Structured Review

Abcam mouse anti beta actin
GCL and GAGE proteins are co-expressed in human cancer cells lines. GCL and GAGE protein expression was examined in 9 human cancer cells lines derived from cervix (HeLa), colon (HCT116), melanoma (MZ2-MEL), breast (BrCa-MZ01, SK-BR3, T47D, M4A4, MCF7) and embryonic cancer (NTERA2) using Western blotting. A375 melanoma cells with exogenous expression of GCL were included as positive control. Antibodies: GCL pAb1, Sigma Aldrich; GCL pAb2, clone A14, Santa Cruz Biotech; GAGE mAb, clone M3 [4] , <t>beta-actin</t> mAb, Ab6276; Abcam.
Mouse Anti Beta Actin, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti beta actin - by Bioz Stars, 2020-09
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1) Product Images from "GAGE Cancer-Germline Antigens Are Recruited to the Nuclear Envelope by Germ Cell-Less (GCL)"

Article Title: GAGE Cancer-Germline Antigens Are Recruited to the Nuclear Envelope by Germ Cell-Less (GCL)

Journal: PLoS ONE

doi: 10.1371/journal.pone.0045819

GCL and GAGE proteins are co-expressed in human cancer cells lines. GCL and GAGE protein expression was examined in 9 human cancer cells lines derived from cervix (HeLa), colon (HCT116), melanoma (MZ2-MEL), breast (BrCa-MZ01, SK-BR3, T47D, M4A4, MCF7) and embryonic cancer (NTERA2) using Western blotting. A375 melanoma cells with exogenous expression of GCL were included as positive control. Antibodies: GCL pAb1, Sigma Aldrich; GCL pAb2, clone A14, Santa Cruz Biotech; GAGE mAb, clone M3 [4] , beta-actin mAb, Ab6276; Abcam.
Figure Legend Snippet: GCL and GAGE proteins are co-expressed in human cancer cells lines. GCL and GAGE protein expression was examined in 9 human cancer cells lines derived from cervix (HeLa), colon (HCT116), melanoma (MZ2-MEL), breast (BrCa-MZ01, SK-BR3, T47D, M4A4, MCF7) and embryonic cancer (NTERA2) using Western blotting. A375 melanoma cells with exogenous expression of GCL were included as positive control. Antibodies: GCL pAb1, Sigma Aldrich; GCL pAb2, clone A14, Santa Cruz Biotech; GAGE mAb, clone M3 [4] , beta-actin mAb, Ab6276; Abcam.

Techniques Used: Expressing, Derivative Assay, Western Blot, Positive Control

2) Product Images from "Alteration of actin dependent signaling pathways associated with membrane microdomains in hyperlipidemia"

Article Title: Alteration of actin dependent signaling pathways associated with membrane microdomains in hyperlipidemia

Journal: Proteome Science

doi: 10.1186/s12953-015-0087-0

Actin dependent signal transduction pathways of identified and quantified detergent resistant membrane microdomains proteins. The interaction map comprises the currently discussed mass spectrometric identified proteins (red bordered boxes) and differentially expressed proteins (green filled red bordered boxes) and were integrated in the over-represented Regulation of actin cytoskeleton , Focal adhesion and Adherens junction signaling pathways. The complex signaling network represents the combination of map04810 , map 04510 and map 04520 KEGG signaling pathways. Abbreviations for the discussed proteins: Ras: Ras-related protein R-Ras; MEK: mitogen-activated protein kinase kinase 1; F2RCD14: coagulation factor II, CD14 antigen; DOCK180: dedicator of cytokinesis protein; VWF: von Willebrand factor; Cav: caveolin; Gβγ: Guanine nucleotide-binding protein G(I)/G(S)/G(O) subunit gamma-12; Arp2/3: Actin-related protein 2/3 complex subunit 1B and 3; PIR121: Cytoplasmic FMR1-interacting protein 1; PFN: profilin; CFN: Cofilin-1; ZYX: Zyxin; MLC: Myosin regulatory light polypeptide 9; MLCK: Myosin light chain kinase 2; mDia: Protein diaphanous homolog 1; ACTN: actinin: VCL: vinculin; TLN: talin; ITG: integrin; Rap-1: Ras-related protein Rap-1A; Rac: Ras-related C3 botulinum toxin substrate 1; ILK: Integrin-linked protein kinase; MLCP: Serine/threonine-protein phosphatase PP1-beta catalytic subunit; RhoA: Transforming protein RhoA; ERM: ezrin/radixin/moesin; GIT1: ARF GTPase-activating protein GIT1; Yes: Tyrosine-protein kinase Yes; IQGAP1: RasGTPase-activating-like protein IQGAP1; CKII: Casein kinase II subunit alpha; Gα12,13: Guanine nucleotide-binding protein subunit alpha-13
Figure Legend Snippet: Actin dependent signal transduction pathways of identified and quantified detergent resistant membrane microdomains proteins. The interaction map comprises the currently discussed mass spectrometric identified proteins (red bordered boxes) and differentially expressed proteins (green filled red bordered boxes) and were integrated in the over-represented Regulation of actin cytoskeleton , Focal adhesion and Adherens junction signaling pathways. The complex signaling network represents the combination of map04810 , map 04510 and map 04520 KEGG signaling pathways. Abbreviations for the discussed proteins: Ras: Ras-related protein R-Ras; MEK: mitogen-activated protein kinase kinase 1; F2RCD14: coagulation factor II, CD14 antigen; DOCK180: dedicator of cytokinesis protein; VWF: von Willebrand factor; Cav: caveolin; Gβγ: Guanine nucleotide-binding protein G(I)/G(S)/G(O) subunit gamma-12; Arp2/3: Actin-related protein 2/3 complex subunit 1B and 3; PIR121: Cytoplasmic FMR1-interacting protein 1; PFN: profilin; CFN: Cofilin-1; ZYX: Zyxin; MLC: Myosin regulatory light polypeptide 9; MLCK: Myosin light chain kinase 2; mDia: Protein diaphanous homolog 1; ACTN: actinin: VCL: vinculin; TLN: talin; ITG: integrin; Rap-1: Ras-related protein Rap-1A; Rac: Ras-related C3 botulinum toxin substrate 1; ILK: Integrin-linked protein kinase; MLCP: Serine/threonine-protein phosphatase PP1-beta catalytic subunit; RhoA: Transforming protein RhoA; ERM: ezrin/radixin/moesin; GIT1: ARF GTPase-activating protein GIT1; Yes: Tyrosine-protein kinase Yes; IQGAP1: RasGTPase-activating-like protein IQGAP1; CKII: Casein kinase II subunit alpha; Gα12,13: Guanine nucleotide-binding protein subunit alpha-13

