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antibodies against aimp3  (Atlas Antibodies)


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    Structured Review

    Atlas Antibodies antibodies against aimp3
    Figure 1. Loss of <t>AIMP3</t> is a feature in bladder cancer and AIMP3 promoter methylation is cancer-specific. (a) AIMP3 TMA-IHC. Top: Normal urothelium demonstrating high levels of cytoplasmic AIMP3 expression (L 320; R 3100). Bottom: AIMP3 is not expressed in an invasive T2G3 tumour (MIBC) (L 320; R 3100). In A, the dashed square indicates the area at a higher magnification (3100) in the photomicro- graphs on the right (R). (b) Distribution of AIMP3 expression levels across tumours of different stages and grades and normal tissues. There is a reduction in AIMP3 expression in cancer as compared to normal bladder tissue. A downward-shift in the percentage of moderate/high expressing tumours exists with stage/grade progression. (c) Promoter methylation of AIMP3 was detected in about 10% of bladder tumours (both MIBC and NMIBC) but was undetected in normal tissues. (d) Relative AIMP3 mRNA expression stratified by tumour stage/grade and methylation status. Methylated tumours demonstrated a significant loss in expression, while a marked difference was also observed between Ta/T1 and T2/higher tumours (p < 0.001). Bars, SE. [Color figure can be viewed in the online issue, which is available at wileyon- linelibrary.com.]
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    Images

    1) Product Images from "Loss of expression of the tumour suppressor gene AIMP3 predicts survival following radiotherapy in muscle-invasive bladder cancer."

    Article Title: Loss of expression of the tumour suppressor gene AIMP3 predicts survival following radiotherapy in muscle-invasive bladder cancer.

    Journal: International journal of cancer

    doi: 10.1002/ijc.29022

    Figure 1. Loss of AIMP3 is a feature in bladder cancer and AIMP3 promoter methylation is cancer-specific. (a) AIMP3 TMA-IHC. Top: Normal urothelium demonstrating high levels of cytoplasmic AIMP3 expression (L 320; R 3100). Bottom: AIMP3 is not expressed in an invasive T2G3 tumour (MIBC) (L 320; R 3100). In A, the dashed square indicates the area at a higher magnification (3100) in the photomicro- graphs on the right (R). (b) Distribution of AIMP3 expression levels across tumours of different stages and grades and normal tissues. There is a reduction in AIMP3 expression in cancer as compared to normal bladder tissue. A downward-shift in the percentage of moderate/high expressing tumours exists with stage/grade progression. (c) Promoter methylation of AIMP3 was detected in about 10% of bladder tumours (both MIBC and NMIBC) but was undetected in normal tissues. (d) Relative AIMP3 mRNA expression stratified by tumour stage/grade and methylation status. Methylated tumours demonstrated a significant loss in expression, while a marked difference was also observed between Ta/T1 and T2/higher tumours (p < 0.001). Bars, SE. [Color figure can be viewed in the online issue, which is available at wileyon- linelibrary.com.]
    Figure Legend Snippet: Figure 1. Loss of AIMP3 is a feature in bladder cancer and AIMP3 promoter methylation is cancer-specific. (a) AIMP3 TMA-IHC. Top: Normal urothelium demonstrating high levels of cytoplasmic AIMP3 expression (L 320; R 3100). Bottom: AIMP3 is not expressed in an invasive T2G3 tumour (MIBC) (L 320; R 3100). In A, the dashed square indicates the area at a higher magnification (3100) in the photomicro- graphs on the right (R). (b) Distribution of AIMP3 expression levels across tumours of different stages and grades and normal tissues. There is a reduction in AIMP3 expression in cancer as compared to normal bladder tissue. A downward-shift in the percentage of moderate/high expressing tumours exists with stage/grade progression. (c) Promoter methylation of AIMP3 was detected in about 10% of bladder tumours (both MIBC and NMIBC) but was undetected in normal tissues. (d) Relative AIMP3 mRNA expression stratified by tumour stage/grade and methylation status. Methylated tumours demonstrated a significant loss in expression, while a marked difference was also observed between Ta/T1 and T2/higher tumours (p < 0.001). Bars, SE. [Color figure can be viewed in the online issue, which is available at wileyon- linelibrary.com.]

