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Cell Signaling Technology Inc anti proliferating cell nuclear antigen pcna
Effects of des-Arg 9 -bradykinin (DABK) and angiotensin II (ANG II) vascular smooth muscle cells (VSMC) growth. [A] Aortic VSMC from Wistar rats treated with ANG II and/or DABK at low concentration (0.1 nM) in the presence or not of losartan (LOS – 10 µM), des-arg9-leu8-bradykinin (DAL – 10 µM) and TIRON (1 mM). Bar graph shows <t>PCNA</t> expression normalized against the housekeeping protein <t>β-actin.</t> Results are represented as mean±SEM of 4 experiments. *P
Anti Proliferating Cell Nuclear Antigen Pcna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "An Interaction of Renin-Angiotensin and Kallikrein-Kinin Systems Contributes to Vascular Hypertrophy in Angiotensin II-Induced Hypertension: In Vivo and In Vitro Studies"

Article Title: An Interaction of Renin-Angiotensin and Kallikrein-Kinin Systems Contributes to Vascular Hypertrophy in Angiotensin II-Induced Hypertension: In Vivo and In Vitro Studies

Journal: PLoS ONE

doi: 10.1371/journal.pone.0111117

Effects of des-Arg 9 -bradykinin (DABK) and angiotensin II (ANG II) vascular smooth muscle cells (VSMC) growth. [A] Aortic VSMC from Wistar rats treated with ANG II and/or DABK at low concentration (0.1 nM) in the presence or not of losartan (LOS – 10 µM), des-arg9-leu8-bradykinin (DAL – 10 µM) and TIRON (1 mM). Bar graph shows PCNA expression normalized against the housekeeping protein β-actin. Results are represented as mean±SEM of 4 experiments. *P
Figure Legend Snippet: Effects of des-Arg 9 -bradykinin (DABK) and angiotensin II (ANG II) vascular smooth muscle cells (VSMC) growth. [A] Aortic VSMC from Wistar rats treated with ANG II and/or DABK at low concentration (0.1 nM) in the presence or not of losartan (LOS – 10 µM), des-arg9-leu8-bradykinin (DAL – 10 µM) and TIRON (1 mM). Bar graph shows PCNA expression normalized against the housekeeping protein β-actin. Results are represented as mean±SEM of 4 experiments. *P

Techniques Used: Concentration Assay, Expressing

2) Product Images from "Inhibition of Intestinal Adenoma Formation in APCMin/+ Mice by Riccardin D, a Natural Product Derived from Liverwort Plant Dumortiera hirsuta"

Article Title: Inhibition of Intestinal Adenoma Formation in APCMin/+ Mice by Riccardin D, a Natural Product Derived from Liverwort Plant Dumortiera hirsuta

Journal: PLoS ONE

doi: 10.1371/journal.pone.0033243

Riccardin D decreased expression of β-catenin and cyclin D1 in intestinal polyps. Intestinal sections were processed for β-catenin and cyclin D1 immunohistochemistry staining. Intestinal sections of control and Riccardin D-treated mice showed brown-colored PCNA-positive (A) and cyclin D1-positive cells (B) in polyps on small intestines and colons (400×). Bar represents the mean ± S.D of six animals. *, p
Figure Legend Snippet: Riccardin D decreased expression of β-catenin and cyclin D1 in intestinal polyps. Intestinal sections were processed for β-catenin and cyclin D1 immunohistochemistry staining. Intestinal sections of control and Riccardin D-treated mice showed brown-colored PCNA-positive (A) and cyclin D1-positive cells (B) in polyps on small intestines and colons (400×). Bar represents the mean ± S.D of six animals. *, p

Techniques Used: Expressing, Immunohistochemistry, Staining, Mouse Assay

3) Product Images from "MEF2D Deficiency in Neonatal Cardiomyocytes Triggers Cell Cycle Re-entry and Programmed Cell Death in Vitro *"

Article Title: MEF2D Deficiency in Neonatal Cardiomyocytes Triggers Cell Cycle Re-entry and Programmed Cell Death in Vitro *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M115.666461

