTH1 (Abclone, A19544), anti phospho-SMAD3 (Ser423/425) (CST, #9520), anti SMAD3(CST, #9523), anti phospho-SMAD2 (Ser465/467), anti SMAD2 (ZENBIO, 382472), anti FABP4 (Proteintech, 12802-1-AP), anti PSPC1 (Proteintech, 16714-1-AP), anti HSP90(Proteintech, 60318-1-Ig), antiβ-Actin (Abclone, AC026), anti PGC1α (Proteintech, 66369-1-Ig). .. The membranes were incubated with the secondary antibody (Proteintech, # SA00001-1, SA00001-2) for 1 h at room temperature after three washes with TBST.



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Inhibitory effects of Ena on HUVEC ferroptosis activated by AGE-elicited neutrophils (A) CCK-8 assay was performed to measure the viability of HUVECs. n = 3 independent experiments. (B) Death rate of HUVECs incubated with neutrophils pretreated by different strategies as detected using flow cytometry. n = 3 independent experiments. (C) Levels of MDA and GSH were quantified to assess the ferroptosis activity. n = 3 independent experiments. (D) Intracellular lipid peroxidation was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (E) Fe 2+ ion content was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (F) JC-1 kit was used to evaluate the mitochondrial membrane potential of HUVECs. Scale bar, 10 μm; n = 3 independent experiments. (G) DCFH-DA fluorescence probe was applied to determine ROS abundance in HUVECs. Scale bar, 200 μm; n = 3 independent experiments. (H) Mitochondrial morphology in HUVECs as analyzed by transmission electron microscopy. Scale bar, 500 nm; n = 3 independent experiments. (I) Western blot detection of <t>PGC1α</t> and KLF9 in HUVECs with different treatments. n = 3 independent experiments. (J) Expression of KLF9 in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (K) Expression of PGC1α in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (L) Schematic diagram of Ena-elicited alleviation on endothelial cell ferroptosis induced by pro-inflammatory neutrophils. Data were shown as mean ± standard deviation (SD) from biological replicates, and statistical comparisons were performed using one-way ANOVA followed by Tukey’s multiple comparisons test in (A–G and I–K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.
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Inhibitory effects of Ena on HUVEC ferroptosis activated by AGE-elicited neutrophils (A) CCK-8 assay was performed to measure the viability of HUVECs. n = 3 independent experiments. (B) Death rate of HUVECs incubated with neutrophils pretreated by different strategies as detected using flow cytometry. n = 3 independent experiments. (C) Levels of MDA and GSH were quantified to assess the ferroptosis activity. n = 3 independent experiments. (D) Intracellular lipid peroxidation was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (E) Fe 2+ ion content was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (F) JC-1 kit was used to evaluate the mitochondrial membrane potential of HUVECs. Scale bar, 10 μm; n = 3 independent experiments. (G) DCFH-DA fluorescence probe was applied to determine ROS abundance in HUVECs. Scale bar, 200 μm; n = 3 independent experiments. (H) Mitochondrial morphology in HUVECs as analyzed by transmission electron microscopy. Scale bar, 500 nm; n = 3 independent experiments. (I) Western blot detection of <t>PGC1α</t> and KLF9 in HUVECs with different treatments. n = 3 independent experiments. (J) Expression of KLF9 in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (K) Expression of PGC1α in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (L) Schematic diagram of Ena-elicited alleviation on endothelial cell ferroptosis induced by pro-inflammatory neutrophils. Data were shown as mean ± standard deviation (SD) from biological replicates, and statistical comparisons were performed using one-way ANOVA followed by Tukey’s multiple comparisons test in (A–G and I–K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.
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Image Search Results


Inhibitory effects of Ena on HUVEC ferroptosis activated by AGE-elicited neutrophils (A) CCK-8 assay was performed to measure the viability of HUVECs. n = 3 independent experiments. (B) Death rate of HUVECs incubated with neutrophils pretreated by different strategies as detected using flow cytometry. n = 3 independent experiments. (C) Levels of MDA and GSH were quantified to assess the ferroptosis activity. n = 3 independent experiments. (D) Intracellular lipid peroxidation was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (E) Fe 2+ ion content was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (F) JC-1 kit was used to evaluate the mitochondrial membrane potential of HUVECs. Scale bar, 10 μm; n = 3 independent experiments. (G) DCFH-DA fluorescence probe was applied to determine ROS abundance in HUVECs. Scale bar, 200 μm; n = 3 independent experiments. (H) Mitochondrial morphology in HUVECs as analyzed by transmission electron microscopy. Scale bar, 500 nm; n = 3 independent experiments. (I) Western blot detection of PGC1α and KLF9 in HUVECs with different treatments. n = 3 independent experiments. (J) Expression of KLF9 in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (K) Expression of PGC1α in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (L) Schematic diagram of Ena-elicited alleviation on endothelial cell ferroptosis induced by pro-inflammatory neutrophils. Data were shown as mean ± standard deviation (SD) from biological replicates, and statistical comparisons were performed using one-way ANOVA followed by Tukey’s multiple comparisons test in (A–G and I–K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Journal: Cell Reports Medicine