    Techniques Used: Methylation, Expressing

    Figure 2. Association between AIMP3 expression, Tp53 transactivity and genomic stability. (a) Relative TP53TG1 mRNA expression stratified by AIMP3 expression levels and TP53 mutation status. Low expressing AIMP3 wt TP53 tumours presented with a loss of TP53TG1 expres- sion comparable to that of mutant Tp53 tumours. Bars, SE. wt, wild-type. (b) Relative AIMP3 expression stratified by FGA. FGA of all tumours were defined as a quantitative expression of genomic instability, assessed by 1-Mb aCGH. Tumours with high levels of AIMP3 exhibited a lower fraction of genome altered (FGA) (p < 0.001). Bars, SE. (c) Dose–response curves of cell lines HeLa, T24, 253J, RT112 and RT4 irradiation (0–5Gy). Bars, SD. (d) AIMP3 protein expression increased with time upon exposure to IR as assessed by western blots and normalised with b actin. Bars, SD (e) Confocal immunofluorescence imaging showing subcellular localisation of AIMP3 in RT4 cells without irradiation (IR2) and with irradiation. (IR1) (3600) (AIMP3-FITC (green-yellow); Actin-TRITC (red-pink); Nuclear DAPI staining (blue); and merged images). Following IR, there is increased nuclear localisation of AIMP3 (Manders coefficient: 0.362 without irradiation com- pared to 0.778 with irradiation). [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
    Figure Legend Snippet: Figure 2. Association between AIMP3 expression, Tp53 transactivity and genomic stability. (a) Relative TP53TG1 mRNA expression stratified by AIMP3 expression levels and TP53 mutation status. Low expressing AIMP3 wt TP53 tumours presented with a loss of TP53TG1 expres- sion comparable to that of mutant Tp53 tumours. Bars, SE. wt, wild-type. (b) Relative AIMP3 expression stratified by FGA. FGA of all tumours were defined as a quantitative expression of genomic instability, assessed by 1-Mb aCGH. Tumours with high levels of AIMP3 exhibited a lower fraction of genome altered (FGA) (p < 0.001). Bars, SE. (c) Dose–response curves of cell lines HeLa, T24, 253J, RT112 and RT4 irradiation (0–5Gy). Bars, SD. (d) AIMP3 protein expression increased with time upon exposure to IR as assessed by western blots and normalised with b actin. Bars, SD (e) Confocal immunofluorescence imaging showing subcellular localisation of AIMP3 in RT4 cells without irradiation (IR2) and with irradiation. (IR1) (3600) (AIMP3-FITC (green-yellow); Actin-TRITC (red-pink); Nuclear DAPI staining (blue); and merged images). Following IR, there is increased nuclear localisation of AIMP3 (Manders coefficient: 0.362 without irradiation com- pared to 0.778 with irradiation). [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

    Techniques Used: Expressing, Mutagenesis, Irradiation, Western Blot, Imaging, Staining

    Figure 3. Reduction of AIMP3 in vitro is associated with increased radioresistance. (a) Western Blot demonstrating significant siRNA- mediated knockdown of AIMP3 between 24 and 96 hrs post-transfection. (b) AIMP3-knockdown cells demonstrate a significant increase in clonogenic survival following irradiation (p < 0.05*). Bars, SD. Relative to cells exposed to IR at IC50 (vertical-banded bars) and those with just transfection-medium exposure with IR at IC50 (horizontal-banded bars), those with AIMP3-knockdown and exposed to IR at IC50 (grey, unbanded bars) have a higher clonogenic survival. Untreated cells were used as reference (100%) for relative changes in clonogenic sur- vival (bars not shown). (c) Clonogenic assay images demonstrating stained and counted colonies in the respective cell lines. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
    Figure Legend Snippet: Figure 3. Reduction of AIMP3 in vitro is associated with increased radioresistance. (a) Western Blot demonstrating significant siRNA- mediated knockdown of AIMP3 between 24 and 96 hrs post-transfection. (b) AIMP3-knockdown cells demonstrate a significant increase in clonogenic survival following irradiation (p < 0.05*). Bars, SD. Relative to cells exposed to IR at IC50 (vertical-banded bars) and those with just transfection-medium exposure with IR at IC50 (horizontal-banded bars), those with AIMP3-knockdown and exposed to IR at IC50 (grey, unbanded bars) have a higher clonogenic survival. Untreated cells were used as reference (100%) for relative changes in clonogenic sur- vival (bars not shown). (c) Clonogenic assay images demonstrating stained and counted colonies in the respective cell lines. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

