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recombinant murine egfr (MedChemExpress)

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MedChemExpress recombinant murine egfr
Recombinant Murine Egfr, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+murine+egfr/EGFR%2C+Mouse/pm41915990-140-0-3
Average 94 stars, based on 1 article reviews

recombinant murine egfr - by Bioz Stars, 2026-10

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Article Title: Vitamin E alleviates experimental autoimmune prostatitis by inhibiting the EGFR/MAPK pathway to reduce M1 macrophage polarization.
Article Snippet: SPR analysis was performed on a Biacore 8 K instrument (Cytiva). .. Recombinant murine EGFR (MedChemExpress, HY-P72989) was immobilized on a CM5 sensor chip via amine coupling in 10 mM sodium acetate (pH 4.5), reaching ~12,600 RU. .. Vitamin E (Selleck, #S4686) was serially diluted in PBST containing 1% DMSO (0.01–5 μM) and injected over the surface at 30 μL/min (association: 100 s, dissociation: 180 s).

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Human cardiac myocytes (HCM) were exposed to hypoxia (1% oxygen) and different time points were assessed. A ERBB1 transcript levels at different time points during hypoxia (n=3 per time point). B ERBB1 protein levels at different time points during hypoxia; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. C Densitometry of ERBB1 western blots. A significant fold change was seen beginning at 8 hours of hypoxia (n=3 per time point). D Schematic illustrating the experimental design of ischemia in mice. Mice receiving no ischemia (−I) were intubated and put on ventilation. Carotid artery catheter was placed, and normal saline was supplied. After thoracotomy, a suture was placed underneath the left coronary artery (LCA). However, no hanging weight was applied. Mice receiving ischemia (+I) was treated the same way, but hanging weight was applied for total occlusion of the LCA. E ErbB1 transcript levels comparing no ischemia (−I) and 45 minutes’ ischemia (+I) in the Area-at-Risk (AAR) (n=7 per group). One observation from each group was removed as outliers. F ERBB1 protein levels comparing no ischemia (−I) and ischemia (+I) in the AAR; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. G Densitometry of ERBB1 western blots (n≥5 per group). *p<0.05, **p<0.01, n.s., nonsignificant. Data are presented as the mean ± SD. (A, C) One-way ANOVA and Bonferroni adjustment for comparisons with values at time zero (E, G) unpaired, two-tailed t-test. A total of 24 mice were used in the studies for Figure 2, and two results were excluded from the analysis. A F5,12=2.37, p=0.102 C F5,12=5.62, p=0.007 E t=−0.16, df=10 G t=−2.72, df=10

Journal: Anesthesiology

Article Title: Transcription-independent induction of ERBB1 through hypoxia-inducible factor HIF2A provides cardio-protection during ischemia and reperfusion

doi: 10.1097/ALN.0000000000003037

Figure Lengend Snippet: Human cardiac myocytes (HCM) were exposed to hypoxia (1% oxygen) and different time points were assessed. A ERBB1 transcript levels at different time points during hypoxia (n=3 per time point). B ERBB1 protein levels at different time points during hypoxia; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. C Densitometry of ERBB1 western blots. A significant fold change was seen beginning at 8 hours of hypoxia (n=3 per time point). D Schematic illustrating the experimental design of ischemia in mice. Mice receiving no ischemia (−I) were intubated and put on ventilation. Carotid artery catheter was placed, and normal saline was supplied. After thoracotomy, a suture was placed underneath the left coronary artery (LCA). However, no hanging weight was applied. Mice receiving ischemia (+I) was treated the same way, but hanging weight was applied for total occlusion of the LCA. E ErbB1 transcript levels comparing no ischemia (−I) and 45 minutes’ ischemia (+I) in the Area-at-Risk (AAR) (n=7 per group). One observation from each group was removed as outliers. F ERBB1 protein levels comparing no ischemia (−I) and ischemia (+I) in the AAR; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. G Densitometry of ERBB1 western blots (n≥5 per group). *p<0.05, **p<0.01, n.s., nonsignificant. Data are presented as the mean ± SD. (A, C) One-way ANOVA and Bonferroni adjustment for comparisons with values at time zero (E, G) unpaired, two-tailed t-test. A total of 24 mice were used in the studies for Figure 2, and two results were excluded from the analysis. A F5,12=2.37, p=0.102 C F5,12=5.62, p=0.007 E t=−0.16, df=10 G t=−2.72, df=10

