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Pesquisa : D12.644.276.382.531 [Categoria DeCS]
Referências encontradas : 19 [refinar]
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  1 / 19 MEDLINE  
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[PMID]:28988771
[Au] Autor:Freed DM; Bessman NJ; Kiyatkin A; Salazar-Cavazos E; Byrne PO; Moore JO; Valley CC; Ferguson KM; Leahy DJ; Lidke DS; Lemmon MA
[Ad] Endereço:Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Cancer Biology Institute, Yale University, West Haven, CT 06516, USA.
[Ti] Título:EGFR Ligands Differentially Stabilize Receptor Dimers to Specify Signaling Kinetics.
[So] Source:Cell;171(3):683-695.e18, 2017 Oct 19.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidermal growth factor receptor (EGFR) regulates many crucial cellular programs, with seven different activating ligands shaping cell signaling in distinct ways. Using crystallography and other approaches, we show how the EGFR ligands epiregulin (EREG) and epigen (EPGN) stabilize different dimeric conformations of the EGFR extracellular region. As a consequence, EREG or EPGN induce less stable EGFR dimers than EGF-making them partial agonists of EGFR dimerization. Unexpectedly, this weakened dimerization elicits more sustained EGFR signaling than seen with EGF, provoking responses in breast cancer cells associated with differentiation rather than proliferation. Our results reveal how responses to different EGFR ligands are defined by receptor dimerization strength and signaling dynamics. These findings have broad implications for understanding receptor tyrosine kinase (RTK) signaling specificity. Our results also suggest parallels between partial and/or biased agonism in RTKs and G-protein-coupled receptors, as well as new therapeutic opportunities for correcting RTK signaling output.
[Mh] Termos MeSH primário: Epigen/química
Epirregulina/química
Receptor do Fator de Crescimento Epidérmico/química
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Mh] Termos MeSH secundário: Cristalografia por Raios X
Epigen/metabolismo
Epirregulina/metabolismo
Transferência Ressonante de Energia de Fluorescência
Seres Humanos
Cinética
Ligantes
Modelos Moleculares
Multimerização Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EPGN protein, human); 0 (EREG protein, human); 0 (Epigen); 0 (Epiregulin); 0 (Ligands); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE


  2 / 19 MEDLINE  
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Barreto, Mauricio L
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[PMID]:25913126
[Au] Autor:Lima-Costa MF; Rodrigues LC; Barreto ML; Gouveia M; Horta BL; Mambrini J; Kehdy FS; Pereira A; Rodrigues-Soares F; Victora CG; Tarazona-Santos E; Epigen-Brazil group
[Ad] Endereço:Fundação Oswaldo Cruz, Instituto de Pesquisas Rene Rachou, Belo Horizonte, Brazil.
[Ti] Título:Genomic ancestry and ethnoracial self-classification based on 5,871 community-dwelling Brazilians (The Epigen Initiative).
[So] Source:Sci Rep;5:9812, 2015 Apr 27.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Brazil never had segregation laws defining membership of an ethnoracial group. Thus, the composition of the Brazilian population is mixed, and its ethnoracial classification is complex. Previous studies showed conflicting results on the correlation between genome ancestry and ethnoracial classification in Brazilians. We used 370,539 Single Nucleotide Polymorphisms to quantify this correlation in 5,851 community-dwelling individuals in the South (Pelotas), Southeast (Bambui) and Northeast (Salvador) Brazil. European ancestry was predominant in Pelotas and Bambui (median = 85.3% and 83.8%, respectively). African ancestry was highest in Salvador (median = 50.5%). The strength of the association between the phenotype and median proportion of African ancestry varied largely across populations, with pseudo R(2) values of 0.50 in Pelotas, 0.22 in Bambui and 0.13 in Salvador. The continuous proportion of African genomic ancestry showed a significant S-shape positive association with self-reported Blacks in the three sites, and the reverse trend was found for self reported Whites, with most consistent classifications in the extremes of the high and low proportion of African ancestry. In self-classified Mixed individuals, the predicted probability of having African ancestry was bell-shaped. Our results support the view that ethnoracial self-classification is affected by both genome ancestry and non-biological factors.