Microarray validation in NRVMs. A , summary of a subset of cell cycle genes dysregulated by 1.5-fold or more in MEF2D depleted NRVMs. The majority of the positive cell cycle genes are up-regulated. Cdt1 , chromatin licensing and DNA replication factor 1; Ccne1 , cyclin E1; Ccne2 , cyclin E2; Mcm3 , minichromosome maintenance complex component 3; Mcm5 , minichromosome maintenance complex component 5; Mcm5 , minichromosome maintenance complex component 6. B , quantitative RT-PCR analysis of cell cycle regulatory genes dysregulated in MEF2D-depleted NRVMs at day 3. Pcna , proliferating cell nuclear antigen. C , Western blot analysis of cell cycle-associated proteins cyclin D1, cyclin D3, and cyclin-dependent kinase 2 ( CDK2 ). D , Western blot densitometry. The data are means ± S.E. ( error bars ). *, p
Figure Legend Snippet: Microarray validation in NRVMs. A , summary of a subset of cell cycle genes dysregulated by 1.5-fold or more in MEF2D depleted NRVMs. The majority of the positive cell cycle genes are up-regulated. Cdt1 , chromatin licensing and DNA replication factor 1; Ccne1 , cyclin E1; Ccne2 , cyclin E2; Mcm3 , minichromosome maintenance complex component 3; Mcm5 , minichromosome maintenance complex component 5; Mcm5 , minichromosome maintenance complex component 6. B , quantitative RT-PCR analysis of cell cycle regulatory genes dysregulated in MEF2D-depleted NRVMs at day 3. Pcna , proliferating cell nuclear antigen. C , Western blot analysis of cell cycle-associated proteins cyclin D1, cyclin D3, and cyclin-dependent kinase 2 ( CDK2 ). D , Western blot densitometry. The data are means ± S.E. ( error bars ). *, p

Techniques Used: Microarray, Quantitative RT-PCR, Western Blot

PI3K/Akt inhibition rescues apoptotic cell death associated with MEF2D depletion. A , summary of apoptosis-associated genes dysregulated by 1.5-fold or more in MEF2D-depleted NRVMs. B , quantitative RT-PCR analysis of the activating E2Fs, E2f1 , E2f2 , and E2f3 , revealed that MEF2D deficiency results in their increased expression. C , two pro-apoptotic transcriptional targets of E2F, Apaf1 and Casp8 , are significantly up-regulated in MEF2D depleted NRVMs. Up-regulation of E2f1 , E2f2 , and E2f3 transcript levels ( D ) and the E2F pro-apoptotic targets Apaf1 and Casp8 ( E ) is abolished when PI3K/Akt activation is inhibited by the addition of GDC-0941 in MEF2D-depleted NRVMs. F , TUNEL assay of NRVMs treated with GDC-0941 demonstrates an abrogation of apoptosis observed in MEF2D-deficient NRVMs 5 days post-transduction. G , post-natal cardiomyocytes are terminally differentiated and are unable to re-enter the cell cycle. MEF2D depletion results in an up-regulation of Mcm3 , Mcm5 , Mcm6 , Pcna , Ccne1 , and Ccne2 and aberrant cell cycle re-entry. E2F transcription factors likely sense unprogrammed cell cycle activation and mediate cardiomyocyte apoptosis by transcriptionally activating pro-apoptotic genes Apaf1 and Casp8. Apaf1 , apoptotic peptidase-activating factor 1; Casp8 , caspase-8. The data are means ± S.E. ( error bars ). *, p
Figure Legend Snippet: PI3K/Akt inhibition rescues apoptotic cell death associated with MEF2D depletion. A , summary of apoptosis-associated genes dysregulated by 1.5-fold or more in MEF2D-depleted NRVMs. B , quantitative RT-PCR analysis of the activating E2Fs, E2f1 , E2f2 , and E2f3 , revealed that MEF2D deficiency results in their increased expression. C , two pro-apoptotic transcriptional targets of E2F, Apaf1 and Casp8 , are significantly up-regulated in MEF2D depleted NRVMs. Up-regulation of E2f1 , E2f2 , and E2f3 transcript levels ( D ) and the E2F pro-apoptotic targets Apaf1 and Casp8 ( E ) is abolished when PI3K/Akt activation is inhibited by the addition of GDC-0941 in MEF2D-depleted NRVMs. F , TUNEL assay of NRVMs treated with GDC-0941 demonstrates an abrogation of apoptosis observed in MEF2D-deficient NRVMs 5 days post-transduction. G , post-natal cardiomyocytes are terminally differentiated and are unable to re-enter the cell cycle. MEF2D depletion results in an up-regulation of Mcm3 , Mcm5 , Mcm6 , Pcna , Ccne1 , and Ccne2 and aberrant cell cycle re-entry. E2F transcription factors likely sense unprogrammed cell cycle activation and mediate cardiomyocyte apoptosis by transcriptionally activating pro-apoptotic genes Apaf1 and Casp8. Apaf1 , apoptotic peptidase-activating factor 1; Casp8 , caspase-8. The data are means ± S.E. ( error bars ). *, p

Techniques Used: Inhibition, Quantitative RT-PCR, Expressing, Activation Assay, TUNEL Assay, Transduction

4) Product Images from "OCT4 maintains self-renewal and reverses senescence in human hair follicle mesenchymal stem cells through the downregulation of p21 by DNA methyltransferases"

Article Title: OCT4 maintains self-renewal and reverses senescence in human hair follicle mesenchymal stem cells through the downregulation of p21 by DNA methyltransferases