Techniques Used: Transduction, Coagulation, Binding Assay

Immunological validation of mass spectrometry data for beta-actin and vinculin. Protein expression of beta-actin (actin cytoplasmatic 1) and vinculin was detected in membrane microdomains enriched fractions by Western Blotting ( a and c respectively), confirming the alteration caused by the hyperlipidemic condition (A) and statin treatment (At) when compared to the control samples (C), detected by LC-MS/MS analysis ( b and d respectively). The Western Blotting experiments were repeated three times. Data are expressed as means ± SD. ** p
Figure Legend Snippet: Immunological validation of mass spectrometry data for beta-actin and vinculin. Protein expression of beta-actin (actin cytoplasmatic 1) and vinculin was detected in membrane microdomains enriched fractions by Western Blotting ( a and c respectively), confirming the alteration caused by the hyperlipidemic condition (A) and statin treatment (At) when compared to the control samples (C), detected by LC-MS/MS analysis ( b and d respectively). The Western Blotting experiments were repeated three times. Data are expressed as means ± SD. ** p

Techniques Used: Mass Spectrometry, Expressing, Western Blot, Liquid Chromatography with Mass Spectroscopy

3) Product Images from "Activation of BMP-Smad1/5/8 Signaling Promotes Survival of Retinal Ganglion Cells after Damage In Vivo"

Article Title: Activation of BMP-Smad1/5/8 Signaling Promotes Survival of Retinal Ganglion Cells after Damage In Vivo

Journal: PLoS ONE

doi: 10.1371/journal.pone.0038690

BMP-Smad1/5/8 signaling is activated in the retina after light damage. A. Exposure to bright light (light damage; LD) is known to induce a significant loss of photoreceptor cells in the ONL. Two days after 8 hrs of LD, there was strong increase in GFAP expression, suggesting the retina was under stress. Smad1/5/8 activation (pSmad 1/5/8) was also observed in retinal ganglion cells and cells in the INL. ONL, outer nuclear layer; INL, inner nuclear layer; GCL, ganclion cell layer. Scale bars: 50 µm. B. 8 hrs of LD induced Id1 expression and this was blocked by injection of the BMP inhibitor, DM. Scale bar: 50 µm. C. Representative Western blot showing the level of Id1 expression after the indicated treatments. D. Id1 expression was induced by LD (3.3 fold increase compared to NT), and the expression was effectively blocked by injection of DM along with LD. The level of Id1 expression was normalized to beta-actin. Y axis shows an arbitrary value. *p
Figure Legend Snippet: BMP-Smad1/5/8 signaling is activated in the retina after light damage. A. Exposure to bright light (light damage; LD) is known to induce a significant loss of photoreceptor cells in the ONL. Two days after 8 hrs of LD, there was strong increase in GFAP expression, suggesting the retina was under stress. Smad1/5/8 activation (pSmad 1/5/8) was also observed in retinal ganglion cells and cells in the INL. ONL, outer nuclear layer; INL, inner nuclear layer; GCL, ganclion cell layer. Scale bars: 50 µm. B. 8 hrs of LD induced Id1 expression and this was blocked by injection of the BMP inhibitor, DM. Scale bar: 50 µm. C. Representative Western blot showing the level of Id1 expression after the indicated treatments. D. Id1 expression was induced by LD (3.3 fold increase compared to NT), and the expression was effectively blocked by injection of DM along with LD. The level of Id1 expression was normalized to beta-actin. Y axis shows an arbitrary value. *p