[Mh] Termos MeSH primário: Epigen/genética
Grupos Étnicos/genética
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Africano/genética
Brasil
Criança
Pré-Escolar
Estudos de Coortes
Grupo com Ancestrais do Continente Europeu/genética
Genética Populacional/métodos
Genômica/métodos
Seres Humanos
Estudos Longitudinais
Meia-Idade
Fenótipo
Polimorfismo de Nucleotídeo Único/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Epigen)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170416
[Lr] Data última revisão:
170416
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150428
[St] Status:MEDLINE
[do] DOI:10.1038/srep09812


  3 / 19 MEDLINE  
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[PMID]:24891618
[Au] Autor:Dahlhoff M; Frances D; Kloepper JE; Paus R; Schäfer M; Niemann C; Schneider MR
[Ad] Endereço:Gene Center, LMU Munich, Munich, Germany.
[Ti] Título:Overexpression of epigen during embryonic development induces reversible, epidermal growth factor receptor-dependent sebaceous gland hyperplasia.
[So] Source:Mol Cell Biol;34(16):3086-95, 2014 Aug.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The epidermal growth factor receptor (EGFR) system is a key regulator of epithelial development and homeostasis. Its functions in the sebaceous gland (SG), however, remain poorly characterized. In this study, using a transgenic mouse line with tissue-specific and inducible expression of the EGFR ligand epigen, we showed that increased activation of the EGFR in skin keratinocytes results in enlarged SGs and increased sebum production. The phenotype can be reverted by interrupting transgene expression and is EGFR dependent, as gland size and sebum levels return to normal values after crossing to the EGFR-impaired mouse line Wa5. Intriguingly, however, the SG enlargement appears only if EGFR activation occurs before birth. Importantly, the enlarged sebaceous glands are associated with an increased expression of the transcription factor MYC and of the transmembrane proteins LRIG1, an established negative-feedback regulator of the EGFR/ERBB tyrosine kinase receptors and a stem cell marker. Our findings identify EGFR signaling as a major pathway determining SG activity and suggest a functional relationship between the EGFR/ERBB system and MYC/LRIG1 in the commitment of stem cells toward specific progenitor cell types, with implications for our understanding of their role in tissue development, homeostasis, and disease.
[Mh] Termos MeSH primário: Fator de Crescimento Epidérmico/biossíntese
Receptor do Fator de Crescimento Epidérmico/biossíntese
Glândulas Sebáceas/embriologia
Glândulas Sebáceas/patologia
[Mh] Termos MeSH secundário: Animais
Fator de Crescimento Epidérmico/genética
Epiderme/crescimento & desenvolvimento
Epiderme/patologia
Epigen
Folículo Piloso/crescimento & desenvolvimento
Folículo Piloso/patologia
Hiperplasia/metabolismo
Queratinócitos/metabolismo
Glicoproteínas de Membrana/biossíntese
Camundongos
Camundongos Transgênicos
Proteínas do Tecido Nervoso/biossíntese
Proteínas Proto-Oncogênicas c-myc/biossíntese
Receptor do Fator de Crescimento Epidérmico/genética
Glândulas Sebáceas/secreção
Sebo/secreção
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Epgn protein, mouse); 0 (Epigen); 0 (Lrig1 protein, mouse); 0 (Membrane Glycoproteins); 0 (Nerve Tissue Proteins); 0 (Proto-Oncogene Proteins c-myc); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (EGFR protein, mouse); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140604
[St] Status:MEDLINE
[do] DOI:10.1128/MCB.00302-14


  4 / 19 MEDLINE  
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[PMID]:24503019
[Au] Autor:Schäfer M; Willrodt AH; Kurinna S; Link AS; Farwanah H; Geusau A; Gruber F; Sorg O; Huebner AJ; Roop DR; Sandhoff K; Saurat JH; Tschachler E; Schneider MR; Langbein L; Bloch W; Beer HD; Werner S
[Ad] Endereço:Department of Biology, Institute of Molecular Health Sciences, ETH Zurich Zurich, Switzerland.
[Ti] Título:Activation of Nrf2 in keratinocytes causes chloracne (MADISH)-like skin disease in mice.
[So] Source:EMBO Mol Med;6(4):442-57, 2014 04.