Journal: Stem Cell Research & Therapy

doi: 10.1186/s13287-018-1120-x

DNMT inhibition decreased OCT4-increased proliferation capacity and differentiation potential in hHFMSCs. a The impact of 5-aza-dC (100 μM, 72 h) and zebularine (100 μM, 48 h) treatment on the expression of DNMTs, p21, OCT4, PCNA, and cyclin D1. b Immunofluorescence of proliferation-associated protein Ki67 (left panels) and OCT4 (right panels) expression and location after DNMT inhibition (bar, 50 μm). c MSP of p21 in hHFMSCs OCT4 treated with DMSO, 5-aza-dC, or zebularine. Cell proliferation curve ( d ) and clone formation assay ( e ) after DNMT inhibition; and the enlarged views showed the difference between DMSO and DNMT inhibitor-treated hHFMSCs OCT4 . The histogram is the formation rate of the three clones. f Effects of DNMT inhibition on hHFMSC cell cycle phase distribution. The percentage of the G1, G2, and S phases in the cell cycle (left of the lower panel) and the PI (right of the lower panel) after DNMT inhibition. “dip” is the abbreviation for diploid. g Osteogenic differentiation after DNMT inhibition. Calcium nodules were detected by Alizarin Red S staining (bar, 50 μm). (* p
Figure Legend Snippet: DNMT inhibition decreased OCT4-increased proliferation capacity and differentiation potential in hHFMSCs. a The impact of 5-aza-dC (100 μM, 72 h) and zebularine (100 μM, 48 h) treatment on the expression of DNMTs, p21, OCT4, PCNA, and cyclin D1. b Immunofluorescence of proliferation-associated protein Ki67 (left panels) and OCT4 (right panels) expression and location after DNMT inhibition (bar, 50 μm). c MSP of p21 in hHFMSCs OCT4 treated with DMSO, 5-aza-dC, or zebularine. Cell proliferation curve ( d ) and clone formation assay ( e ) after DNMT inhibition; and the enlarged views showed the difference between DMSO and DNMT inhibitor-treated hHFMSCs OCT4 . The histogram is the formation rate of the three clones. f Effects of DNMT inhibition on hHFMSC cell cycle phase distribution. The percentage of the G1, G2, and S phases in the cell cycle (left of the lower panel) and the PI (right of the lower panel) after DNMT inhibition. “dip” is the abbreviation for diploid. g Osteogenic differentiation after DNMT inhibition. Calcium nodules were detected by Alizarin Red S staining (bar, 50 μm). (* p

Techniques Used: Inhibition, Expressing, Immunofluorescence, Tube Formation Assay, Clone Assay, Staining

OCT4 increased proliferation capacity and differentiation potential in hHFMSCs. Cell proliferation curve ( a ) and cell population doubling time ( b ) of hHFMSCs EGFP and hHFMSCs OCT4 . c Clone formation assay of hHFMSCs EGFP and hHFMSCs OCT4 ; the enlarged views show the difference between the two cell clones. The histogram is the formation rate for each clone (bar, 200 μm). d Representative sphere images and bar graph of the percentages of spheres in hHFMSCs EGFP and hHFMSCs OCT . e Western blot results for the expression of proliferation-associated proteins PCNA and cyclin D1 in hHFMSCs EGFP and hHFMSCs OCT4 . f Immunofluorescence of proliferation-associated protein Ki67 expression and location in hHFMSCs EGFP and hHFMSCs OCT4 (bar, 50 μm). g Effects of OCT4 on hHFMSC cell cycle phase distribution. The percentage of the G1, G2, and S phase in the cell cycle (left of the lower panel) and the PI (right of the lower panel) of the hHFMSCs EGFP and hHFMSCs OCT4 . “dip” is the abbreviation for diploid. h Osteogenic differentiation in hHFMSCs EGFP and hHFMSCs OCT4 . Calcium nodules were detected by Alizarin Red S staining (bar, 200 μm). (* p
Figure Legend Snippet: OCT4 increased proliferation capacity and differentiation potential in hHFMSCs. Cell proliferation curve ( a ) and cell population doubling time ( b ) of hHFMSCs EGFP and hHFMSCs OCT4 . c Clone formation assay of hHFMSCs EGFP and hHFMSCs OCT4 ; the enlarged views show the difference between the two cell clones. The histogram is the formation rate for each clone (bar, 200 μm). d Representative sphere images and bar graph of the percentages of spheres in hHFMSCs EGFP and hHFMSCs OCT . e Western blot results for the expression of proliferation-associated proteins PCNA and cyclin D1 in hHFMSCs EGFP and hHFMSCs OCT4 . f Immunofluorescence of proliferation-associated protein Ki67 expression and location in hHFMSCs EGFP and hHFMSCs OCT4 (bar, 50 μm). g Effects of OCT4 on hHFMSC cell cycle phase distribution. The percentage of the G1, G2, and S phase in the cell cycle (left of the lower panel) and the PI (right of the lower panel) of the hHFMSCs EGFP and hHFMSCs OCT4 . “dip” is the abbreviation for diploid. h Osteogenic differentiation in hHFMSCs EGFP and hHFMSCs OCT4 . Calcium nodules were detected by Alizarin Red S staining (bar, 200 μm). (* p