Techniques Used: Expressing, Activation Assay, Injection, Western Blot

NMDA damage induces expression of Id1, a known target of BMP-Smad1/5/8 signaling. A. Representative images from at least 3 animals per treatment are shown. Injection of 100 mM NMDA induced Id1 expression (red) in Hes5-GFP+ Müller cells (green). Id1 expression was blocked by coinjection of BMP inhibitors, LDN-193189 (LDN) or dorsomorphin (DM). Scale bar: 50 µm. B. Representative Western blot showing the level of Id1 expression 2 days after injection of the indicated factors. C. Quantification of the Western blots. More than a 2 fold increase in Id1 expression was observed after NMDA damage, and this increase was blocked effectively by LDN or DM. The level of Id1 expression was normalized to beta-actin. *p
Figure Legend Snippet: NMDA damage induces expression of Id1, a known target of BMP-Smad1/5/8 signaling. A. Representative images from at least 3 animals per treatment are shown. Injection of 100 mM NMDA induced Id1 expression (red) in Hes5-GFP+ Müller cells (green). Id1 expression was blocked by coinjection of BMP inhibitors, LDN-193189 (LDN) or dorsomorphin (DM). Scale bar: 50 µm. B. Representative Western blot showing the level of Id1 expression 2 days after injection of the indicated factors. C. Quantification of the Western blots. More than a 2 fold increase in Id1 expression was observed after NMDA damage, and this increase was blocked effectively by LDN or DM. The level of Id1 expression was normalized to beta-actin. *p

Techniques Used: Expressing, Injection, Western Blot

4) Product Images from "Genomic Analysis of Individual Differences in Ethanol Drinking: Evidence for Non-Genetic Factors in C57BL/6 Mice"

Article Title: Genomic Analysis of Individual Differences in Ethanol Drinking: Evidence for Non-Genetic Factors in C57BL/6 Mice

Journal: PLoS ONE

doi: 10.1371/journal.pone.0021100

RAB3A expression in high and low drinking mice. A . Western blot of nucleus accumbens total protein probed with RAB3A and beta-actin. B . Quantitation of western blot analysis, area under the curve (AUC) RAB3A expression normalized to total beta-actin. LOW
Figure Legend Snippet: RAB3A expression in high and low drinking mice. A . Western blot of nucleus accumbens total protein probed with RAB3A and beta-actin. B . Quantitation of western blot analysis, area under the curve (AUC) RAB3A expression normalized to total beta-actin. LOW

Techniques Used: Expressing, Mouse Assay, Western Blot, Quantitation Assay

5) Product Images from "Gastric tumor development in Smad3-deficient mice initiates from forestomach/glandular transition zone along the lesser curvature"

Article Title: Gastric tumor development in Smad3-deficient mice initiates from forestomach/glandular transition zone along the lesser curvature

Journal: Laboratory investigation; a journal of technical methods and pathology

doi: 10.1038/labinvest.2012.47

STAT3 and phosphoSTAT3 expression in Smad3 knockdown gastric cancer cell lines Immunoblot analyses of the Smad3 protein and phospho-STAT3 levels in AGS and MKN28 cells using beta-actin as a loading control. The shRNA-mediated knockdown of Smad3 increased the phosphorylated form of STAT3 in both AGS and MKN28 gastric cancer cells.
Figure Legend Snippet: STAT3 and phosphoSTAT3 expression in Smad3 knockdown gastric cancer cell lines Immunoblot analyses of the Smad3 protein and phospho-STAT3 levels in AGS and MKN28 cells using beta-actin as a loading control. The shRNA-mediated knockdown of Smad3 increased the phosphorylated form of STAT3 in both AGS and MKN28 gastric cancer cells.

Techniques Used: Expressing, shRNA

6) Product Images from "Chinese Medicine Formula Lingguizhugan Decoction Improves Beta-Oxidation and Metabolism of Fatty Acid in High-Fat-Diet-Induced Rat Model of Fatty Liver Disease"

Article Title: Chinese Medicine Formula Lingguizhugan Decoction Improves Beta-Oxidation and Metabolism of Fatty Acid in High-Fat-Diet-Induced Rat Model of Fatty Liver Disease

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

doi: 10.1155/2013/429738

LGZG improved fatty acid beta-oxidation via regulation of TR β 1 and CPT1A expression. The relative mRNA and protein expression of TR β 1 and CPT1A were detected by real-time PCR and western blot. (a) The influence of LGZG and its decomposed recipes on the protein expression of hepatic TR β 1 and CPT1A; (b) the influence of LGZG and its decomposed recipes on the relative mRNA of hepatic TR β 1 and CPT1A (normalized by β -actin). * P
Figure Legend Snippet: LGZG improved fatty acid beta-oxidation via regulation of TR β 1 and CPT1A expression. The relative mRNA and protein expression of TR β 1 and CPT1A were detected by real-time PCR and western blot. (a) The influence of LGZG and its decomposed recipes on the protein expression of hepatic TR β 1 and CPT1A; (b) the influence of LGZG and its decomposed recipes on the relative mRNA of hepatic TR β 1 and CPT1A (normalized by β -actin). * P

Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot

7) Product Images from "Functional Analysis of Prognostic Gene Expression Network Genes in Metastatic Breast Cancer Models"

Article Title: Functional Analysis of Prognostic Gene Expression Network Genes in Metastatic Breast Cancer Models