[Is] ISSN:1757-4684
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The transcription factor Nrf2 is a key regulator of the cellular stress response, and pharmacological Nrf2 activation is a promising strategy for skin protection and cancer prevention. We show here that prolonged Nrf2 activation in keratinocytes causes sebaceous gland enlargement and seborrhea in mice due to upregulation of the growth factor epigen, which we identified as a novel Nrf2 target. This was accompanied by thickening and hyperkeratosis of hair follicle infundibula. These abnormalities caused dilatation of infundibula, hair loss, and cyst development upon aging. Upregulation of epigen, secretory leukocyte peptidase inhibitor (Slpi), and small proline-rich protein 2d (Sprr2d) in hair follicles was identified as the likely cause of infundibular acanthosis, hyperkeratosis, and cyst formation. These alterations were highly reminiscent to the phenotype of chloracne/"metabolizing acquired dioxin-induced skin hamartomas" (MADISH) patients. Indeed, SLPI, SPRR2, and epigen were strongly expressed in cysts of MADISH patients and upregulated by dioxin in human keratinocytes in an NRF2-dependent manner. These results identify novel Nrf2 activities in the pilosebaceous unit and point to a role of NRF2 in MADISH pathogenesis.
[Mh] Termos MeSH primário: Cloracne/metabolismo
Queratinócitos/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Cloracne/genética
Modelos Animais de Doenças
Epigen/genética
Epigen/metabolismo
Folículo Piloso/metabolismo
Seres Humanos
Camundongos
Camundongos Transgênicos
Fator 2 Relacionado a NF-E2/genética
Inibidor Secretado de Peptidases Leucocitárias/genética
Inibidor Secretado de Peptidases Leucocitárias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Epigen); 0 (NF-E2-Related Factor 2); 0 (Secretory Leukocyte Peptidase Inhibitor)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140208
[St] Status:MEDLINE
[do] DOI:10.1002/emmm.201303281


  5 / 19 MEDLINE  
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[PMID]:24374012
[Au] Autor:Schneider MR; Yarden Y
[Ad] Endereço:Institute of Molecular Animal Breeding and Biotechnology, Gene Center, LMU Munich, Munich, Germany.
[Ti] Título:Structure and function of epigen, the last EGFR ligand.
[So] Source:Semin Cell Dev Biol;28:57-61, 2014 Apr.
[Is] ISSN:1096-3634
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Epigen is the latest addition to the mammalian family of EGFR ligands. Epigen was initially identified as a novel expressed sequence tag with homology to the EGF family by high throughput sequencing of a mouse keratinocyte complementary DNA library, and received its name for its ability to act as an epithelial mitogen. In vitro studies attributed to epigen several unique features, such as persistent and potent biological actions involving low affinity receptor binding, as well as sub-maximal receptor activation and inactivation. Similarly to the other EGFR ligands, the expression of epigen is up-regulated by hormones and in certain cancer types. While the biological functions of epigen remain to be uncovered, it appears to play a role in epidermal structures, such as the mammary gland and the sebaceous gland. The latter organ, in particular, was greatly enlarged in transgenic mice overexpressing epigen. Interestingly, mice lacking epigen develop and grow normally, probably due to functional compensation by other EGFR ligands. Future studies are likely to reveal the biological roles of the unique receptor binding properties of epigen, as well as its potential harnessing during disease.
[Mh] Termos MeSH primário: Fator de Crescimento Epidérmico/metabolismo
Epigen/metabolismo
Neoplasias/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Epigen/genética
Técnicas de Inativação de Genes
Seres Humanos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Epigen); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131231
[St] Status:MEDLINE


  6 / 19 MEDLINE  
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[PMID]:24354788
[Au] Autor:Nagai K; Arai H; Okudera M; Yamamura T; Oki H; Komiyama K
[Ad] Endereço:Department of Pathology, Nihon University School of Dentistry, Tokyo, Japan.
[Ti] Título:Epiregulin is critical for the acinar cell regeneration of the submandibular gland in a mouse duct ligation model.
[So] Source:J Oral Pathol Med;43(5):378-87, 2014 May.
[Is] ISSN:1600-0714
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Acinar cell regeneration from tubular structures has been reported to occur in duct-deligated salivary glands. However, the detailed process of acinar cell regeneration has not been clarified. We have developed a mouse duct ligation model to clarify the mechanisms underlying acinar cell regeneration, and we analyzed the epidermal growth factor receptor (EGFR) and epidermal growth factor (EGF) ligands using the model. We studied these ligands expressions in the course of acinar cell regeneration using immunohistochemistry and RT-PCR methods. In the duct-ligated portion of the submandibular gland (SMG) that underwent atrophy, newly formed acinar cells were observed arising from the tubular structures after the release of the duct obstruction. The constitutive expression of EGFR was observed by immunohistochemistry in both the duct-ligated and duct-deligated animals as well as in normal controls. The EGFR phosphorylation detected on the tubular structures after duct ligation paralleled the acinar cell regeneration. RT-PCR showed an increase in the epiregulin and heparin-binding EGF levels from day 0 to day 3 after the release of the duct obstruction. The EGF level was increased only after day 7. In vitro, cultured cells isolated from ligated SMGs proliferated and produced EGF ligands following the addition of epiregulin to the culture medium. These findings suggest that the tubular structures localized in an atrophic gland are the source of acinar cell regeneration of the salivary gland. The induction of EGF ligands, in particular epiregulin, may play an important role in acinar cell regeneration in this model.