    Techniques Used: In Vitro, Western Blot, Knockdown, Transfection, Irradiation, Clonogenic Assay, Staining

    Figure 4. Reduced expression of AIMP3 is associated with reduced survival following radiotherapy and higher risk of recurrence. (a) AIMP3 expression in the BCON TMA. Example of AIMP3-negative (top) and AIMP3-positive (bottom) tumours that were treated with either radical radiotherapy alone or radical radiotherapy supplemented with carbogen and nicotinamide. (b) Kaplan-Meier plot illustrates that the adjusted HR for death in AIMP3-positive group was half the HR for death in the AIMP3-negative group in the BCON cohort. (c) Kaplan Meier plot depicts the HR for death in patients with tumour recurrence following radiotherapy was 8.8 relative to patients without recurrence. (d) AIMP3 expression was evaluated on a radical cystectomy TMA set. Kaplan Meier plot demonstrates no significant differences in the HR for death between the AIMP3-positive and negative groups. [Color figure can be viewed in the online issue, which is available at wileyonlineli- brary.com.]
    Figure Legend Snippet: Figure 4. Reduced expression of AIMP3 is associated with reduced survival following radiotherapy and higher risk of recurrence. (a) AIMP3 expression in the BCON TMA. Example of AIMP3-negative (top) and AIMP3-positive (bottom) tumours that were treated with either radical radiotherapy alone or radical radiotherapy supplemented with carbogen and nicotinamide. (b) Kaplan-Meier plot illustrates that the adjusted HR for death in AIMP3-positive group was half the HR for death in the AIMP3-negative group in the BCON cohort. (c) Kaplan Meier plot depicts the HR for death in patients with tumour recurrence following radiotherapy was 8.8 relative to patients without recurrence. (d) AIMP3 expression was evaluated on a radical cystectomy TMA set. Kaplan Meier plot demonstrates no significant differences in the HR for death between the AIMP3-positive and negative groups. [Color figure can be viewed in the online issue, which is available at wileyonlineli- brary.com.]

    Techniques Used: Expressing

    Related Articles

    Incubation:

    Article Title: Loss of expression of the tumour suppressor gene AIMP3 predicts survival following radiotherapy in muscle-invasive bladder cancer.
    Article Snippet: Pratik M.S.. Gurung, Abhi Veerakumarasivam, Magali Williamson, Nicholas Counsell, James Douglas, Wei S. Tan, Andrew Feber, Simon J. Crabb, Susan C. Short, Alex Freeman, Thomas Powles, Peter J. Hoskin, Catharine M. West and John D. Kelly 1 Division of Surgery and Interventional Science, University College London (UCL), London, United Kingdom 2 Perdana University Graduate School of Medicine, Perdana University, Serdang, Selangor Darul Ehsan, Malaysia 3 Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor Darul Ehsan, Malaysia 4 Cancer Research UK and UCL Clinical Trials Centre, London, United Kingdom 5 Cancer Research UK Centre, University of Southampton School of Medicine, Southampton, United Kingdom 6 UCL Cancer Institute, Cancer Biology, UCL, London, United Kingdom 7 Cancer Sciences Unit, University of Southampton, Southampton, United Kingdom 8 Section of Oncology and Clinical Research, Leeds Institute of Molecular Medicine, Leeds, United Kingdom 9 Department of Histopathology, UCL, London, United Kingdom 10 Bart’s Cancer Institute, Queen Mary University of London, London, United Kingdom 11 Department of Oncology, Mount Vernon Hospital, Northwood, Middlesex, United Kingdom 12 Academic Department of Radiation Oncology, University of Manchester, Manchester, United Kingdom .. Pratik M.S.. Gurung, Abhi Veerakumarasivam, Magali Williamson, Nicholas Counsell, James Douglas, Wei S. Tan, Andrew Feber, Simon J. Crabb, Susan C. Short, Alex Freeman, Thomas Powles, Peter J. Hoskin, Catharine M. West and John D. Kelly 1 Division of Surgery and Interventional Science, University College London (UCL), London, United Kingdom 2 Perdana University Graduate School of Medicine, Perdana University, Serdang, Selangor Darul Ehsan, Malaysia 3 Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor Darul Ehsan, Malaysia 4 Cancer Research UK and UCL Clinical Trials Centre, London, United Kingdom 5 Cancer Research UK Centre, University of Southampton School of Medicine, Southampton, United Kingdom 6 UCL Cancer Institute, Cancer Biology, UCL, London, United Kingdom 7 Cancer Sciences Unit, University of Southampton, Southampton, United Kingdom 8 Section of Oncology and Clinical Research, Leeds Institute of Molecular Medicine, Leeds, United Kingdom 9 Department of Histopathology, UCL, London, United Kingdom 10 Bart’s Cancer Institute, Queen Mary University of London, London, United Kingdom 11 Department of Oncology, Mount Vernon Hospital, Northwood, Middlesex, United Kingdom 12 Academic Department of Radiation Oncology, University of Manchester, Manchester, United Kingdom .. Pratik M.S.. Gurung, Abhi Veerakumarasivam, Magali Williamson, Nicholas Counsell, James Douglas, Wei S. Tan, Andrew Feber, Simon J. Crabb, Susan C. Short, Alex Freeman, Thomas Powles, Peter J. Hoskin, Catharine M. West and John D. Kelly 1 Division of Surgery and Interventional Science, University College London (UCL), London, United Kingdom 2 Perdana University Graduate School of Medicine, Perdana University, Serdang, Selangor Darul Ehsan, Malaysia 3 Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor Darul Ehsan, Malaysia 4 Cancer Research UK and UCL Clinical Trials Centre, London, United Kingdom 5 Cancer Research UK Centre, University of Southampton School of Medicine, Southampton, United Kingdom 6 UCL Cancer Institute, Cancer Biology, UCL, London, United Kingdom 7 Cancer Sciences Unit, University of Southampton, Southampton, United Kingdom 8 Section of Oncology and Clinical Research, Leeds Institute of Molecular Medicine, Leeds, United Kingdom 9 Department of Histopathology, UCL, London, United Kingdom 10 Bart’s Cancer Institute, Queen Mary University of London, London, United Kingdom 11 Department of Oncology, Mount Vernon Hospital, Northwood, Middlesex, United Kingdom 12 Academic Department of Radiation Oncology, University of Manchester, Manchester, United Kingdom



