Flow Cytometry: The reagent is designed for analysis of human blood cells using 10 µl reagent / 100 µl of whole blood or 10⁶ cells in a suspension. The content of a vial (1 ml) is sufficient for 100 tests.

Reactivité

Horse, Human

Réactivité croisée

This antibody does not cross react with Mouse or Rat.

Immunogène

Human epidermoid carcinoma line A431.

Hôte

Mouse

Clonalité

Monoclonal

Clone

EGFR1

Isotype

IgG2b

Chaînes légères

kappa

Conjuguer

Excitation: 565nm, Emission: 578nm

Purification

This antibody is conjugated with R-phycoerythrin (PE) under optimum conditions. The conjugate is purified by size-exclusion chromatography; removing unconjugated antibody and free fluorochrome.

Forme du produit

Liquid

Formulation

Supplied in Phosphate Buffered Saline, pH 7.4, with 15 mM Sodium Azide.

Stockage

Shipped at 4°C. Store in the dark at 2-8°C. Do not freeze!

Synonymes

9030024J15Rik, AI552599, Avian erythroblastic leukemia viral (v erb b) oncogene homolog , Avian erythroblastic leukemia viral (verbb) oncogene homolog , Cell growth inhibiting protein 40 , Cell proliferation inducing protein 61 , EGF R, EGFR_HUMAN, Epidermal growth factor receptor, Epidermal growth factor receptor (avian erythroblastic leukemia viral (v erb b) oncogene homolog) , Epidermal growth factor receptor (erythroblastic leukemia viral (v erb b) oncogene homolog avian) , erb-b2 receptor tyrosine kinase 1, Erbb, erbb 1, Erbb1, Errp, Erythroblastic leukemia viral (v erb-b) oncogene homolog, HER1, mENA , NISBD2, Oncogen ERBB, Oncogene ERBB , OTTMUSP00000005385, OTTMUSP00000005386, PIG61, Proto oncogene c ErbB 1, Proto-oncogene c-ErbB-1, Receptor tyrosine protein kinase ErbB 1 , Receptor tyrosine protein kinase ErbB1 , Receptor tyrosine-protein kinase ErbB-1, RP23-295E4.1, SA7, Species antigen 7, Urogastrone, v-erb-b Avian erythroblastic leukemia viral oncogen homolog, wa2, Wa5

Contrôles isotype

Mouse IgG2b [MPC-11] (PE) (A86382)

Avertissement

Ce produit est uniquement destiné à la recherche. Il n'est pas destiné à un usage diagnostique ou thérapeutique.

Images (1)

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Figure 1: Flow Cytometry - Anti-EGFR Antibody [EGFR1] (PE) (A86602)

Surface staining of EGFR on A431 cells with Anti-EGFR Antibody (A86602).

Références pour cet ID de clone (4)

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Long-term expansion of human functional epidermal precursor cells: promotion of extensive amplification by low TGF-beta1 concentrations.

Références : Anti-EGFR Antibody [EGFR1] (PE) (ab130738)

Résumé :

We have previously introduced the concept of high proliferative potential-quiescent (HPP-Q) cells to refer to primitive human hematopoietic progenitors, on which transforming growth factor-beta1 (TGF-beta1) exerts a pleiotropic effect. TGF-beta1 confers to these slow-dividing cells a mitogenic receptor(low) phenotype and maintains immature properties by preventing differentiation and apoptosis. However, the effect of TGF-beta1 on long-term expansion has not yet been clearly demonstrated. Here, we describe the characterization of a human skin keratinocyte subpopulation, highly enriched for primitive epidermal precursors, on the basis of high adhesion capacity (Adh+++) and low expression of the epidermal growth factor receptor (Adh+++EGF-Rlow). In our standard culture condition without feeder cells, the mean estimated output for cells from an unfractionated population of primary foreskin keratinocytes was 10(7)-10(8), increasing to 10(12)-10(13) in cultures initiated with selected Adh+++EGF-Rlow precursors. Characterization of these cells revealed a hitherto unknown property of TGF-beta1: its addition at a very low concentration (10 pg/ml) in long-term cultures induces a very significant additional increase of expansion. In this optimized system, outputs obtained in cultures initiated with Adh+++EGF-Rlow cells repeatedly reached 10(16)-10(17) ( approximately 60 population doublings, approximately 4 x 10(18) keratinocytes produced per clonogenic cell present in the initial population). At the molecular level, this effect is associated with an increase in Smad1, Smad2 and Smad3 phosphorylation and an increase in alpha6 and beta1 integrin expression. No such effect could be observed on mature keratinocytes with low adhesion capacity (Adh-/+). We finally demonstrated that the progeny of Adh+++EGF-Rlow precursors after long-term expansion is still capable of generating a pluristratified epidermis in a model for skin reconstruction. In conclusion, after further characterizing the phenotype of primitive epidermal precursors, we demonstrated a new function of TGF-beta1, which is to promote undifferentiated keratinocyte amplification.

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Expression of a truncated 100 kDa HER2 splice variant acts as an endogenous inhibitor of tumour cell proliferation.