[Mh] Termos MeSH primário: Células Acinares/fisiologia
Epirregulina/análise
Regeneração/fisiologia
Ductos Salivares/metabolismo
Doenças da Glândula Submandibular/metabolismo
Glândula Submandibular/metabolismo
[Mh] Termos MeSH secundário: Anfirregulina
Animais
Atrofia
Betacelulina/análise
Técnicas de Cultura de Células
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Modelos Animais de Doenças
Família de Proteínas EGF/análise
Fator de Crescimento Epidérmico/análise
Fator de Crescimento Epidérmico/efeitos dos fármacos
Epigen/análise
Epirregulina/farmacologia
Feminino
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/análise
Calicreínas/análise
Calicreínas/efeitos dos fármacos
Ligadura
Camundongos
Camundongos Endogâmicos C57BL
Peptidilprolil Isomerase/análise
Antígeno Nuclear de Célula em Proliferação/análise
Receptor do Fator de Crescimento Epidérmico/análise
Receptor do Fator de Crescimento Epidérmico/efeitos dos fármacos
Ductos Salivares/efeitos dos fármacos
Ductos Salivares/patologia
Glândula Submandibular/patologia
Doenças da Glândula Submandibular/patologia
Fator de Crescimento Transformador alfa/análise
Fator de Crescimento Transformador alfa/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amphiregulin); 0 (Areg protein, mouse); 0 (Betacellulin); 0 (Btc protein, mouse); 0 (EGF Family of Proteins); 0 (Epgn protein, mouse); 0 (Epigen); 0 (Epiregulin); 0 (Ereg protein, mouse); 0 (Heparin-binding EGF-like Growth Factor); 0 (Proliferating Cell Nuclear Antigen); 0 (Transforming Growth Factor alpha); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.21.- (Kallikreins); EC 3.4.99.- (epidermal growth factor binding protein, mouse); EC 5.2.1.8 (Peptidylprolyl Isomerase)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:131221
[St] Status:MEDLINE
[do] DOI:10.1111/jop.12145


  7 / 19 MEDLINE  
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[PMID]:23899604
[Au] Autor:Dahlhoff M; Emrich D; Wolf E; Schneider MR
[Ad] Endereço:Institute of Molecular Animal Breeding and Biotechnology, Laboratory for Functional Genome Analysis (LAFUGA), Gene Center, LMU Munich, 81377 Munich, Germany. Electronic address: dahlhoff@lmb.uni-muenchen.de.
[Ti] Título:Increased activation of the epidermal growth factor receptor in transgenic mice overexpressing epigen causes peripheral neuropathy.
[So] Source:Biochim Biophys Acta;1832(12):2068-76, 2013 Dec.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In the mammalian nervous system, axons are commonly surrounded by myelin, a lipid-rich sheath that is essential for precise and rapid conduction of nerve impulses. In the peripheral nervous system (PNS), myelin sheaths are formed by Schwann cells which wrap around individual axons. While the tyrosine kinase receptors ERBB2 and ERBB3 are established mediators of peripheral myelination, less is known about the functions of the related epidermal growth factor receptor (EGFR) in the regulation of PNS myelination. Here, we report a peripheral neurodegenerative disease caused by increased EGFR activation. Specifically, we characterize a symmetric and distally pronounced, late-onset muscular atrophy in transgenic mice overexpressing the EGFR ligand epigen. Histological examination revealed a demyelinating neuropathy and axon degeneration, and molecular analysis of signaling pathways showed reduced protein kinase B (PKB, AKT) activation in the nerves of Epigen-tg mice, indicating that the muscular phenotype is secondary to PNS demyelination and axon degeneration. Crossing of Epigen-tg mice into an EGFR-deficient background revealed the pathology to be completely EGFR-dependent. This mouse line provides a new model for studying molecular events associated with early stages of peripheral neuropathies, an essential prerequisite for the development of successful therapeutic interventions.
