- 44-784G - Invitrogen Antibodies EGFR antibody

Submitted references Extreme Trait Whole-Genome Sequencing Identifies PTPRO as a Novel Candidate Gene in Emphysema with Severe Airflow Obstruction.

Radder JE, Zhang Y, Gregory AD, Yu S, Kelly NJ, Leader JK, Kaminski N, Sciurba FC, Shapiro SD
American journal of respiratory and critical care medicine 2017 Jul 15;196(2):159-171

Targeting miR-146a to treat delayed wound healing in human diabetic organ-cultured corneas.

Winkler MA, Dib C, Ljubimov AV, Saghizadeh M
PloS one 2014;9(12):e114692

Normalization of wound healing and stem cell marker patterns in organ-cultured human diabetic corneas by gene therapy of limbal cells.

Saghizadeh M, Dib CM, Brunken WJ, Ljubimov AV
Experimental eye research 2014 Dec;129:66-73

Differentially expressed wound healing-related microRNAs in the human diabetic cornea.

Funari VA, Winkler M, Brown J, Dimitrijevich SD, Ljubimov AV, Saghizadeh M
PloS one 2013;8(12):e84425

Enhanced wound healing, kinase and stem cell marker expression in diabetic organ-cultured human corneas upon MMP-10 and cathepsin F gene silencing.

Saghizadeh M, Epifantseva I, Hemmati DM, Ghiam CA, Brunken WJ, Ljubimov AV
Investigative ophthalmology & visual science 2013 Dec 17;54(13):8172-80

Adenovirus-driven overexpression of proteinases in organ-cultured normal human corneas leads to diabetic-like changes.

Saghizadeh M, Kramerov AA, Yaghoobzadeh Y, Hu J, Ljubimova JY, Black KL, Castro MG, Ljubimov AV
Brain research bulletin 2010 Feb 15;81(2-3):262-72

Sialyl Lewis X modification of the epidermal growth factor receptor regulates receptor function during airway epithelial wound repair.

Allahverdian S, Wang A, Singhera GK, Wong BW, Dorscheid DR
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 2010 Apr;40(4):607-18

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot using EGFR (pY845) polyclonal antibody, rabbit.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Immunofluorescence analysis of EGFR [pY845] was performed using 90% confluent log phase A-431 cells treated with 200 ng/mL of EGF for 10 minutes. The cells were fixed with 4% paraformaldehyde for 10 minutes, permeabilized with 0.1% Triton™ X-100 for 10 minutes, and blocked with 1% BSA for 1 hour at room temperature. The cells were labeled with Phospho-EGFR (Tyr845) Rabbit Polyclonal Antibody (Product # 44-784G) at 1:250 dilution in 0.1% BSA and incubated overnight at 4 degree Celsius and then labeled with Goat anti-Rabbit IgG (H+L) Superclonal™ Secondary Antibody, Alexa Fluor® 488 conjugate (Product # A27034) at a dilution of 1:2000 for 45 minutes at room temperature (Panel a: green). Nuclei (Panel b: blue) were stained with SlowFade® Gold Antifade Mountant with DAPI (Product # S36938). F-actin (Panel c: red) was stained with Rhodamine Phalloidin (Product # R415, 1:300). Panel d represents the merged image showing membranous and cytoplasmic localization. Panel e represents cells treated with antagonist, Afatinib (1µM for 6hrs) followed by EGF (200 ng/mL for 10 minutes), showing reduced Phospho-EGFR staining. Panel f shows untreated cells with no signal. Panel g represents control cells with no primary antibody to assess background. The images were captured at 60X magnification.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Immunofluorescence analysis of EGFR (pY845) was done on 70% confluent log phase HeLa cells treated with EGF (200 ng/mL for 10 min). The cells were fixed with 4% paraformaldehyde for 15 minutes, permeabilized with 0.25% Triton™ X-100 for 10 minutes, and blocked with 5% BSA for 1 hour at room temperature. The cells were labeled with EGFR (pY845) Rabbit polyclonal Antibody (Product # 44-784G) at 1:250 dilution in 1% BSA and incubated for 3 hours at room temperature and then labeled with Alexa Fluor 488 Goat Anti-Rabbit IgG Secondary Antibody (Product # A-11008) at a dilution of 1:400 for 30 minutes at room temperature (Panel a: green). Nuclei (Panel b: blue) were stained with SlowFade® Gold Antifade Mountant DAPI (Product # S36938). F-actin (Panel c: red) was stained with Alexa Fluor 594 Phalloidin (Product # A12381). Panel d is a merged image showing cytoplasmic localization. Panel e shows untreated cells. Panel f shows no primary antibody control. The images were captured at 20X magnification.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 Western blot analysis of EGFR and p-EGFR expression in transfected HCEC. Total extracted protein from HCEC transfected with pre-miRNA precursors or their inhibitors (antagomirs, AM) and Cy3-labeled pre-miRNA (control) was separated on gradient SDS-PAGE gels, transferred to nitrocellulose and probed with antibodies to EGFR or p-EGFR. Antibodies to beta-tubulin or beta-actin were used as equal loading controls and for semi-quantitation. In both wounded and non-wounded HCEC, miR-146a mimic treatment decreased whereas its antagomir increased protein levels of p-EGFR (A,B). MiR-424 mimic and antagomir treatments did not change the expression of p-EGFR in non-wounded cells (A,B). However, in wounded cells, miR-424 mimic decreased whereas its antagomir increased protein levels of p-EGFR (A,B). In both wounded and non-wounded HCEC, miR-146a mimic treatment decreased whereas its antagomir significantly increased protein levels of total EGFR (C,D). MiR-424 mimic and antagomir treatments did not significantly change the expression of EGFR both in wounded and non-wounded cells (C,D). Band intensities were quantified using ImageJ software and plotted relative to the loading controls. Blots in A were developed with alkaline phosphatase system, blots in C, with ECL reagent. *, p < 0.05.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 Western analyses of activated signaling molecules in transfected primary normal LEC. A. Total extracted protein from normal LEC transfected with pre-miRNA precursors or their inhibitors and Cy3-labeled pre-miRNA (control) was separated on gradient SDS-PAGE gels, transferred to nitrocellulose and probed with primary antibodies. Antibodies to beta-tubulin or beta-actin were used as loading controls and for semi-quantitation. MiR-146a treatment decreased, whereas its inhibitor increased, protein levels of p-EGFR, p-ERK1/2, p-p38, and not significantly, p-Akt. B. Quantitation of activated signaling molecules. The bar graph represents average +- SEM of pooled values (n = 4) of densitometric scans. *P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 6 MiR-424 and wound healing-related signaling molecules. In wounded HCEC cultures, miR-424 elevated in diabetes decreased staining for p-p38, p-Akt and especially, for p-EGFR. Conversely, antagomir (AM) treatment increased the expression of all tested activated signaling intermediates above control levels. Exposure times are the same for all panels in a row. W, wound area. Bar = 60 mum.

44-784G

Antibody data