Journal: PLoS ONE

doi: 10.1371/journal.pone.0111813

Knockdown of Tpx2 does not induce prototypical MET in 6DT1 cells. A) E-cadherin mRNA levels in 6DT1 shCtrl, 6DT1-shTpx2#1, and 6DT1-shTpx2#2 cells were measured by qRT-PCR and displayed relative to levels in shRNA control cells. Error bars represent standard deviations. B) Western blot analysis for E-cadherin, beta-catenin, N-cadherin, and vimentin of cell lines described in a). Beta-actin serves as loading control. 67NR and 4T1 cells serve as positive and negative controls for the different EMT markers. C) 6DT1-shCtrl, 6DT1-shTpx2#1 and 6DT1-shTpx2#2 cells (and 67NR and 4T1 cells as controls) were immunofluorescently stained for E-cadherin and actin cytoskeleton was labeled with phalloidin (green). DAPI was used for nuclear staining. Confocal images are shown at 63x magnification.
Figure Legend Snippet: Knockdown of Tpx2 does not induce prototypical MET in 6DT1 cells. A) E-cadherin mRNA levels in 6DT1 shCtrl, 6DT1-shTpx2#1, and 6DT1-shTpx2#2 cells were measured by qRT-PCR and displayed relative to levels in shRNA control cells. Error bars represent standard deviations. B) Western blot analysis for E-cadherin, beta-catenin, N-cadherin, and vimentin of cell lines described in a). Beta-actin serves as loading control. 67NR and 4T1 cells serve as positive and negative controls for the different EMT markers. C) 6DT1-shCtrl, 6DT1-shTpx2#1 and 6DT1-shTpx2#2 cells (and 67NR and 4T1 cells as controls) were immunofluorescently stained for E-cadherin and actin cytoskeleton was labeled with phalloidin (green). DAPI was used for nuclear staining. Confocal images are shown at 63x magnification.

Techniques Used: Quantitative RT-PCR, shRNA, Western Blot, Staining, Labeling

Related Articles

Produced:

Article Title: Vascular ?-amyloid and early astrocyte alterations impair cerebrovascular function and cerebral metabolism in transgenic arcA? mice
Article Snippet: .. Primary antibodies Primary antibodies used for immunohistochemistry and western blotting: glucose transporter 1 (GLUT1, Alpha Diagnostic, GT11-A; GLUT1, Abcam, ab40084), glucose transporter 3 (GLUT3, Alpha Diagnostic, GT31-A), endothelial cells (CD31/PECAM1, BD Pharmingen, 553370), APP/Aβ (6E10, Covance/Signet, SIG-39300), Aβ (in-house produced antibody recognising fibrillar Aβ), laminin (Sigma-Aldrich, L9393), β actin (Abcam, ab6276), lactate transporter 1/monocarboxylate transporter 1 (MCT1, Alpha Diagnostic, MCT-13A), glial fibrillary acidic protein (GFAP, Advanced Immunochemical Inc., 031223), alpha smooth muscle actin (Sigma-Aldrich, A2547), β dystroglycan (Abcam, ab49515). .. Decreased endothelial and astrocytic GLUT1 expression in mid-stage arcAβ mice Western blot analysis of cortex and brain homogenates from mid-stage TG arcAβ mice and their NTG littermates revealed that the expression of the endothelial GLUT1 protein (55 kDa isoform) was reduced in the TG animals (Fig. d).

Western Blot:

Article Title: Validating gamma oscillations and delayed auditory responses as translational biomarkers of autism
Article Snippet: .. Western blotting was performed as published, using anti-NLGN3 (rabbit polyclonal, sc-50395, Santa Cruz, 1:200) and anti-β-actin (mouse monoclonal, Abcam ab6276, 1:5000) ( ). .. The effect of the mGluR5 antagonist MPEP (6-Methyl-2-(phenylethynyl)pyridine, Sigma) was assessed on AEP and PPI phenotypes.

Article Title: Vascular ?-amyloid and early astrocyte alterations impair cerebrovascular function and cerebral metabolism in transgenic arcA? mice
Article Snippet: .. Primary antibodies Primary antibodies used for immunohistochemistry and western blotting: glucose transporter 1 (GLUT1, Alpha Diagnostic, GT11-A; GLUT1, Abcam, ab40084), glucose transporter 3 (GLUT3, Alpha Diagnostic, GT31-A), endothelial cells (CD31/PECAM1, BD Pharmingen, 553370), APP/Aβ (6E10, Covance/Signet, SIG-39300), Aβ (in-house produced antibody recognising fibrillar Aβ), laminin (Sigma-Aldrich, L9393), β actin (Abcam, ab6276), lactate transporter 1/monocarboxylate transporter 1 (MCT1, Alpha Diagnostic, MCT-13A), glial fibrillary acidic protein (GFAP, Advanced Immunochemical Inc., 031223), alpha smooth muscle actin (Sigma-Aldrich, A2547), β dystroglycan (Abcam, ab49515). .. Decreased endothelial and astrocytic GLUT1 expression in mid-stage arcAβ mice Western blot analysis of cortex and brain homogenates from mid-stage TG arcAβ mice and their NTG littermates revealed that the expression of the endothelial GLUT1 protein (55 kDa isoform) was reduced in the TG animals (Fig. d).