Article Snippet: Proteins were transferred to nitrocellulose membranes by Trans-Blot Turbo system (Cat#1704150, Biorad) and were detected using specific primary antibodies as specified: Human ERBB1 (Cell signaling, Cat#4267; , , , , and ), murine ERBB1 (Abcam, Cat#ab52894; , , and ), RBM4 (Santa Cruz, Cat#sc373852), phosphorylated AKT (Cell signaling, Cat#9271), total AKT (Cell signaling, Cat#9272), β-actin (EMD Millipore, Cat#cp01).

Techniques: Western Blot, Two Tailed Test

(A-C) HIF1A and HIF2A were knocked down in HCM using short hairpin RNAs (shRNA) by lentiviral transfection. shControl HCM were transfected with lentivirus containing an empty vector. A ERBB1 transcript levels in normoxic (Nx) and hypoxic (1% oxygen; Hx) conditions (n≥4 per group). HCM were exposed to normoxia or hypoxia for 16 hours. B ERBB1 protein levels in normoxic (Nx) and hypoxic (Hx) conditions; β-ACTIN was used as a loading control. One representative blot from two independent experiments is shown. C Densitometry of ERBB1 western blots (n≥2 per group). No significant difference was found comparing Nx and Hx conditions in shHIF2A HCM. D ErbB1 transcript levels comparing no ischemia (−I) and ischemia (+I) in the AAR in Myosin Cre+ and Hif2aloxP/loxP Myosin Cre+ mice. Mice underwent no ischemia or 45 minutes of ischemia by total occlusion of the LCA. Heart samples were collected from n≥6 mice per group. One observation was removed as an outlier from the +I group of Hif2aloxP/loxP Myosin Cre+ mice. E ERBB1 protein levels in the AAR comparing no ischemia (−I) and ischemia (+I) in the AAR in Myosin Cre+ and Hif2aloxP/loxP Myosin Cre+ mice; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. F Densitometry of ERBB1 western blots (n≥6 per group). *p<0.05, **p<0.01, n.s., nonsignificant. One observation was removed as an outlier from the −I group of Myosin Cre+ mice. Two animals did not survive and were excluded from the −I group of Hif2aloxP/loxP Myosin Cre+ mice. Data are presented as the mean ± SD. (A, C, D, and F) Two-way ANOVA and Bonferroni adjustment for comparisons between Nx and Hx, −I and +I. A total of 42 mice were used in the studies for Figure 3, and four results were excluded from the analysis. A F5,27=0.93, p=0.474 C F5,11=3.68, p=0.033 D F3,24=0.83, p=0.490 F F3,22=8.99, p<0.001

Journal: Anesthesiology

Article Title: Transcription-independent induction of ERBB1 through hypoxia-inducible factor HIF2A provides cardio-protection during ischemia and reperfusion