Techniques Used: Tube Formation Assay, Clone Assay, Western Blot, Expressing, Immunofluorescence, Staining

5) Product Images from "Herbal composition of Cinnamomum cassia, Pinus densiflora, Curcuma longa and Glycyrrhiza glabra prevents atherosclerosis by upregulating p27 (Kip1) expression"

Article Title: Herbal composition of Cinnamomum cassia, Pinus densiflora, Curcuma longa and Glycyrrhiza glabra prevents atherosclerosis by upregulating p27 (Kip1) expression

Journal: BMC Complementary and Alternative Medicine

doi: 10.1186/s12906-016-1224-8

Effect of cinnamon extract on cell cycle progression and cell cycle-related proteins. VSMCs cultured in serum-starved medium were stimulated with 25 ng/mL PDGF-BB and the effect in the presence of Kiom-18 extract (5–50 μg/ml) on the DNA synthesis ( a ) and the histogram data ( b ) for each phase of the cell cycle is shown. The cell cycle progression data are representative of three independent experiments. Moreover, the effect of Kiom-18 extract on cell cycle regulatory proteins stimulated by PDGF-BB, including cyclin D1/E1, CDK2/4, Rb, and PCNA as negative regulatory molecules ( c ), was measured using SDS-PAGE followed by immunoblotting. Total β-actin was used for normalization. These results were analyzed using densitometry; the values represent the percentage of the control stimulated by PDGF-BB. All values are expressed as the mean ± SEM ( n = 3). Significant differences from the PDGF control (PDGF-stimulated) are shown by * p
Figure Legend Snippet: Effect of cinnamon extract on cell cycle progression and cell cycle-related proteins. VSMCs cultured in serum-starved medium were stimulated with 25 ng/mL PDGF-BB and the effect in the presence of Kiom-18 extract (5–50 μg/ml) on the DNA synthesis ( a ) and the histogram data ( b ) for each phase of the cell cycle is shown. The cell cycle progression data are representative of three independent experiments. Moreover, the effect of Kiom-18 extract on cell cycle regulatory proteins stimulated by PDGF-BB, including cyclin D1/E1, CDK2/4, Rb, and PCNA as negative regulatory molecules ( c ), was measured using SDS-PAGE followed by immunoblotting. Total β-actin was used for normalization. These results were analyzed using densitometry; the values represent the percentage of the control stimulated by PDGF-BB. All values are expressed as the mean ± SEM ( n = 3). Significant differences from the PDGF control (PDGF-stimulated) are shown by * p

Techniques Used: Cell Culture, DNA Synthesis, SDS Page

6) Product Images from "Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation"

Article Title: Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation

Journal: Oncotarget

doi: 10.18632/oncotarget.16279

Effects of macrophage depletion with clodronate liposomes on transplantation-induced arterial remodeling and inflammation ( A ) Time course of early adventitial macrophage infiltration and subsequent neointimal hyperplasia revealed by hematoxylin and eosin (H E) staining and immunohistochemistry. Macrophages were stained with anti-CD68; T cells stained with anti-CD3; and proliferating cells stained with anti-PCNA. ( B ) Histology images showing that macrophage depletion inhibited the growth of neointima, diminished infiltrating macrophages in the adventitia, reduced the number of PCNA + cells, and reduced inflammatory responses (samples of day 14). ( C ) Effects of clodronate on the expression levels of various inflammatory molecules measured with qPCR. ( D ) Proportion of smooth muscle cells (stained with anti-a-SM actin, indicated by arrows) and non-muscle cells (arrowheads) in the neointima of untreated and clodronate-treated vessels. Data are mean ± SD. * P
Figure Legend Snippet: Effects of macrophage depletion with clodronate liposomes on transplantation-induced arterial remodeling and inflammation ( A ) Time course of early adventitial macrophage infiltration and subsequent neointimal hyperplasia revealed by hematoxylin and eosin (H E) staining and immunohistochemistry. Macrophages were stained with anti-CD68; T cells stained with anti-CD3; and proliferating cells stained with anti-PCNA. ( B ) Histology images showing that macrophage depletion inhibited the growth of neointima, diminished infiltrating macrophages in the adventitia, reduced the number of PCNA + cells, and reduced inflammatory responses (samples of day 14). ( C ) Effects of clodronate on the expression levels of various inflammatory molecules measured with qPCR. ( D ) Proportion of smooth muscle cells (stained with anti-a-SM actin, indicated by arrows) and non-muscle cells (arrowheads) in the neointima of untreated and clodronate-treated vessels. Data are mean ± SD. * P