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    Image Search Results


    Differential expression and prognostic value of EEF1E1. ( A ) Differential expression of EEF1E1 in TCGA-LIHC cohort, ( B ) OEP000321 cohort and ( C ) GSE14520 cohort. ( D ) Risk accumulation curve of EEF1E1 mRNA expression for early recurrence in TCGA-LIHC and ( E ) OEP000321 cohort. ( F ) Correlation between EEF1E1 mRNA expression with Rad-scores. ( G ) IHC stains image of EEF1E1 protein levels in HCC and para cancer tissues. (**** p < 0.0001).

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: CT Radiomics Combined with Metabolic-Biomarkers Enables Early Recurrence Prediction in Hepatocellular Carcinoma

    doi: 10.2147/JHC.S547186

    Figure Lengend Snippet: Differential expression and prognostic value of EEF1E1. ( A ) Differential expression of EEF1E1 in TCGA-LIHC cohort, ( B ) OEP000321 cohort and ( C ) GSE14520 cohort. ( D ) Risk accumulation curve of EEF1E1 mRNA expression for early recurrence in TCGA-LIHC and ( E ) OEP000321 cohort. ( F ) Correlation between EEF1E1 mRNA expression with Rad-scores. ( G ) IHC stains image of EEF1E1 protein levels in HCC and para cancer tissues. (**** p < 0.0001).

    Article Snippet: The main steps were as follows: rabbit anti-human EEF1E1 (Proteintech Cat No: 10805-1-AP, 1:200 dilution) was incubated at 4°C overnight, followed by incubation with horseradish peroxidase (HRP)-conjugated secondary antibody (ZSGB-BIO, ZB-2301) for one h at 37°C, and staining with 3,3-diaminobenzidine tetrahydrochloride (DAB).

    Techniques: Quantitative Proteomics, Expressing

    Relation between EEF1E1 protein levels and HCC recurrence status. ( A ) IHC stains image of EEF1E1 protein levels in different recurrence risk of HCC tissues. ( B ) Statistical analysis was performed using the Chi-square test to compare the relative levels of EEF1E1 negative (EEF1E1 − ) or positive (EEF1E1 + ) between HCC with recurrence and HCC without recurrence ( p = 0.010). ( C ) Boxplot of IHC scores of EEF1E1 between non-recurrence and recurrence patients. ( D ) Risk accumulation curve of EEF1E1 protein level for early recurrence in IHC validation cohort. ( E ) Correlation between Rad-scores and EEF1E1 IHC scores.