Article Title: GAGE Cancer-Germline Antigens Are Recruited to the Nuclear Envelope by Germ Cell-Less (GCL)
Article Snippet: .. Immunoassays Antibodies used in this study were: Mouse anti-GAGE (M3 ; immunocytochemistry [ICC], 1/100 dilution; western blot [WB], 1/5000 dilution), rabbit anti-Myc (A14; Santa Cruz Biotech, Heidelberg, Germany; ICC, 1/100), rabbit anti-GCL (Santa Cruz Biotech; WB, 1/1000), rabbit anti-GCL (Sigma Aldrich, Brondby, Denmark; WB, 1/1000), mouse anti-beta-Actin (Ab6276; Abcam, Cambridge, UK; WB, 1/200.000); FITC-conjugated goat anti-mouse IgG (Dako, Glostrup, Denmark; ICC, 1/400), Cy3-conjugated goat anti-rabbit IgG (Jackson ImmunoResearch Laboratories, West Grove, PA, USA; ICC, 1/400). ..

Incubation:

Article Title: Tyrosine kinase B protein expression is reduced in the cerebellum of patients with bipolar disorder
Article Snippet: .. The membranes were blocked with 5% nonfat milk in 0.1% Tween-20/ Tris-buffered saline (TBS-T) (RT, 3 h) and then incubated (4 °C, 16 h) with the rabbit polyclonal anti-TrkB antibody (H-181, #sc-8316, Santa Cruz Biotechnology; 1:500 dilution in 1% nonfat milk/TBS-T) or the mouse monoclonal anti-β-actin antibody (AC-15, #ab6276, Abcam, Cambridge, MA, USA; 1:20,000). .. After TBS-T washing, the membranes were incubated (RT, 2 h) with the peroxidase-conjugated goat anti-rabbit IgG secondary antibody (#170-6515, Bio-Rad; 1:5,000 dilution in 1% nonfat milk/TBS-T) or peroxidase-conjugated horse anti-mouse IgG secondary antibody (#PI-2000, Vector Laboratories; 1:5,000).

Immunocytochemistry:

Article Title: GAGE Cancer-Germline Antigens Are Recruited to the Nuclear Envelope by Germ Cell-Less (GCL)
Article Snippet: .. Immunoassays Antibodies used in this study were: Mouse anti-GAGE (M3 ; immunocytochemistry [ICC], 1/100 dilution; western blot [WB], 1/5000 dilution), rabbit anti-Myc (A14; Santa Cruz Biotech, Heidelberg, Germany; ICC, 1/100), rabbit anti-GCL (Santa Cruz Biotech; WB, 1/1000), rabbit anti-GCL (Sigma Aldrich, Brondby, Denmark; WB, 1/1000), mouse anti-beta-Actin (Ab6276; Abcam, Cambridge, UK; WB, 1/200.000); FITC-conjugated goat anti-mouse IgG (Dako, Glostrup, Denmark; ICC, 1/400), Cy3-conjugated goat anti-rabbit IgG (Jackson ImmunoResearch Laboratories, West Grove, PA, USA; ICC, 1/400). ..

Immunohistochemistry:

Article Title: Vascular ?-amyloid and early astrocyte alterations impair cerebrovascular function and cerebral metabolism in transgenic arcA? mice
Article Snippet: .. Primary antibodies Primary antibodies used for immunohistochemistry and western blotting: glucose transporter 1 (GLUT1, Alpha Diagnostic, GT11-A; GLUT1, Abcam, ab40084), glucose transporter 3 (GLUT3, Alpha Diagnostic, GT31-A), endothelial cells (CD31/PECAM1, BD Pharmingen, 553370), APP/Aβ (6E10, Covance/Signet, SIG-39300), Aβ (in-house produced antibody recognising fibrillar Aβ), laminin (Sigma-Aldrich, L9393), β actin (Abcam, ab6276), lactate transporter 1/monocarboxylate transporter 1 (MCT1, Alpha Diagnostic, MCT-13A), glial fibrillary acidic protein (GFAP, Advanced Immunochemical Inc., 031223), alpha smooth muscle actin (Sigma-Aldrich, A2547), β dystroglycan (Abcam, ab49515). .. Decreased endothelial and astrocytic GLUT1 expression in mid-stage arcAβ mice Western blot analysis of cortex and brain homogenates from mid-stage TG arcAβ mice and their NTG littermates revealed that the expression of the endothelial GLUT1 protein (55 kDa isoform) was reduced in the TG animals (Fig. d).