doi: 10.1097/ALN.0000000000003037

Figure Lengend Snippet: (A-C) HIF1A and HIF2A were knocked down in HCM using short hairpin RNAs (shRNA) by lentiviral transfection. shControl HCM were transfected with lentivirus containing an empty vector. A ERBB1 transcript levels in normoxic (Nx) and hypoxic (1% oxygen; Hx) conditions (n≥4 per group). HCM were exposed to normoxia or hypoxia for 16 hours. B ERBB1 protein levels in normoxic (Nx) and hypoxic (Hx) conditions; β-ACTIN was used as a loading control. One representative blot from two independent experiments is shown. C Densitometry of ERBB1 western blots (n≥2 per group). No significant difference was found comparing Nx and Hx conditions in shHIF2A HCM. D ErbB1 transcript levels comparing no ischemia (−I) and ischemia (+I) in the AAR in Myosin Cre+ and Hif2aloxP/loxP Myosin Cre+ mice. Mice underwent no ischemia or 45 minutes of ischemia by total occlusion of the LCA. Heart samples were collected from n≥6 mice per group. One observation was removed as an outlier from the +I group of Hif2aloxP/loxP Myosin Cre+ mice. E ERBB1 protein levels in the AAR comparing no ischemia (−I) and ischemia (+I) in the AAR in Myosin Cre+ and Hif2aloxP/loxP Myosin Cre+ mice; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. F Densitometry of ERBB1 western blots (n≥6 per group). *p<0.05, **p<0.01, n.s., nonsignificant. One observation was removed as an outlier from the −I group of Myosin Cre+ mice. Two animals did not survive and were excluded from the −I group of Hif2aloxP/loxP Myosin Cre+ mice. Data are presented as the mean ± SD. (A, C, D, and F) Two-way ANOVA and Bonferroni adjustment for comparisons between Nx and Hx, −I and +I. A total of 42 mice were used in the studies for Figure 3, and four results were excluded from the analysis. A F5,27=0.93, p=0.474 C F5,11=3.68, p=0.033 D F3,24=0.83, p=0.490 F F3,22=8.99, p<0.001

Techniques: shRNA, Transfection, Plasmid Preparation, Western Blot

A ERBB1 transcript levels comparing healthy control (C) tissues and tissues from ischemic heart disease (IHD) patients (n=10 in both groups). B ERBB1 protein levels comparing C tissues and IHD patients’ tissue; β-ACTIN was used as a loading control. One representative blot from two independent experiments is shown. C Densitometry of ERBB1 western blots for C tissues and IHD patients’ tissue (n=5 in both groups). ***p<0.001, n.s., nonsignificant. Data are presented as the mean ± SD. (A, C) Two-tailed Satterthwaite t-test. A t=−2.07, df=11.32 c t=−5.37, df=4.09

Journal: Anesthesiology

Article Title: Transcription-independent induction of ERBB1 through hypoxia-inducible factor HIF2A provides cardio-protection during ischemia and reperfusion

doi: 10.1097/ALN.0000000000003037

Figure Lengend Snippet: A ERBB1 transcript levels comparing healthy control (C) tissues and tissues from ischemic heart disease (IHD) patients (n=10 in both groups). B ERBB1 protein levels comparing C tissues and IHD patients’ tissue; β-ACTIN was used as a loading control. One representative blot from two independent experiments is shown. C Densitometry of ERBB1 western blots for C tissues and IHD patients’ tissue (n=5 in both groups). ***p<0.001, n.s., nonsignificant. Data are presented as the mean ± SD. (A, C) Two-tailed Satterthwaite t-test. A t=−2.07, df=11.32 c t=−5.37, df=4.09

Techniques: Western Blot, Two Tailed Test

A RBM4 transcript levels after knockdown of RBM4 (n≥5 per group). B RBM4 protein levels after knockdown of RBM4. One representative blot from three independent experiments is shown. C ERBB1 protein levels in Nx and Hx; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. D Densitometry of ERBB1 western blots (n=4 per group). *p<0.05, ***p<0.001, n.s., nonsignificant. Data are presented as the mean ± SD. A unpaired, two-tailed t-test. D Two-way ANOVA and Bonferroni adjustment for comparisons between Nx and Hx. A t=12.56, df=9 D F3,12=12.32, p<0.001

Journal: Anesthesiology

Article Title: Transcription-independent induction of ERBB1 through hypoxia-inducible factor HIF2A provides cardio-protection during ischemia and reperfusion

doi: 10.1097/ALN.0000000000003037

Figure Lengend Snippet: A RBM4 transcript levels after knockdown of RBM4 (n≥5 per group). B RBM4 protein levels after knockdown of RBM4. One representative blot from three independent experiments is shown. C ERBB1 protein levels in Nx and Hx; β-ACTIN was used as a loading control. One representative blot from three independent experiments is shown. D Densitometry of ERBB1 western blots (n=4 per group). *p<0.05, ***p<0.001, n.s., nonsignificant. Data are presented as the mean ± SD. A unpaired, two-tailed t-test. D Two-way ANOVA and Bonferroni adjustment for comparisons between Nx and Hx. A t=12.56, df=9 D F3,12=12.32, p<0.001