[Mh] Termos MeSH primário: Fator de Crescimento Epidérmico/fisiologia
Atrofia Muscular/etiologia
Doenças do Sistema Nervoso Periférico/etiologia
Receptor do Fator de Crescimento Epidérmico/fisiologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Doenças Desmielinizantes
Epigen
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Atrofia Muscular/metabolismo
Atrofia Muscular/patologia
Bainha de Mielina/metabolismo
Doenças do Sistema Nervoso Periférico/metabolismo
Doenças do Sistema Nervoso Periférico/patologia
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EPGN protein, human); 0 (Epgn protein, mouse); 0 (Epigen); 0 (RNA, Messenger); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (EGFR protein, mouse); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130801
[St] Status:MEDLINE


  8 / 19 MEDLINE  
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[PMID]:23142483
[Au] Autor:Dahlhoff M; Schäfer M; Wolf E; Schneider MR
[Ad] Endereço:Institute of Molecular Animal Breeding and Biotechnology, Gene Center, LMU Munich, Feodor-Lynen-Str. 25, 81377 Munich, Germany.
[Ti] Título:Genetic deletion of the EGFR ligand epigen does not affect mouse embryonic development and tissue homeostasis.
[So] Source:Exp Cell Res;319(4):529-35, 2013 Feb 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The epidermal growth factor receptor (EGFR) is a tyrosine kinase receptor with manifold functions during development, tissue homeostasis and disease. EGFR activation, the formation of homodimers or heterodimers (with the related ERBB2-4 receptors) and downstream signaling is initiated by the binding of a family of structurally related growth factors, the EGFR ligands. Genetic deletion experiments clarified the biological function of all family members except for the last characterized ligand, epigen. We employed gene targeting in mouse embryonic stem cells to generate mice lacking epigen expression. Loss of epigen did not affect mouse development, fertility, or organ physiology. Quantitative RT-PCR analysis revealed increased expression of betacellulin and EGF in a few organs of epigen-deficient mice, suggesting a functional compensation by these ligands. In conclusion, we completed the genetic analysis of EGFR ligands and show that epigen has non-essential functions or functions that can be compensated by other EGFR ligands during growth and tissue homeostasis.
[Mh] Termos MeSH primário: Estruturas Animais/fisiologia
Desenvolvimento Embrionário/genética
Fator de Crescimento Epidérmico/genética
Homeostase/genética
[Mh] Termos MeSH secundário: Estruturas Animais/embriologia
Estruturas Animais/crescimento & desenvolvimento
Estruturas Animais/metabolismo
Animais
Epigen
Feminino
Deleção de Genes
Ligantes
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
Gravidez
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Epgn protein, mouse); 0 (Epigen); 0 (Ligands); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (EGFR protein, mouse); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1303
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121113
[St] Status:MEDLINE


  9 / 19 MEDLINE  
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[PMID]:22451941
[Au] Autor:Voutilainen M; Lindfors PH; Lefebvre S; Ahtiainen L; Fliniaux I; Rysti E; Murtoniemi M; Schneider P; Schmidt-Ullrich R; Mikkola ML
[Ad] Endereço:Developmental Biology Program, Institute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.
[Ti] Título:Ectodysplasin regulates hormone-independent mammary ductal morphogenesis via NF-κB.
[So] Source:Proc Natl Acad Sci U S A;109(15):5744-9, 2012 Apr 10.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ductal growth of the mammary gland occurs in two distinct stages. The first round of branching morphogenesis occurs during embryogenesis, and the second round commences at the onset of puberty. Currently, relatively little is known about the genetic networks that control the initial phases of ductal expansion, which, unlike pubertal development, proceeds independent of hormonal input in female mice. Here we identify NF-κB downstream of the TNF-like ligand ectodysplasin (Eda) as a unique regulator of embryonic and prepubertal ductal morphogenesis. Loss of Eda, or inhibition of NF-κB, led to smaller ductal trees with fewer branches. On the other hand, overexpression of Eda caused a dramatic NF-κB-dependent phenotype in both female and male mice characterized by precocious and highly increased ductal growth and branching that correlated with enhanced cell proliferation. We have identified several putative transcriptional target genes of Eda/NF-κB, including PTHrP, Wnt10a, and Wnt10b, as well as Egf family ligands amphiregulin and epigen. We developed a mammary bud culture system that allowed us to manipulate mammary development ex vivo and found that recombinant PTHrP, Wnt3A, and Egf family ligands stimulate embryonic branching morphogenesis, suggesting that these pathways may cooperatively mediate the effects of Eda.