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    Abcam rabbit anti mouse α sma
    Candidate stem cell marker CD146 associated with small blood vessels in the odontoblast layer are reduced in the Bmp2-cKO Sp7-Cre-EGFP model, and αSma + stem cells in the cervical and apical regions of the periodontium are also greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP model. ( a – d ) Candidate stem cell marker CD146 immunocytochemistry localized within the dental pulp ( a – d , purple arrows) and in association with blood vessels adjacent to the odontoblast layer ( a – d , blue arrows) on capillaries. CD146 protein expression is greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP in 1-month-old mice (×200). a and b are from the third molars, and c and d are from incisor cervical loop region. Candidate stem cells, marked with <t>α-SMA</t> immunocytochemistry are noted all within the periodontium of the first and second molars (data shown in Supplementary Figure S7 ) and in the less developed dental follicle cells of the third molars ( e and f , black arrow), and apical papilla region ( g and h , black arrow). Expression of α-SMA stem cell marker is greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP mice ( h ) as compared to control ( g ), example from the second molar, 1 month of age, and shown at ×200. Bmp2, bone morphogenetic protein-2.
    Rabbit Anti Mouse α Sma, supplied by Abcam, used in various techniques. Bioz Stars score: 88/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam mouse anti human β actin
    PRKDC knockdown in NGP cells confirms DNA-PKcs-dependent radiosensitizing activity of NU7026. (A) PRKDC mRNA expression in NGP cells at 144 h after transduction with nonspecific control shRNA (SHC002) or PRKDC shRNA. PRKDC mRNA levels were determined by qPCR and ΔCt values were normalized to the household gene <t>β-actin.</t> Normalized ΔCt values of untreated non-transduced NGP cells (no virus) were set at zero, giving ΔΔCt. Data represent the mean (n = 4) +/- SD. (B) FACS analysis of the effects of treatment with 0.63 Gy IR on the sub-G1 fraction of normal NGP cells and NGP cells transduced with SHC002 or PRKDC shRNA. Results are obtained at 96 h after IR-exposure of the cells. (C) Sub-G1 fraction of NGP cells transduced with SHC002 or PRKDC shRNA after non-treatment and after treatment with 0.63 Gy IR, at 48, 72 and 96 h after irradiation. (D) Western Blot analysis of protein levels of DNA-PKcs and cleaved PARP in non-irradiated and irradiated normal NGP cells and NGP cells transduced with SHC002 or PRKDC shRNA. Results were obtained at 120 h after irradiation, which was equal to 168 h after transduction. β-actin protein levels were used as loading control.
    Mouse Anti Human β Actin, supplied by Abcam, used in various techniques. Bioz Stars score: 92/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam mouse anti α actin
    Myosin II is associated with RNAP II, TFIIB, <t>α-actin</t> and β-actin in the nucleus. Nuclear extracts were immunoprecipitated (IP) with indicated antibodies, followed by immunoblotting (IB). Rabbit IgG was used as negative control. ( A ) RNAP
    Mouse Anti α Actin, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam ms anti β actin
    Exposure to LNP-cm CFTR Enriches Membrane-Integrated CFTR In Vitro (A) CFTR-WT is core-glycosylated (CG) in the endoplasmic reticulum, after which it moves through the trans -Golgi network to become complex-glycosylated (CxG) and reaches the plasma membrane, where it acts as a chloride channel. CFTR-F508del fails to achieve complex glycosylation and rapidly undergoes degradation. (B) Western blot detection of CFTR in untreated and treated CF cell lysates (lanes 3 and 4). Lanes 1 and 2 contained complex- and core-glycosylated CFTR migration standards. <t>β-Actin</t> was used as a loading control. (C and D) Immunocytochemistry detection of CFTR was performed on treated (CF + LNP− cm CFTR ) and untreated cells (CF-WT or CF) grown either under (C) standard growth conditions or (D) at the air-liquid interface until polarization. White arrows highlight the CFTR-enriched plasma membrane. Red, CFTR; blue, nucleus; green, actin.
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    Candidate stem cell marker CD146 associated with small blood vessels in the odontoblast layer are reduced in the Bmp2-cKO Sp7-Cre-EGFP model, and αSma + stem cells in the cervical and apical regions of the periodontium are also greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP model. ( a – d ) Candidate stem cell marker CD146 immunocytochemistry localized within the dental pulp ( a – d , purple arrows) and in association with blood vessels adjacent to the odontoblast layer ( a – d , blue arrows) on capillaries. CD146 protein expression is greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP in 1-month-old mice (×200). a and b are from the third molars, and c and d are from incisor cervical loop region. Candidate stem cells, marked with α-SMA immunocytochemistry are noted all within the periodontium of the first and second molars (data shown in Supplementary Figure S7 ) and in the less developed dental follicle cells of the third molars ( e and f , black arrow), and apical papilla region ( g and h , black arrow). Expression of α-SMA stem cell marker is greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP mice ( h ) as compared to control ( g ), example from the second molar, 1 month of age, and shown at ×200. Bmp2, bone morphogenetic protein-2.

    Journal: International Journal of Oral Science

    Article Title: Bone morphogenetic protein-2 gene controls tooth root development in coordination with formation of the periodontium

    doi: 10.1038/ijos.2013.41

    Figure Lengend Snippet: Candidate stem cell marker CD146 associated with small blood vessels in the odontoblast layer are reduced in the Bmp2-cKO Sp7-Cre-EGFP model, and αSma + stem cells in the cervical and apical regions of the periodontium are also greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP model. ( a – d ) Candidate stem cell marker CD146 immunocytochemistry localized within the dental pulp ( a – d , purple arrows) and in association with blood vessels adjacent to the odontoblast layer ( a – d , blue arrows) on capillaries. CD146 protein expression is greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP in 1-month-old mice (×200). a and b are from the third molars, and c and d are from incisor cervical loop region. Candidate stem cells, marked with α-SMA immunocytochemistry are noted all within the periodontium of the first and second molars (data shown in Supplementary Figure S7 ) and in the less developed dental follicle cells of the third molars ( e and f , black arrow), and apical papilla region ( g and h , black arrow). Expression of α-SMA stem cell marker is greatly reduced in the Bmp2-cKO Sp7-Cre-EGFP mice ( h ) as compared to control ( g ), example from the second molar, 1 month of age, and shown at ×200. Bmp2, bone morphogenetic protein-2.

