Review

p53 signaling – phospho antibody microarray pft196 (Full Moon BioSystems)

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Full Moon BioSystems p53 signaling – phospho antibody microarray pft196

Measurement of cell biology assays in IMR-32 cells coordinately knocked-down for <t>both</t> <t>p53</t> and GAS5: A . Measurement of Apoptosis reveals that additional loss of p53 rescues the drop in apoptosis from GAS5 alone, B . Measurement of cell viability indicates further loss of cell viability when p53 is additionally knocked-down, C and D . Measurement of cell cycle populations after additional loss of p53 reveals significant rescue of cell cycle arrest at the cost of a dramatic increase in apoptosis. E and F . Compensation of the exogenous expression of wild type p53 in SK-N-AS cells in concert with GAS5 knockdown induces a state of cell cycle arrest. All experiments were performed in triplicate. * and ** p < 0.05, Student's t-test.

P53 Signaling – Phospho Antibody Microarray Pft196, supplied by Full Moon BioSystems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p53 signaling – phospho antibody microarray pft196/product/Full Moon BioSystems
Average 90 stars, based on 1 article reviews

p53 signaling – phospho antibody microarray pft196 - by Bioz Stars, 2026-03

90/100 stars

Images

1) Product Images from "The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma"

Article Title: The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma

Journal: Oncotarget

doi: 10.18632/oncotarget.14244

Measurement of cell biology assays in IMR-32 cells coordinately knocked-down for both p53 and GAS5: A . Measurement of Apoptosis reveals that additional loss of p53 rescues the drop in apoptosis from GAS5 alone, B . Measurement of cell viability indicates further loss of cell viability when p53 is additionally knocked-down, C and D . Measurement of cell cycle populations after additional loss of p53 reveals significant rescue of cell cycle arrest at the cost of a dramatic increase in apoptosis. E and F . Compensation of the exogenous expression of wild type p53 in SK-N-AS cells in concert with GAS5 knockdown induces a state of cell cycle arrest. All experiments were performed in triplicate. * and ** p < 0.05, Student's t-test.

Figure Legend Snippet: Measurement of cell biology assays in IMR-32 cells coordinately knocked-down for both p53 and GAS5: A . Measurement of Apoptosis reveals that additional loss of p53 rescues the drop in apoptosis from GAS5 alone, B . Measurement of cell viability indicates further loss of cell viability when p53 is additionally knocked-down, C and D . Measurement of cell cycle populations after additional loss of p53 reveals significant rescue of cell cycle arrest at the cost of a dramatic increase in apoptosis. E and F . Compensation of the exogenous expression of wild type p53 in SK-N-AS cells in concert with GAS5 knockdown induces a state of cell cycle arrest. All experiments were performed in triplicate. * and ** p < 0.05, Student's t-test.

Techniques Used: Expressing, Knockdown

A . qRT-PCR of GAS5, p53, BRCA1, and GADD45A expression in IMR-32 cells after transfection with: Negative Control siRNA, GAS5 & Negative Control siRNA, GAS5 & BRCA1 siRNA, and GAS5 & GADD45A siRNA. Samples were normalized to the Ct value of GAPDH, with relative expression calculated by normalizing to the ΔΔCt of the Negative Control siRNA sample. Data were expressed as a means of +/- SD using three biological replicates. B . Western blot analysis of p53, BRCA1-phospho1457, and GADD45A in IMR-32 cells after transfection with: Negative Control siRNA, GAS5 & Negative Control siRNA, GAS5 & BRCA1 siRNA, and GAS5 & GADD45A siRNA. GAPDH was used as a load control. C and D . Measurement of cell cycle populations after knockdown with GAS5 and BRCA1 reveals limited rescue of cell cycle arrest with only a minimal increase in apoptosis. E and F . Measurement of cell cycle populations after knockdown with GAS5 and GADD45A reveals dramatic rescue of cell cycle arrest with greater increase in apoptosis. All experiments were performed in triplicate. * and ** p < 0.05, Student's t-test.