Techniques: Western Blot, Two Tailed Test

(A-D) ERBB1 was knocked down using shRNA in HCM via lentiviral transfection. The shControl was transfected with lentivirus containing an empty vector. A ERBB1 transcript levels after knockdown of ERBB1 (n=3 per group). B ERBB1 protein levels in normoxia (Nx) and hypoxia (Hx); β-ACTIN was used as a loading control. HCM cells were exposed to normoxia (Nx) or hypoxia (1% oxygen) for 16 hours. One representative blot from two independent experiments is shown. C pAkt (Ser473) levels were assessed in shControl and shERBB1 HCM after 16 hours of normoxia (Nx) or hypoxia (Hx), followed with or without subsequent 20 nM amphiregulin (AREG) treatment for 10 minutes (+A). One representative blot from three independent experiments is shown. D Densitometry of phosphorylated Akt western blots, which is expressed as a ratio of phosphorylated Akt to total Akt (pAkt/tAkt) (n=3 per group). *p<0.05, n.s., nonsignificant. Data are presented as the mean ± SD. A unpaired, two-tailed t-test. D Three-way ANOVA and Bonferroni adjustment for comparisons between Nx and Hx, as well as between with and without +A. A t=2.87, df=4 D F7,16=3.8, p=0.013

Journal: Anesthesiology

Article Title: Transcription-independent induction of ERBB1 through hypoxia-inducible factor HIF2A provides cardio-protection during ischemia and reperfusion

doi: 10.1097/ALN.0000000000003037

Figure Lengend Snippet: (A-D) ERBB1 was knocked down using shRNA in HCM via lentiviral transfection. The shControl was transfected with lentivirus containing an empty vector. A ERBB1 transcript levels after knockdown of ERBB1 (n=3 per group). B ERBB1 protein levels in normoxia (Nx) and hypoxia (Hx); β-ACTIN was used as a loading control. HCM cells were exposed to normoxia (Nx) or hypoxia (1% oxygen) for 16 hours. One representative blot from two independent experiments is shown. C pAkt (Ser473) levels were assessed in shControl and shERBB1 HCM after 16 hours of normoxia (Nx) or hypoxia (Hx), followed with or without subsequent 20 nM amphiregulin (AREG) treatment for 10 minutes (+A). One representative blot from three independent experiments is shown. D Densitometry of phosphorylated Akt western blots, which is expressed as a ratio of phosphorylated Akt to total Akt (pAkt/tAkt) (n=3 per group). *p<0.05, n.s., nonsignificant. Data are presented as the mean ± SD. A unpaired, two-tailed t-test. D Three-way ANOVA and Bonferroni adjustment for comparisons between Nx and Hx, as well as between with and without +A. A t=2.87, df=4 D F7,16=3.8, p=0.013

Techniques: shRNA, Transfection, Plasmid Preparation, Western Blot, Two Tailed Test

Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice were given tamoxifen daily at a dose of 1 mg via intraperitoneal injection for 5 consecutive days. Animals were then given a recovery period of 7 days. A ERBB1 protein levels after tamoxifen-induced in vivo knockout of ErbB1 in cardiac myocyte; β-ACTIN was used as a loading control. Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice underwent 45 minutes of ischemia by total occlusion of LCA. One representative blot from three independent experiments is shown. B Densitometry of ERBB1 western blots (n=4 per group). C Schematic of how surgery was performed. Infarct size was measured after double staining with 1% Evan’s blue and 1% triphenyltetrazolium chloride (TTC). Infarct sizes were normalized by percentage of infarct size to the AAR. D Infarct size after 45 minutes of ischemia and 2 hours of reperfusion in Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice (n=5 per group). E Representative infarct staining results from Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice. F Cardiac troponin I (TnI) levels determined by ELISA. Blood was collected from the portal vein after 45 minutes of ischemia and 2 hours of reperfusion in Myosin Cre+ (n=6) and ErbB1loxP/loxP Myosin Cre+ mice (n=7). The difference between infarct size measurement and cardiac TnI sample number are addressed in the methods section. *p<0.05, ***p<0.001, n.s., nonsignificant. Data are presented as the mean ± SD. (B, D, and F) unpaired, two-tailed t-test. A total of 10 mice were used in the studies for Figure 5, and none of the results were excluded from the analysis. B t=3.32, df=6 D t=−5.33, df=8 F t=−2.67, df=12