    Article Snippet: Immunohistochemistry Immunohistochemistry was performed as previously described., Primary antibodies included polyclonal rabbit anti-mouse vascular endothelial growth factor A (VEGF-A), Ab9571 (1∶200), rabbit anti-mouse CD146, Ab75769 (1∶200) and rabbit anti-mouse α-SMA, Ab5694 (1∶200), were obtained from Abcam Limited (Boston, MA, USA).

    Techniques: Marker, Immunocytochemistry, Expressing, Mouse Assay

    PRKDC knockdown in NGP cells confirms DNA-PKcs-dependent radiosensitizing activity of NU7026. (A) PRKDC mRNA expression in NGP cells at 144 h after transduction with nonspecific control shRNA (SHC002) or PRKDC shRNA. PRKDC mRNA levels were determined by qPCR and ΔCt values were normalized to the household gene β-actin. Normalized ΔCt values of untreated non-transduced NGP cells (no virus) were set at zero, giving ΔΔCt. Data represent the mean (n = 4) +/- SD. (B) FACS analysis of the effects of treatment with 0.63 Gy IR on the sub-G1 fraction of normal NGP cells and NGP cells transduced with SHC002 or PRKDC shRNA. Results are obtained at 96 h after IR-exposure of the cells. (C) Sub-G1 fraction of NGP cells transduced with SHC002 or PRKDC shRNA after non-treatment and after treatment with 0.63 Gy IR, at 48, 72 and 96 h after irradiation. (D) Western Blot analysis of protein levels of DNA-PKcs and cleaved PARP in non-irradiated and irradiated normal NGP cells and NGP cells transduced with SHC002 or PRKDC shRNA. Results were obtained at 120 h after irradiation, which was equal to 168 h after transduction. β-actin protein levels were used as loading control.

    Journal: PLoS ONE

    Article Title: DNA-Dependent Protein Kinase As Molecular Target for Radiosensitization of Neuroblastoma Cells

    doi: 10.1371/journal.pone.0145744

    Figure Lengend Snippet: PRKDC knockdown in NGP cells confirms DNA-PKcs-dependent radiosensitizing activity of NU7026. (A) PRKDC mRNA expression in NGP cells at 144 h after transduction with nonspecific control shRNA (SHC002) or PRKDC shRNA. PRKDC mRNA levels were determined by qPCR and ΔCt values were normalized to the household gene β-actin. Normalized ΔCt values of untreated non-transduced NGP cells (no virus) were set at zero, giving ΔΔCt. Data represent the mean (n = 4) +/- SD. (B) FACS analysis of the effects of treatment with 0.63 Gy IR on the sub-G1 fraction of normal NGP cells and NGP cells transduced with SHC002 or PRKDC shRNA. Results are obtained at 96 h after IR-exposure of the cells. (C) Sub-G1 fraction of NGP cells transduced with SHC002 or PRKDC shRNA after non-treatment and after treatment with 0.63 Gy IR, at 48, 72 and 96 h after irradiation. (D) Western Blot analysis of protein levels of DNA-PKcs and cleaved PARP in non-irradiated and irradiated normal NGP cells and NGP cells transduced with SHC002 or PRKDC shRNA. Results were obtained at 120 h after irradiation, which was equal to 168 h after transduction. β-actin protein levels were used as loading control.

    Article Snippet: After blocking, membranes were incubated with mouse anti-human β-actin (clone AC-15) monoclonal antibody (1:20000; Abcam) or mouse anti-human α-tubulin (clone DM1A) monoclonal antibody (1:10000) in OBB with 0.1% (v/v) Tween-20 (OBB-T) (overnight; 4°C).

    Techniques: Activity Assay, Expressing, Transduction, shRNA, Real-time Polymerase Chain Reaction, FACS, Irradiation, Western Blot

    Combination treatment with NU7026 and IR induces apoptosis in NGP cells. (A) Effects of NU7026 plus IR combination therapy versus monotherapy on the cell cycle status of NGP cells. For combination treatment, cells were pre-treated with 10 μM NU7026 for 1 h before exposure to 0.63 Gy IR. Samples were analyzed by FACS analysis at 96 h after treatment. (B) FACS analysis of the effects of combination therapy versus monotherapy on the sub-G1 fraction of cells at 48, 72 and 96 h after treatment. (C) Western Blot detection of total DNA-PKcs and activated DNA-PKcs (via phosphorylation at serine 2056) levels and PARP cleavage after combination therapy versus monotherapy with 10 μM NU7026 and/or 0.63 Gy IR, at 1 h and 96 h after IR-exposure, respectively. β-actin protein levels were used as loading control.

    Journal: PLoS ONE

    Article Title: DNA-Dependent Protein Kinase As Molecular Target for Radiosensitization of Neuroblastoma Cells

    doi: 10.1371/journal.pone.0145744

    Figure Lengend Snippet: Combination treatment with NU7026 and IR induces apoptosis in NGP cells. (A) Effects of NU7026 plus IR combination therapy versus monotherapy on the cell cycle status of NGP cells. For combination treatment, cells were pre-treated with 10 μM NU7026 for 1 h before exposure to 0.63 Gy IR. Samples were analyzed by FACS analysis at 96 h after treatment. (B) FACS analysis of the effects of combination therapy versus monotherapy on the sub-G1 fraction of cells at 48, 72 and 96 h after treatment. (C) Western Blot detection of total DNA-PKcs and activated DNA-PKcs (via phosphorylation at serine 2056) levels and PARP cleavage after combination therapy versus monotherapy with 10 μM NU7026 and/or 0.63 Gy IR, at 1 h and 96 h after IR-exposure, respectively. β-actin protein levels were used as loading control.