Figure Legend Snippet: A . qRT-PCR of GAS5, p53, BRCA1, and GADD45A expression in IMR-32 cells after transfection with: Negative Control siRNA, GAS5 & Negative Control siRNA, GAS5 & BRCA1 siRNA, and GAS5 & GADD45A siRNA. Samples were normalized to the Ct value of GAPDH, with relative expression calculated by normalizing to the ΔΔCt of the Negative Control siRNA sample. Data were expressed as a means of +/- SD using three biological replicates. B . Western blot analysis of p53, BRCA1-phospho1457, and GADD45A in IMR-32 cells after transfection with: Negative Control siRNA, GAS5 & Negative Control siRNA, GAS5 & BRCA1 siRNA, and GAS5 & GADD45A siRNA. GAPDH was used as a load control. C and D . Measurement of cell cycle populations after knockdown with GAS5 and BRCA1 reveals limited rescue of cell cycle arrest with only a minimal increase in apoptosis. E and F . Measurement of cell cycle populations after knockdown with GAS5 and GADD45A reveals dramatic rescue of cell cycle arrest with greater increase in apoptosis. All experiments were performed in triplicate. * and ** p < 0.05, Student's t-test.

Techniques Used: Quantitative RT-PCR, Expressing, Transfection, Negative Control, Western Blot, Control, Knockdown

A . qRT-PCR of HDM2 (MDM2) expression in IMR-32 cells after transfection with: Negative Control siRNA & Vector only (VO), GAS5 siRNA + VO, GAS5 siRNA complemented with FL-expressing plasmid and GAS5 siRNA complemented with C2-expressing plasmid. Samples were normalized to the Ct value of GAPDH, with relative expression calculated by normalizing to the ΔΔCt of the Negative Control siRNA & Vector only sample. Data were expressed as a means of +/- SD using three biological replicates. B . Western blot analysis of p53 and HDM2 (MDM2) in IMR-32 cells after transfection with: Negative Control siRNA & Vector only (VO), GAS5 siRNA + VO, GAS5 siRNA complemented with FL-expressing plasmid, and GAS5 siRNA complemented with C2-expressing plasmid. GAPDH was used as a load control. * and ** p < 0.05, Student's t-test. C . Schematic illustration of the effects of GAS5 knockdown in neuroblastoma cells. Briefly, loss of GAS5 induces ser1457 phosphorylation of BRCA1, an ATM-specific phosphorylation site. Simultaneously, loss of GAS5 also induces multiple p53 phosphorylation events, leading to increased stability and a decrease in cellular HDM2 levels (likely due to auto- ubiquitination). Phospho-activated p53 and BRCA1 then induce increased transcription of GADD45A, leading to the induction cell cycle arrest.

Figure Legend Snippet: A . qRT-PCR of HDM2 (MDM2) expression in IMR-32 cells after transfection with: Negative Control siRNA & Vector only (VO), GAS5 siRNA + VO, GAS5 siRNA complemented with FL-expressing plasmid and GAS5 siRNA complemented with C2-expressing plasmid. Samples were normalized to the Ct value of GAPDH, with relative expression calculated by normalizing to the ΔΔCt of the Negative Control siRNA & Vector only sample. Data were expressed as a means of +/- SD using three biological replicates. B . Western blot analysis of p53 and HDM2 (MDM2) in IMR-32 cells after transfection with: Negative Control siRNA & Vector only (VO), GAS5 siRNA + VO, GAS5 siRNA complemented with FL-expressing plasmid, and GAS5 siRNA complemented with C2-expressing plasmid. GAPDH was used as a load control. * and ** p < 0.05, Student's t-test. C . Schematic illustration of the effects of GAS5 knockdown in neuroblastoma cells. Briefly, loss of GAS5 induces ser1457 phosphorylation of BRCA1, an ATM-specific phosphorylation site. Simultaneously, loss of GAS5 also induces multiple p53 phosphorylation events, leading to increased stability and a decrease in cellular HDM2 levels (likely due to auto- ubiquitination). Phospho-activated p53 and BRCA1 then induce increased transcription of GADD45A, leading to the induction cell cycle arrest.