Références : Anti-EGFR Antibody [EGFR1] (PE) (ab130738)

Résumé :

Overexpression of the HER2 (neu/c-erbB-2) oncogene frequently coincides with an aggressive clinical course of certain human adenocarcinomas. Expression and secretion of aberrant HER2 splice variants has been reported in various cell lines and tissues and can interfere with the oncogenic HER2 activity. Here we demonstrate, using two different approaches, that expression of a truncated 100 kDa HER2 variant which encodes the extracellular domain of HER2 (HER-ECD) inhibits growth factor-mediated tumour cell proliferation. A HER2-ECD cDNA encoding the truncated variant was overexpressed in MCF7 breast cancer cells. HER2-ECD overexpression decreased spontaneous proliferation of MCF7 cells as well as heregulin-mediated soft agar colony formation. Concomitantly, heregulin-induced phosphorylation of HER4 as well as downstream activation of p44/p42 MAP-kinases was decreased. To confirm these data, ribozymes were targeted to the 3'-untranslated region of the 2.3 kb HER2-ECD mRNA which is spontaneously expressed in MKN7 gastric cancer cells. HER2-ECD-targeted ribozymes downregulated HER2-ECD expression and enhanced EGF-mediated soft agar colony formation of MKN7 cells. In parallel, EGF-induced activation of p44/p42 MAP-kinases and activation of c-Fos expression were increased in ribozyme-transfected MKN7 cells. Finally, in RT-PCR we found a trend towards a progressive loss of 2.3 kb HER2-ECD mRNA expression in more advanced gastric tumours. These data show that the HER2-ECD variant inhibits growth factor-mediated tumour cell proliferation suggesting an important role during the progression of human cancer.

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Changing patterns of localization of putative stem cells in developing human hair follicles.

Références : Anti-EGFR Antibody [EGFR1] (PE) (ab130738)

Résumé :

In rodents, the hair follicle stem cells lie in a well-defined bulge in the outer root sheath; however, the bulge as a stem cell site of human hair follicle epithelium is still controversial. Epidermal stem cells are thought to express high levels of beta1 integrin and low levels of E-cadherin and beta- and gamma-catenin. In order to clarify the ontogenic distribution of possible stem cells during hair follicle development, the expression patterns of beta1 integrin subunits, E-cadherin, and beta- and gamma-catenins in the skin samples from human fetuses of a series of estimated gestational ages (EGA) were examined. beta1 integrin-rich, E-cadherin-, and beta- and gamma-catenin-poor cells, possible stem cells, were localized to the entire hair germ (65-84 d EGA) and later to the outermost cells of hair peg (85-104 d EGA). In the bulbous hair peg (105-135 d EGA) and in the differentiated lanugo hair follicle (>135 d EGA), they were settled in the bulge and the outermost layer of the outer root sheath. This sequential localization was similar to that of cells rich in epidermal growth factor receptor expression and positive with keratin 19, a putative marker of epidermal stem cells. In addition, these beta1 integrin-rich, E-cadherin-, and beta- and gamma-catenin-poor cells showed similar, undifferentiated morphologic features by electron microscopy. This information of ontogenic localization of possible hair follicle stem cells contributes to the further understanding of mechanisms of human hair follicle morphogenesis and supports the idea that the human fetal hair follicle bulge is a site of stem cells for follicular epithelium.

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Glial progenitor-like phenotype in low-grade glioma and enhanced CD133-expression and neuronal lineage differentiation potential in high-grade glioma.

Références : Anti-EGFR Antibody [EGFR1] (PE) (ab130738)

Résumé :

BACKGROUND:

While neurosphere- as well as xenograft tumor-initiating cells have been identified in gliomas, the resemblance between glioma cells and neural stem/progenitor cells as well as the prognostic value of stem/progenitor cell marker expression in glioma are poorly clarified.

METHODOLOGY/PRINCIPAL FINDINGS:

Viable glioma cells were characterized for surface marker expression along the glial genesis hierarchy. Six low-grade and 17 high-grade glioma specimens were flow-cytometrically analyzed for markers characteristics of stem cells (CD133); glial progenitors (PDGFRalpha, A2B5, O4, and CD44); and late oligodendrocyte progenitors (O1). In parallel, the expression of glial fibrillary acidic protein (GFAP), synaptophysin and neuron-specific enolase (NSE) was immunohistochemically analyzed in fixed tissue specimens. Irrespective of the grade and morphological diagnosis of gliomas, glioma cells concomitantly expressed PDGFRalpha, A2B5, O4, CD44 and GFAP. In contrast, O1 was weakly expressed in all low-grade and the majority of high-grade glioma specimens analyzed. Co-expression of neuronal markers was observed in all high-grade, but not low-grade, glioma specimens analyzed. The rare CD133 expressing cells in low-grade glioma specimens typically co-expressed vessel endothelial marker CD31. In contrast, distinct CD133 expression profiles in up to 90% of CD45-negative glioma cells were observed in 12 of the 17 high-grade glioma specimens and the majority of these CD133 expressing cells were CD31 negative. The CD133 expression correlates inversely with length of patient survival. Surprisingly, cytogenetic analysis showed that gliomas contained normal and abnormal cell karyotypes with hitherto indistinguishable phenotype.

CONCLUSIONS/SIGNIFICANCE:

This study constitutes an important step towards clarification of lineage commitment and differentiation blockage of glioma cells. Our data suggest that glioma cells may resemble expansion of glial lineage progenitor cells with compromised differentiation capacity downstream of A2B5 and O4 expression. The concurrent expression of neuronal markers demonstrates that high-grade glioma cells are endowed with multi-lineage differentiation potential in vivo. Importantly, enhanced CD133 expression marks a poor prognosis in gliomas.

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