Techniques Used: Transplantation Assay, Staining, Immunohistochemistry, Expressing, Real-time Polymerase Chain Reaction

7) Product Images from "Epigenetic reactivation of estrogen receptor-? (ER?) by genistein enhances hormonal therapy sensitivity in ER?-negative breast cancer"

Article Title: Epigenetic reactivation of estrogen receptor-? (ER?) by genistein enhances hormonal therapy sensitivity in ER?-negative breast cancer

Journal: Molecular Cancer

doi: 10.1186/1476-4598-12-9

GE and TAM inhibited the expression of PCNA and increased ERα expression in vivo . Immunohistochemical analysis was performed in tumor samples to detect PCNA-positive cells for proliferation index (left panel) and ERα in vivo expression (right panel). A ) and B ) PCNA and ERα expression in MDA-MB-231 tumor xenogratfs ( Protocol 1). C ) and D ) PCNA and ERα expression in C3(1)-SV40 Tag transgenic mice tumors ( Protocol 2). Immunohistochemical data in terms of percentage of positive cells are presented as mean ± SD from each group. PCNA-positive and ERα-positive cells were counted in 5 different areas of the sections, and data are summarized in terms of percent positive cells from all tumor samples. Representative photograph from one field of each experimental group. Columns, mean; Bars, SD from 5 or 10 mice per group; *, p
Figure Legend Snippet: GE and TAM inhibited the expression of PCNA and increased ERα expression in vivo . Immunohistochemical analysis was performed in tumor samples to detect PCNA-positive cells for proliferation index (left panel) and ERα in vivo expression (right panel). A ) and B ) PCNA and ERα expression in MDA-MB-231 tumor xenogratfs ( Protocol 1). C ) and D ) PCNA and ERα expression in C3(1)-SV40 Tag transgenic mice tumors ( Protocol 2). Immunohistochemical data in terms of percentage of positive cells are presented as mean ± SD from each group. PCNA-positive and ERα-positive cells were counted in 5 different areas of the sections, and data are summarized in terms of percent positive cells from all tumor samples. Representative photograph from one field of each experimental group. Columns, mean; Bars, SD from 5 or 10 mice per group; *, p

Techniques Used: Expressing, In Vivo, Immunohistochemistry, Multiple Displacement Amplification, Transgenic Assay, Mouse Assay

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Incubation:

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Article Snippet: .. Protein samples (20 μg) were separated on NuPage® Novex® 4%–12% Bis-Tris gels (Life Technologies, Carlsbad, CA, USA), then transferred to PVDF membranes (Rockford, IL, USA), which were blocked with non-fat milk and incubated with primary antibodies (OXPHOS complexes; 1:2500, Abcam, Cambridge, UK), Drp-1 (1:2000, Novus Biotechnology, Littleton, CO, USA), Opa-1 (1:2000, Novus Biotechnology, Littleton, CO, USA), LC3A/B (1:2000, Cell Signaling Technology, Danvers, MA, USA), Tom-20 (1:2000, Santa Cruz Biotechnology, Dallas, TX, USA) and MnSOD (1:2000, Millipore, Billerica, MA, USA), Pink-1 (1:1000, BioVision Incorporated, Milpitas, CA, USA), Fis-1 (1:500, Santa Cruz Biotechnology, Dallas, TX, USA) and Parkin (1:500, Cell Signaling Technology, Danvers, MA, USA) for overnight. .. Membranes were then incubated in secondary antibodies (goat anti-rabbit or rabbit anti-mouse IgG horseradish peroxidase-conjugated secondary antibodies, 1:5000 for OPA-1, MnSOD, Tom-20, OXPHOS complexes; 1:2000 for Drp-1, Pink-1, LC3A/B; 1:500 for Parkin; Santa Cruz Biotechnology, Dallas, TX, USA) for 1 h. Protein expression was detected by SuperSignal West Pico Chemiluminescent substrate (Thermo, Waltham, MA, USA) and Fujifilm LAS-3000 (Fujifilm, Tokyo, Japan).

