goat anti p21 (R&D Systems)
Structured Review

Goat Anti P21, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p21/Human+p21%2FCIP1%2FCDKN1A+Antibody/pmc03594263-132-9-11
Average 93 stars, based on 13 article reviews
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1) Product Images from "A high-content cellular senescence screen identifies candidate tumor suppressors, including EPHA3"
Article Title: A high-content cellular senescence screen identifies candidate tumor suppressors, including EPHA3
Journal: Cell Cycle
doi: 10.4161/cc.23515
Figure Legend Snippet: Figure 1. Identification of senescence-inducing kinase siRNAs. ( A ) Schematic overview of the high-content senescence screen. ( B ) Scatterplot analysis of data from the kinome HCS screen in p53+ cells. Cells were stained for Ki67, p53, p21 CIP1 and Hoechst at day 3, and multiparametric analysis was performed to determine siRNAs displaying decreased proliferation (< 0.5 StDev Ki67%) and an increased nuclear size (> 2.0 StDev Hoechst mean area). High, medium and low cell number indicators are assigned as the third parameter. ( C ) Senescence scores per gene are the sum of the senescence scores of its siRNA pool and the four individual siRNAs, omitting siRNAs conferring less than 50% specific gene knockdown. Scoring details are depicted in . References to studies establishing bona fide tumor suppressor functions for human ( Hs ) or mouse ( Mm ) genes are indicated.
Techniques Used: Staining, Knockdown
Figure Legend Snippet: Figure 2. Delineation of senescence signatures. ( A ) hTERT-RPE1 p53 shRNA cells were transfected with kinome siRNAs in the absence of doxycycline and immunostained for p53 and p21 CIP1 following 72 h culture. Percentages of cells expressing p53, p21 CIP1 above threshold levels were calculated, and averages from four 384 wells are shown. ( B ) hTERT-RPE1 p53 shRNA cells were transfected with kinome siRNAs in the absence or presence of doxycycline and immunostained for Ki67. Percentages of cells expressing Ki67 protein above threshold levels were calculated, and averages from four 384 wells are shown. * indicates p ≤ 0,05 and ** indicates p ≤ 0,01. ( C ) Senescence scores per gene are the sum of the senescence scores of the siRNA pool plus four individual siRNAs, omitting siRNAs conferring less than 50% knockdown. Detailed scoring information is depicted in . ( D ) Quantitative p16 INK4A mRNA expression analyses during senescence induction. hTERT-RPE1 p53 shRNA cells were transfected with pooled siRNAs in the absence of doxycycline. RNA expression was quantitated using TaqMan analyses after 3 days of transfection. ( E ) Schematic model summarizing kinome screen data, using data depicted in ( A ) and ( D ). In an incipient tumor, modeled by hTERT-RPE1 cells, loss of selected tumor suppressors activates p53- and/or p16 INK4A -dependent senescence, and overt DNA damage. In a premalignant tumor, senescence may serve as a cell-intrinsic tumor suppressor mechanism to subvert oncogenic transformation. Loss of p16 INK4A and/or p53 promotes malignancy.
Techniques Used: shRNA, Transfection, Expressing, Knockdown, RNA Expression, Transformation Assay
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![( A ) MCF7-PALR and MCF7-ABER cells were treated with Ctr-ASO-M or SUV-ASO-Ms (0.1 μM). CCK8 assays reveal the cell growth under PAL (0.5 μM) or ABE (0.1 μM) treatment ( N = 3 biological replicates). ( B ) CCK8 assays calculating IC 50 values of SUV-ASO-Ms in MCF7-TAMR, MCF7-PALR, and MCF7-ABER cells ( N = 3 biological replicates). ( C ) Synergy Finder is calculating ZIP scores in MCF7-TAMR to study the synergistic effect between SUV-ASO-Ms and CDK4/6i (PAL and ABE). ( D and E ) MCF7-PALR and MCF7-ABER cells were treated with Ctr-ASO-M or SUV-ASO-Ms (0.1 μM) alone or in combination with CDK4/6i (PAL, 0.5 μM and ABE, 0.1 μM). Flow cytometry analysis (D) and β-Gal activity assays (20× magnification) (E) showing the cell cycle distribution and senescence of the cells. ( F ) Schematic depicting the experimental design of the MCF7-ABER xenograft tumors conducted to assess the efficacy of SUV-ASO2-M or a combination of SUV-ASO2-M with ABE in vivo. ( G to I ) After being treated with Ctr-ASO-M or SUV-ASO2-M in combination with Veh or ABE, the tumor growth curves (G), the harvested tumors (H), and the tumor weight (I) were measured. ( J and K ) RT-qPCR and Western blotting detection of SUV39H2 mRNA (J) and protein (K) in tumors from xenografts. ( L ) IHC staining of <t>p21</t> in tumors from xenografts. H scores were calculated for p21 in all samples. Data were presented as means ± SD [(A to E), N = 3 biological replicates; (G), (I), (J) to (L), N = 5 biological replicates]. The P values were calculated by one-way ANOVA followed by Tukey’s test for multiple-group comparison.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_1863/pmc13651863/pmc13651863__sciadv.aea2001-f4.jpg)