Journal: Anesthesiology

Article Title: Transcription-independent induction of ERBB1 through hypoxia-inducible factor HIF2A provides cardio-protection during ischemia and reperfusion

doi: 10.1097/ALN.0000000000003037

Figure Lengend Snippet: Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice were given tamoxifen daily at a dose of 1 mg via intraperitoneal injection for 5 consecutive days. Animals were then given a recovery period of 7 days. A ERBB1 protein levels after tamoxifen-induced in vivo knockout of ErbB1 in cardiac myocyte; β-ACTIN was used as a loading control. Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice underwent 45 minutes of ischemia by total occlusion of LCA. One representative blot from three independent experiments is shown. B Densitometry of ERBB1 western blots (n=4 per group). C Schematic of how surgery was performed. Infarct size was measured after double staining with 1% Evan’s blue and 1% triphenyltetrazolium chloride (TTC). Infarct sizes were normalized by percentage of infarct size to the AAR. D Infarct size after 45 minutes of ischemia and 2 hours of reperfusion in Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice (n=5 per group). E Representative infarct staining results from Myosin Cre+ and ErbB1loxP/loxP Myosin Cre+ mice. F Cardiac troponin I (TnI) levels determined by ELISA. Blood was collected from the portal vein after 45 minutes of ischemia and 2 hours of reperfusion in Myosin Cre+ (n=6) and ErbB1loxP/loxP Myosin Cre+ mice (n=7). The difference between infarct size measurement and cardiac TnI sample number are addressed in the methods section. *p<0.05, ***p<0.001, n.s., nonsignificant. Data are presented as the mean ± SD. (B, D, and F) unpaired, two-tailed t-test. A total of 10 mice were used in the studies for Figure 5, and none of the results were excluded from the analysis. B t=3.32, df=6 D t=−5.33, df=8 F t=−2.67, df=12

Techniques: Injection, In Vivo, Knock-Out, Western Blot, Double Staining, Staining, Enzyme-linked Immunosorbent Assay, Two Tailed Test

During myocardial ischemia and reperfusion injury, the heart experiences significant hypoxia. Hypoxia stabilizes transcription factor HIF2A, which is then recruited by RBM4 to the RNA hypoxia response element (rHRE). This complex initiates the translation of ErbB1 mRNA to produce ERBB1 protein. Also upregulated during myocardial injury is AREG. HIF2A binds to the AREG promotor and increases the transcription of AREG gene. Finally, increased AREG protein binds to the increased ERBB1 receptors and activate important ERBB1 downstream signaling cascades, such as Akt, to provide cardio-protection.

Journal: Anesthesiology

Article Title: Transcription-independent induction of ERBB1 through hypoxia-inducible factor HIF2A provides cardio-protection during ischemia and reperfusion

doi: 10.1097/ALN.0000000000003037

Figure Lengend Snippet: During myocardial ischemia and reperfusion injury, the heart experiences significant hypoxia. Hypoxia stabilizes transcription factor HIF2A, which is then recruited by RBM4 to the RNA hypoxia response element (rHRE). This complex initiates the translation of ErbB1 mRNA to produce ERBB1 protein. Also upregulated during myocardial injury is AREG. HIF2A binds to the AREG promotor and increases the transcription of AREG gene. Finally, increased AREG protein binds to the increased ERBB1 receptors and activate important ERBB1 downstream signaling cascades, such as Akt, to provide cardio-protection.

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