Techniques Used: Quantitative RT-PCR, Expressing, Transfection, Negative Control, Plasmid Preparation, Western Blot, Control, Knockdown, Phospho-proteomics, Ubiquitin Proteomics

Image Search Results

Journal: Oncotarget

Article Title: The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma

doi: 10.18632/oncotarget.14244

Figure Lengend Snippet: Measurement of cell biology assays in IMR-32 cells coordinately knocked-down for both p53 and GAS5: A . Measurement of Apoptosis reveals that additional loss of p53 rescues the drop in apoptosis from GAS5 alone, B . Measurement of cell viability indicates further loss of cell viability when p53 is additionally knocked-down, C and D . Measurement of cell cycle populations after additional loss of p53 reveals significant rescue of cell cycle arrest at the cost of a dramatic increase in apoptosis. E and F . Compensation of the exogenous expression of wild type p53 in SK-N-AS cells in concert with GAS5 knockdown induces a state of cell cycle arrest. All experiments were performed in triplicate. * and ** p < 0.05, Student's t-test.

Article Snippet: The remaining cell pellet (containing 1.5 × 10 6 cells) was prepared according to manufacturer's protocols (Antibody Array Assay Kit, Cat. No. KAS02, Full Moon BioSystems) and coupled to an ELISA-based array platform (p53 Signaling – Phospho Antibody Microarray, Cat. No. PFT196, Full Moon BioSystems).

Techniques: Expressing, Knockdown

Journal: Oncotarget

Article Title: The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma

doi: 10.18632/oncotarget.14244

Figure Lengend Snippet: A . qRT-PCR of GAS5, p53, BRCA1, and GADD45A expression in IMR-32 cells after transfection with: Negative Control siRNA, GAS5 & Negative Control siRNA, GAS5 & BRCA1 siRNA, and GAS5 & GADD45A siRNA. Samples were normalized to the Ct value of GAPDH, with relative expression calculated by normalizing to the ΔΔCt of the Negative Control siRNA sample. Data were expressed as a means of +/- SD using three biological replicates. B . Western blot analysis of p53, BRCA1-phospho1457, and GADD45A in IMR-32 cells after transfection with: Negative Control siRNA, GAS5 & Negative Control siRNA, GAS5 & BRCA1 siRNA, and GAS5 & GADD45A siRNA. GAPDH was used as a load control. C and D . Measurement of cell cycle populations after knockdown with GAS5 and BRCA1 reveals limited rescue of cell cycle arrest with only a minimal increase in apoptosis. E and F . Measurement of cell cycle populations after knockdown with GAS5 and GADD45A reveals dramatic rescue of cell cycle arrest with greater increase in apoptosis. All experiments were performed in triplicate. * and ** p < 0.05, Student's t-test.

Techniques: Quantitative RT-PCR, Expressing, Transfection, Negative Control, Western Blot, Control, Knockdown

Journal: Oncotarget

Article Title: The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma

doi: 10.18632/oncotarget.14244

Figure Lengend Snippet: A . qRT-PCR of HDM2 (MDM2) expression in IMR-32 cells after transfection with: Negative Control siRNA & Vector only (VO), GAS5 siRNA + VO, GAS5 siRNA complemented with FL-expressing plasmid and GAS5 siRNA complemented with C2-expressing plasmid. Samples were normalized to the Ct value of GAPDH, with relative expression calculated by normalizing to the ΔΔCt of the Negative Control siRNA & Vector only sample. Data were expressed as a means of +/- SD using three biological replicates. B . Western blot analysis of p53 and HDM2 (MDM2) in IMR-32 cells after transfection with: Negative Control siRNA & Vector only (VO), GAS5 siRNA + VO, GAS5 siRNA complemented with FL-expressing plasmid, and GAS5 siRNA complemented with C2-expressing plasmid. GAPDH was used as a load control. * and ** p < 0.05, Student's t-test. C . Schematic illustration of the effects of GAS5 knockdown in neuroblastoma cells. Briefly, loss of GAS5 induces ser1457 phosphorylation of BRCA1, an ATM-specific phosphorylation site. Simultaneously, loss of GAS5 also induces multiple p53 phosphorylation events, leading to increased stability and a decrease in cellular HDM2 levels (likely due to auto- ubiquitination). Phospho-activated p53 and BRCA1 then induce increased transcription of GADD45A, leading to the induction cell cycle arrest.

Techniques: Quantitative RT-PCR, Expressing, Transfection, Negative Control, Plasmid Preparation, Western Blot, Control, Knockdown, Phospho-proteomics, Ubiquitin Proteomics

Review

Structured Review

Images

1) Product Images from "The long non-coding RNA GAS5 differentially regulates cell cycle arrest and apoptosis through activation of BRCA1 and p53 in human neuroblastoma"

Similar Products

Image Search Results