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    Cell Signaling Technology Inc anti pcna
    4SC‐202 inhibits HH/GLI signaling in SMOi‐resistant cancer cells. ( a ) Western blot analysis of GLI1 expression in cells with lentiviral shRNA‐mediated knockdown of SUFU (shSUFU) or control knockdown (shControl). Beta Actin served as loading control. ( b ) qPCR analysis of GLI1 mRNA expression in SUFU knockdown (shSUFU) and control cells (shControl) transduced with lentiviral nontargeting scrambled shRNA. ( c and d ) qPCR analysis of GLI1 ( c ) and HHIP mRNA expression ( d ) as readout for HH/GLI signaling activity in SUFU‐depleted SMOi‐resistant cells showing resistance to vismodegib but sensitivity to 4SC‐202 treatment. ( e ) Western blot analysis of SUFU‐depleted Daoy cells treated with vismodegib or 4SC‐202 at the concentrations indicated. β‐Tubulin served as loading control. Vismodegib was unable to reduce GLI1 protein levels, while 4SC‐202 treatment effectively abolished GLI1 protein expression. ( f ) Relative densitometric quantification of GLI1/β‐Tubulin protein levels shown in ( e ). ( g ) ChIP analysis of MYC‐tagged GLI1 binding to the GLI target promoter PTCH in response to control or 4SC‐202 treatment. Enrichment of GLI1 bound promoter DNA was measured by qPCR. IgG isotype antibody was used as control. ( h ) Murine BCC cells were subcutaneously injected into dorsal flanks of 12 NSG mice. 4SC‐202 was administered by oral gavage at 80 mg/kg/day. The tumor volume at day 0 (i.e., start of drug treatment (arrow)) was set to 100%. ( i ) Western blot analysis of solvent (allografts #1–#4) and 4SC‐202 treated (allografts #5–#8) BCC lysates probed for proliferation‐cell‐nuclear‐antigen <t>(Pcna)</t> and Ccnd1 expression. <t>Erk1/2</t> expression served as loading control. ( j ) Analysis of in vitro cell proliferation of murine BCC cells in response to 4SC‐202 and entinostat treatment. ChIP: chromatin immunoprecipitation. ** p
    Anti Pcna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 73 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti pcna/product/Cell Signaling Technology Inc
    Average 93 stars, based on 73 article reviews
    Price from $9.99 to $1999.99
    anti pcna - by Bioz Stars, 2020-07
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    Cell Signaling Technology Inc anti proliferating cell nuclear antigen pcna antibodies
    Activation of NF-κB in the gingiva from insulin-resistant obese rodents. (A) Representative immunoblots of NF-κB <t>(p65)</t> from gingival nuclear proteins from Zucker rats. (B) Data from 3 experiments were normalized with <t>PCNA</t> and actin and quantified by densitometry. The p65 subunit of NF-κB was increased significantly in ZF rats. The data are expressed as mean ± SD. ZL vs . ZF, n = 6.* p
    Anti Proliferating Cell Nuclear Antigen Pcna Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti proliferating cell nuclear antigen pcna antibodies/product/Cell Signaling Technology Inc
    Average 88 stars, based on 9 article reviews
    Price from $9.99 to $1999.99
    anti proliferating cell nuclear antigen pcna antibodies - by Bioz Stars, 2020-07
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    4SC‐202 inhibits HH/GLI signaling in SMOi‐resistant cancer cells. ( a ) Western blot analysis of GLI1 expression in cells with lentiviral shRNA‐mediated knockdown of SUFU (shSUFU) or control knockdown (shControl). Beta Actin served as loading control. ( b ) qPCR analysis of GLI1 mRNA expression in SUFU knockdown (shSUFU) and control cells (shControl) transduced with lentiviral nontargeting scrambled shRNA. ( c and d ) qPCR analysis of GLI1 ( c ) and HHIP mRNA expression ( d ) as readout for HH/GLI signaling activity in SUFU‐depleted SMOi‐resistant cells showing resistance to vismodegib but sensitivity to 4SC‐202 treatment. ( e ) Western blot analysis of SUFU‐depleted Daoy cells treated with vismodegib or 4SC‐202 at the concentrations indicated. β‐Tubulin served as loading control. Vismodegib was unable to reduce GLI1 protein levels, while 4SC‐202 treatment effectively abolished GLI1 protein expression. ( f ) Relative densitometric quantification of GLI1/β‐Tubulin protein levels shown in ( e ). ( g ) ChIP analysis of MYC‐tagged GLI1 binding to the GLI target promoter PTCH in response to control or 4SC‐202 treatment. Enrichment of GLI1 bound promoter DNA was measured by qPCR. IgG isotype antibody was used as control. ( h ) Murine BCC cells were subcutaneously injected into dorsal flanks of 12 NSG mice. 4SC‐202 was administered by oral gavage at 80 mg/kg/day. The tumor volume at day 0 (i.e., start of drug treatment (arrow)) was set to 100%. ( i ) Western blot analysis of solvent (allografts #1–#4) and 4SC‐202 treated (allografts #5–#8) BCC lysates probed for proliferation‐cell‐nuclear‐antigen (Pcna) and Ccnd1 expression. Erk1/2 expression served as loading control. ( j ) Analysis of in vitro cell proliferation of murine BCC cells in response to 4SC‐202 and entinostat treatment. ChIP: chromatin immunoprecipitation. ** p