    Article Snippet: After blocking, membranes were incubated with mouse anti-human β-actin (clone AC-15) monoclonal antibody (1:20000; Abcam) or mouse anti-human α-tubulin (clone DM1A) monoclonal antibody (1:10000) in OBB with 0.1% (v/v) Tween-20 (OBB-T) (overnight; 4°C).

    Techniques: FACS, Western Blot

    Myosin II is associated with RNAP II, TFIIB, α-actin and β-actin in the nucleus. Nuclear extracts were immunoprecipitated (IP) with indicated antibodies, followed by immunoblotting (IB). Rabbit IgG was used as negative control. ( A ) RNAP

    Journal: Gastroenterology

    Article Title: NUCLEAR MYOSIN II REGULATES THE ASSEMBLY OF PREINITIATION COMPLEX FOR ICAM-1 GENE TRANSCRIPTION

    doi: 10.1053/j.gastro.2009.03.040

    Figure Lengend Snippet: Myosin II is associated with RNAP II, TFIIB, α-actin and β-actin in the nucleus. Nuclear extracts were immunoprecipitated (IP) with indicated antibodies, followed by immunoblotting (IB). Rabbit IgG was used as negative control. ( A ) RNAP

    Article Snippet: Primary antibodies were: mouse anti-α-actin (Abcam), mouse antiβ-actin (Sigma) and goat anti-pMLC (Thr18/Ser19, Santa Cruz).

    Techniques: Immunoprecipitation, Negative Control

    Myosin II and actin exist in the nuclei of HCCSMCs. ( A to H ) Immunostaining and confocal microscopy of α-actin (green), β-actin (green) and pT18/S19MLC 20 (red) in HCCSMCs. TO PRO 3 (blue) was used for counterstaining of nuclei. ( I ) Western

    Journal: Gastroenterology

    Article Title: NUCLEAR MYOSIN II REGULATES THE ASSEMBLY OF PREINITIATION COMPLEX FOR ICAM-1 GENE TRANSCRIPTION

    doi: 10.1053/j.gastro.2009.03.040

    Figure Lengend Snippet: Myosin II and actin exist in the nuclei of HCCSMCs. ( A to H ) Immunostaining and confocal microscopy of α-actin (green), β-actin (green) and pT18/S19MLC 20 (red) in HCCSMCs. TO PRO 3 (blue) was used for counterstaining of nuclei. ( I ) Western

    Article Snippet: Primary antibodies were: mouse anti-α-actin (Abcam), mouse antiβ-actin (Sigma) and goat anti-pMLC (Thr18/Ser19, Santa Cruz).

    Techniques: Immunostaining, Confocal Microscopy, Western Blot

    Exposure to LNP-cm CFTR Enriches Membrane-Integrated CFTR In Vitro (A) CFTR-WT is core-glycosylated (CG) in the endoplasmic reticulum, after which it moves through the trans -Golgi network to become complex-glycosylated (CxG) and reaches the plasma membrane, where it acts as a chloride channel. CFTR-F508del fails to achieve complex glycosylation and rapidly undergoes degradation. (B) Western blot detection of CFTR in untreated and treated CF cell lysates (lanes 3 and 4). Lanes 1 and 2 contained complex- and core-glycosylated CFTR migration standards. β-Actin was used as a loading control. (C and D) Immunocytochemistry detection of CFTR was performed on treated (CF + LNP− cm CFTR ) and untreated cells (CF-WT or CF) grown either under (C) standard growth conditions or (D) at the air-liquid interface until polarization. White arrows highlight the CFTR-enriched plasma membrane. Red, CFTR; blue, nucleus; green, actin.

    Journal: Molecular Therapy

    Article Title: Lipid Nanoparticle-Delivered Chemically Modified mRNA Restores Chloride Secretion in Cystic Fibrosis

    doi: 10.1016/j.ymthe.2018.05.014

    Figure Lengend Snippet: Exposure to LNP-cm CFTR Enriches Membrane-Integrated CFTR In Vitro (A) CFTR-WT is core-glycosylated (CG) in the endoplasmic reticulum, after which it moves through the trans -Golgi network to become complex-glycosylated (CxG) and reaches the plasma membrane, where it acts as a chloride channel. CFTR-F508del fails to achieve complex glycosylation and rapidly undergoes degradation. (B) Western blot detection of CFTR in untreated and treated CF cell lysates (lanes 3 and 4). Lanes 1 and 2 contained complex- and core-glycosylated CFTR migration standards. β-Actin was used as a loading control. (C and D) Immunocytochemistry detection of CFTR was performed on treated (CF + LNP− cm CFTR ) and untreated cells (CF-WT or CF) grown either under (C) standard growth conditions or (D) at the air-liquid interface until polarization. White arrows highlight the CFTR-enriched plasma membrane. Red, CFTR; blue, nucleus; green, actin.

    Article Snippet: Antibodies used were Ms-anti-CFTR Ab596 (University of North Carolina), 1:2,000, and Ms-anti-β-actin (Abcam), 1:10,000.

    Techniques: In Vitro, Western Blot, Migration, Immunocytochemistry