[Mh] Termos MeSH primário: Ectodisplasinas/metabolismo
Hormônios/farmacologia
Glândulas Mamárias Animais/crescimento & desenvolvimento
Glândulas Mamárias Animais/metabolismo
Morfogênese/efeitos dos fármacos
NF-kappa B/metabolismo
[Mh] Termos MeSH secundário: Anfirregulina
Androgênios/farmacologia
Animais
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Família de Proteínas EGF
Desenvolvimento Embrionário/efeitos dos fármacos
Fator de Crescimento Epidérmico/metabolismo
Epigen
Epitélio/efeitos dos fármacos
Epitélio/crescimento & desenvolvimento
Epitélio/metabolismo
Feminino
Glicoproteínas/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Ligantes
Masculino
Glândulas Mamárias Animais/efeitos dos fármacos
Glândulas Mamárias Animais/patologia
Camundongos
Camundongos Transgênicos
Proteína Relacionada ao Hormônio Paratireóideo/metabolismo
Transcrição Genética/efeitos dos fármacos
Proteínas Wnt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amphiregulin); 0 (Androgens); 0 (Areg protein, mouse); 0 (EGF Family of Proteins); 0 (Ectodysplasins); 0 (Epgn protein, mouse); 0 (Epigen); 0 (Glycoproteins); 0 (Hormones); 0 (Intercellular Signaling Peptides and Proteins); 0 (Ligands); 0 (NF-kappa B); 0 (Parathyroid Hormone-Related Protein); 0 (Wnt Proteins); 62229-50-9 (Epidermal Growth Factor)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:150225
[Lr] Data última revisão:
150225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120328
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1110627109


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[PMID]:22193422
[Au] Autor:Oshima G; Wennerberg J; Yamatodani T; Kjellén E; Mineta H; Johnsson A; Ekblad L
[Ad] Endereço:Department of Otorhinolaryngology, Head and Neck Surgery, Lund University, 221 85 Lund, Sweden.
[Ti] Título:Autocrine epidermal growth factor receptor ligand production and cetuximab response in head and neck squamous cell carcinoma cell lines.
[So] Source:J Cancer Res Clin Oncol;138(3):491-9, 2012 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Predictive strategies for the treatment efficacy of cetuximab are currently not available for head and neck cancer. We investigated the correlation between the expression of epidermal growth factor receptor (EGFR) ligands and EGFR expression, and the growth inhibitory activity of cetuximab in a panel of head and neck squamous cell carcinoma (HNSCC) cell lines. METHODS: The growth inhibiting effect of cetuximab was measured for eight HNSCC cell lines and correlated with the autocrine production of five EGFR ligands as measured by ELISA, and the mRNA expression of two ligands, as measured by quantitative RT-PCR. EGFR expression was assessed by western blot analysis. RESULTS: There was a good correlation between the expression of four of the EGFR ligands (TGF-α, amphiregulin, epiregulin and epigen) and the growth inhibiting effect of cetuximab. TGF-α had the highest predictive potential but had to be combined with epigen for full prediction. EGFR expression also correlated with cetuximab sensitivity but less clearly. CONCLUSIONS: The results indicate that the expression of several EGFR ligands has to be used to predict sensitivity to cetuximab in HNSCC. This has to be further evaluated in clinical samples.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Antineoplásicos/farmacologia
Carcinoma de Células Escamosas/tratamento farmacológico
Fator de Crescimento Epidérmico/biossíntese
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Receptor do Fator de Crescimento Epidérmico/metabolismo
Fator de Crescimento Transformador alfa/biossíntese
[Mh] Termos MeSH secundário: Anfirregulina
Anticorpos Monoclonais Humanizados
Western Blotting
Carcinoma de Células Escamosas/metabolismo
Linhagem Celular Tumoral
Cetuximab
Família de Proteínas EGF
Ensaio de Imunoadsorção Enzimática
Epigen
Epirregulina
Regulação Neoplásica da Expressão Gênica
Glicoproteínas/biossíntese
Neoplasias de Cabeça e Pescoço/metabolismo
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/biossíntese
Ligantes
Valor Preditivo dos Testes
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AREG protein, human); 0 (Amphiregulin); 0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (EGF Family of Proteins); 0 (EPGN protein, human); 0 (EREG protein, human); 0 (Epigen); 0 (Epiregulin); 0 (Glycoproteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Ligands); 0 (Transforming Growth Factor alpha); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); PQX0D8J21J (Cetuximab)
[Em] Mês de entrada:1204
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111224
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-011-1127-5



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