    Journal: International Journal of Cancer

    Article Title: Targeting class I histone deacetylases by the novel small molecule inhibitor 4 SC‐202 blocks oncogenic hedgehog‐ GLI signaling and overcomes smoothened inhibitor resistance

    doi: 10.1002/ijc.31117

    Figure Lengend Snippet: 4SC‐202 inhibits HH/GLI signaling in SMOi‐resistant cancer cells. ( a ) Western blot analysis of GLI1 expression in cells with lentiviral shRNA‐mediated knockdown of SUFU (shSUFU) or control knockdown (shControl). Beta Actin served as loading control. ( b ) qPCR analysis of GLI1 mRNA expression in SUFU knockdown (shSUFU) and control cells (shControl) transduced with lentiviral nontargeting scrambled shRNA. ( c and d ) qPCR analysis of GLI1 ( c ) and HHIP mRNA expression ( d ) as readout for HH/GLI signaling activity in SUFU‐depleted SMOi‐resistant cells showing resistance to vismodegib but sensitivity to 4SC‐202 treatment. ( e ) Western blot analysis of SUFU‐depleted Daoy cells treated with vismodegib or 4SC‐202 at the concentrations indicated. β‐Tubulin served as loading control. Vismodegib was unable to reduce GLI1 protein levels, while 4SC‐202 treatment effectively abolished GLI1 protein expression. ( f ) Relative densitometric quantification of GLI1/β‐Tubulin protein levels shown in ( e ). ( g ) ChIP analysis of MYC‐tagged GLI1 binding to the GLI target promoter PTCH in response to control or 4SC‐202 treatment. Enrichment of GLI1 bound promoter DNA was measured by qPCR. IgG isotype antibody was used as control. ( h ) Murine BCC cells were subcutaneously injected into dorsal flanks of 12 NSG mice. 4SC‐202 was administered by oral gavage at 80 mg/kg/day. The tumor volume at day 0 (i.e., start of drug treatment (arrow)) was set to 100%. ( i ) Western blot analysis of solvent (allografts #1–#4) and 4SC‐202 treated (allografts #5–#8) BCC lysates probed for proliferation‐cell‐nuclear‐antigen (Pcna) and Ccnd1 expression. Erk1/2 expression served as loading control. ( j ) Analysis of in vitro cell proliferation of murine BCC cells in response to 4SC‐202 and entinostat treatment. ChIP: chromatin immunoprecipitation. ** p

    Article Snippet: Western blot analysis, chromatin immunoprecipitation (ChIP) and immunohistochemistry For protein detection by Western blot analysis, the following primary antibodies were applied: anti‐GLI1 (V812), anti‐Beta Actin (D6A8), anti‐HDAC1 (D5C6U), anti‐HDAC2 (D6S5P), anti‐HDAC3 (7G6C5), anti‐p44/42 MAPK (Erk1/2), anti‐PCNA (D3H8P), anti‐Cyclin D1 (92G2), anti‐β‐Tubulin (9F3, all Cell Signaling) and anti‐SUFU (sc‐10933, Santa Cruz Biotechnology).

    Techniques: Western Blot, Expressing, shRNA, Real-time Polymerase Chain Reaction, Transduction, Activity Assay, Chromatin Immunoprecipitation, Binding Assay, Injection, Mouse Assay, In Vitro

    miR-16-2-3p regulates the PDPK1/Akt signaling pathway in MPMCs. At 72 h after transfection with (A) pre16-2-3p/preNC or (B) si16-2-3p/siNC, MPMCs were subjected to western blot analysis to detect PDPK1, p-Akt, total Akt and PCNA expression. Independent experiments were repeated at least 3 times. miR, microRNA; PDPK1, 3-phosphoinositide-dependent protein kinase-1; Akt, protein kinase B; MPMC, maxillary primordium mesenchymal cells; pre16-2-3p, precursor miR-16-2-3p; preNC, precursor negative control; si, small interfering; NC, negative control; p, phosphorylated; PCNA, proliferating cell nuclear antigen.

    Journal: International Journal of Molecular Medicine

    Article Title: miR-16-2-3p inhibits cell proliferation and migration and induces apoptosis by targeting PDPK1 in maxillary primordium mesenchymal cells

    doi: 10.3892/ijmm.2019.4070

    Figure Lengend Snippet: miR-16-2-3p regulates the PDPK1/Akt signaling pathway in MPMCs. At 72 h after transfection with (A) pre16-2-3p/preNC or (B) si16-2-3p/siNC, MPMCs were subjected to western blot analysis to detect PDPK1, p-Akt, total Akt and PCNA expression. Independent experiments were repeated at least 3 times. miR, microRNA; PDPK1, 3-phosphoinositide-dependent protein kinase-1; Akt, protein kinase B; MPMC, maxillary primordium mesenchymal cells; pre16-2-3p, precursor miR-16-2-3p; preNC, precursor negative control; si, small interfering; NC, negative control; p, phosphorylated; PCNA, proliferating cell nuclear antigen.