Article Title: Enalaprilat reverses neutrophil polarization imbalance via targeting taurine-STING axis for treatment of diabetic wounds

doi: 10.1016/j.xcrm.2026.102714

Figure Lengend Snippet: Inhibitory effects of Ena on HUVEC ferroptosis activated by AGE-elicited neutrophils (A) CCK-8 assay was performed to measure the viability of HUVECs. n = 3 independent experiments. (B) Death rate of HUVECs incubated with neutrophils pretreated by different strategies as detected using flow cytometry. n = 3 independent experiments. (C) Levels of MDA and GSH were quantified to assess the ferroptosis activity. n = 3 independent experiments. (D) Intracellular lipid peroxidation was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (E) Fe 2+ ion content was visualized by fluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (F) JC-1 kit was used to evaluate the mitochondrial membrane potential of HUVECs. Scale bar, 10 μm; n = 3 independent experiments. (G) DCFH-DA fluorescence probe was applied to determine ROS abundance in HUVECs. Scale bar, 200 μm; n = 3 independent experiments. (H) Mitochondrial morphology in HUVECs as analyzed by transmission electron microscopy. Scale bar, 500 nm; n = 3 independent experiments. (I) Western blot detection of PGC1α and KLF9 in HUVECs with different treatments. n = 3 independent experiments. (J) Expression of KLF9 in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (K) Expression of PGC1α in HUVECs incubated with neutrophils pretreated by different approaches as detected using immunofluorescence staining. Scale bar, 10 μm; n = 3 independent experiments. (L) Schematic diagram of Ena-elicited alleviation on endothelial cell ferroptosis induced by pro-inflammatory neutrophils. Data were shown as mean ± standard deviation (SD) from biological replicates, and statistical comparisons were performed using one-way ANOVA followed by Tukey’s multiple comparisons test in (A–G and I–K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Expression vectors encoding ZNF460, GGT1, KLF9 and PGC1α were constructed by GeneChem (Shanghai, China) via cloning the open reading frames of the indicated genes into a pcDNA3.1 plasmid vector.

Techniques: CCK-8 Assay, Incubation, Flow Cytometry, Activity Assay, Fluorescence, Staining, Membrane, Transmission Assay, Electron Microscopy, Western Blot, Expressing, Immunofluorescence, Standard Deviation

SAC promotes PGC1α/FBP1 axis in AKI mouse kidneys. (A) Representative images of multiplex immunofluorescence staining in renal tissues showing DAPI (blue, nuclei), LRP2 (green, proximal tubules), and FBP1 (red) (original magnification ×40; Scale bar: 50 μm). (B) Quantitative assessment of FBP1-positive area. (C) Representative photomicrographs of FOXO1 staining in renal tissues (original magnification ×40; Scale bar: 50 μm). (D) Quantitative assessment of FOXO1-positive cells. (E) Representative photomicrographs of PGC1α staining in renal tissues (original magnification ×40; Scale bar: 50 μm). (F) Quantitative assessment of PGC1α-positive Area. NS represents not significant. * p < 0.05. ** p < 0.01. *** p < 0.001.

Journal: Renal Failure

Article Title: Salvianolic acid C alleviates acute kidney injury by restoring fructose-1,6-bisphosphatase 1-mediated gluconeogenesis

doi: 10.1080/0886022X.2026.2629902

Figure Lengend Snippet: SAC promotes PGC1α/FBP1 axis in AKI mouse kidneys. (A) Representative images of multiplex immunofluorescence staining in renal tissues showing DAPI (blue, nuclei), LRP2 (green, proximal tubules), and FBP1 (red) (original magnification ×40; Scale bar: 50 μm). (B) Quantitative assessment of FBP1-positive area. (C) Representative photomicrographs of FOXO1 staining in renal tissues (original magnification ×40; Scale bar: 50 μm). (D) Quantitative assessment of FOXO1-positive cells. (E) Representative photomicrographs of PGC1α staining in renal tissues (original magnification ×40; Scale bar: 50 μm). (F) Quantitative assessment of PGC1α-positive Area. NS represents not significant. * p < 0.05. ** p < 0.01. *** p < 0.001.

Article Snippet: Primary antibodies used were Cleaved-caspase-3 (Cat# 9661, Cell Signaling Technology, Danvers, MA, USA), FOXO1 (Cat# GB12286, Servicebio, Wuhan, China), and PGC1α (Cat# 66369-1-IG, Servicebio, Wuhan, Hubei, China).

Techniques: Multiplex Assay, Immunofluorescence, Staining