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: CT Radiomics Combined with Metabolic-Biomarkers Enables Early Recurrence Prediction in Hepatocellular Carcinoma

    doi: 10.2147/JHC.S547186

    Figure Lengend Snippet: Relation between EEF1E1 protein levels and HCC recurrence status. ( A ) IHC stains image of EEF1E1 protein levels in different recurrence risk of HCC tissues. ( B ) Statistical analysis was performed using the Chi-square test to compare the relative levels of EEF1E1 negative (EEF1E1 − ) or positive (EEF1E1 + ) between HCC with recurrence and HCC without recurrence ( p = 0.010). ( C ) Boxplot of IHC scores of EEF1E1 between non-recurrence and recurrence patients. ( D ) Risk accumulation curve of EEF1E1 protein level for early recurrence in IHC validation cohort. ( E ) Correlation between Rad-scores and EEF1E1 IHC scores.

    Article Snippet: The main steps were as follows: rabbit anti-human EEF1E1 (Proteintech Cat No: 10805-1-AP, 1:200 dilution) was incubated at 4°C overnight, followed by incubation with horseradish peroxidase (HRP)-conjugated secondary antibody (ZSGB-BIO, ZB-2301) for one h at 37°C, and staining with 3,3-diaminobenzidine tetrahydrochloride (DAB).

    Techniques: Biomarker Discovery

    Existing studies frame rocaglates as pure eIF4A/translation inhibitors. This study conceptually redefines rocaglates as translation remodelers that reprogram both the translation machinery, e.g., increasing eEF1ε1 translational activity, as well as the translatome, including the upregulation of numerous proteins, e.g., GEF-H1, that mediate rocaglate cytotoxicity in cancer cells. As a proof of concept, GEF-H1 activates RHOA, leading to increased JNK phosphorylation and apoptotic signaling resulting in reduced cell viability.

    Journal: Cell reports

    Article Title: Proteomics reveal cap-dependent translation inhibitors remodel the translation machinery and translatome

    doi: 10.1016/j.celrep.2021.109806

    Figure Lengend Snippet: Existing studies frame rocaglates as pure eIF4A/translation inhibitors. This study conceptually redefines rocaglates as translation remodelers that reprogram both the translation machinery, e.g., increasing eEF1ε1 translational activity, as well as the translatome, including the upregulation of numerous proteins, e.g., GEF-H1, that mediate rocaglate cytotoxicity in cancer cells. As a proof of concept, GEF-H1 activates RHOA, leading to increased JNK phosphorylation and apoptotic signaling resulting in reduced cell viability.

    Article Snippet: eEF1ε1 , Proteintech , Cat#10805-1-AP; RRID:AB_2097140.

    Techniques: Activity Assay, Phospho-proteomics

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: Proteomics reveal cap-dependent translation inhibitors remodel the translation machinery and translatome

    doi: 10.1016/j.celrep.2021.109806

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: eEF1ε1 , Proteintech , Cat#10805-1-AP; RRID:AB_2097140.

    Techniques: Plasmid Preparation, Derivative Assay, Recombinant, Protease Inhibitor, cDNA Synthesis, SYBR Green Assay, Mass Spectrometry, Construct, Software

    The expression of EEF1E1 in HCC. (A) Comparing the expression of EEF1E1 in cancer and normal. (B) Comparing the expression of EEF1E1 in cancer and paracancerous. (C) The expression of EEF1E1 in HCC from Human protein Atlas.

    Journal: Frontiers in Oncology

    Article Title: A Novel HCC Prognosis Predictor EEF1E1 Is Related to Immune Infiltration and May Be Involved in EEF1E1/ATM/p53 Signaling

    doi: 10.3389/fonc.2021.700972

    Figure Lengend Snippet: The expression of EEF1E1 in HCC. (A) Comparing the expression of EEF1E1 in cancer and normal. (B) Comparing the expression of EEF1E1 in cancer and paracancerous. (C) The expression of EEF1E1 in HCC from Human protein Atlas.

    Article Snippet: The immunohistochemistry of EEF1E1 expression in HCC was downloaded from Human Protein Atlas ( ) ( http://www.proteinatlas.org ).

    Techniques: Expressing