    Article Snippet: Following blocking of nonspecific binding with 5% non-fat milk in TBS containing 0.1% Tween-20 (TBS-T) at 25°C for 1 h, the membranes were incubated with the following primary antibodies: Anti-PDPK1 (cat. no. 3062; 1:1,000; Cell Signaling Technology, Inc., Danvers, MA, USA), anti-phosphorylated protein kinase B (p-Akt; cat. no. 2965S; 1:1000; Cell Signaling Technology, Inc.), anti-proliferating cell nuclear antigen (PCNA; cat. no. 2586S; 1:1,000; Cell Signaling Technology, MA, USA), anti-cleaved caspase-3 (cat. no. 9660; 1:1,000; Cell Signaling Technology, Inc.), anti-matrix metalloproteinase-9 (MMP-9; cat. no. 10375-2-AP; 1:2,000; Proteintech Group, Wuhan, China), anti-MMP-2 (cat. no. 10373-2-AP; 1:2,000; Proteintech Group), and anti-β-actin (cat. no. 10230-1-AP; 1:2,000; Proteintech Group).

    Techniques: Transfection, Western Blot, Expressing, Negative Control

    Activation of NF-κB in the gingiva from insulin-resistant obese rodents. (A) Representative immunoblots of NF-κB (p65) from gingival nuclear proteins from Zucker rats. (B) Data from 3 experiments were normalized with PCNA and actin and quantified by densitometry. The p65 subunit of NF-κB was increased significantly in ZF rats. The data are expressed as mean ± SD. ZL vs . ZF, n = 6.* p

    Journal: Journal of Dental Research

    Article Title: Obesity-associated Gingival Vascular Inflammation and Insulin Resistance

    doi: 10.1177/0022034514532102

    Figure Lengend Snippet: Activation of NF-κB in the gingiva from insulin-resistant obese rodents. (A) Representative immunoblots of NF-κB (p65) from gingival nuclear proteins from Zucker rats. (B) Data from 3 experiments were normalized with PCNA and actin and quantified by densitometry. The p65 subunit of NF-κB was increased significantly in ZF rats. The data are expressed as mean ± SD. ZL vs . ZF, n = 6.* p

    Article Snippet: Immunoblotting was performed with anti-NF-κB (p65) (1:1,000 dilution; Santa Cruz Biotechnology, Inc.) and anti-proliferating cell nuclear antigen (PCNA) antibodies (1:1,000 dilution; Cell Signaling Technology).

    Techniques: Activation Assay, Western Blot

    Effects of des-Arg 9 -bradykinin (DABK) and angiotensin II (ANG II) vascular smooth muscle cells (VSMC) growth. [A] Aortic VSMC from Wistar rats treated with ANG II and/or DABK at low concentration (0.1 nM) in the presence or not of losartan (LOS – 10 µM), des-arg9-leu8-bradykinin (DAL – 10 µM) and TIRON (1 mM). Bar graph shows PCNA expression normalized against the housekeeping protein β-actin. Results are represented as mean±SEM of 4 experiments. *P

    Journal: PLoS ONE

    Article Title: An Interaction of Renin-Angiotensin and Kallikrein-Kinin Systems Contributes to Vascular Hypertrophy in Angiotensin II-Induced Hypertension: In Vivo and In Vitro Studies

    doi: 10.1371/journal.pone.0111117

    Figure Lengend Snippet: Effects of des-Arg 9 -bradykinin (DABK) and angiotensin II (ANG II) vascular smooth muscle cells (VSMC) growth. [A] Aortic VSMC from Wistar rats treated with ANG II and/or DABK at low concentration (0.1 nM) in the presence or not of losartan (LOS – 10 µM), des-arg9-leu8-bradykinin (DAL – 10 µM) and TIRON (1 mM). Bar graph shows PCNA expression normalized against the housekeeping protein β-actin. Results are represented as mean±SEM of 4 experiments. *P

    Article Snippet: In other series of experiments membranes from VSMC were then incubated with anti-B1R (1∶1000) (Santa Cruz Biotechnology, Santa Cruz, California, USA) or anti-proliferating-cell nuclear antigen (PCNA) (Cell Signaling) and also anti-β-actin (Santa Cruz Biotechnology, Santa Cruz, California, USA) at 4°C. β-actin was used as a housekeeping protein.

    Techniques: Concentration Assay, Expressing