EGF receptor ligands | ScienceGate

The growth factor/receptor combination of hepatocyte growth factor (HGF)/c-met has been postulated to be critical for mesenchymal-to-epithelial conversion and tubule formation in the developing kidney. We therefore isolated and immortalized cells from embryonic kidneys of met -/- transgenic mice to determine whether these cells were epithelial and able to chemotax and form tubules in vitro. The cells were immortalized with retrovirus expressing human papillomavirus 16 (HPV 16) E6/E7 genes. Two rapidly dividing clones were isolated and found to express the epithelial cell markers cytokeratin, zonula occludens-1, and E-cadherin but not to express the fibroblast marker vimentin. The met -/- cells were able to chemotax in response to epidermal growth factor and transforming growth factor-alpha (TGF-alpha) and form tubules in vitro in response to TGF-alpha but not HGF. These experiments suggest that the HGF/c-met axis is not essential for epithelial cell development in the embryonic kidney and demonstrate that other growth factors are capable of supporting early tubulogenesis.

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Mouse Chromosomal Location of Three EGF Receptor Ligands: Amphiregulin (Areg), Betacellulin (Btc), and Heparin-Binding EGF (Hegfl)

Genomics ◽

10.1006/geno.1995.1116 ◽

1995 ◽

Vol 28 (1) ◽

pp. 116-118 ◽

Cited By ~ 15

Author(s):

Bhavani G. Pathak ◽

Debra J. Gilbert ◽

Charles A. Harrison ◽

Noreen C. Luetteke ◽

Xiaorong Chen ◽

...

Keyword(s):

Egf Receptor ◽

Chromosomal Location ◽

Heparin Binding ◽

Receptor Ligands

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Concentration of epidermal growth factor (EGF) receptor ligands in the urine of breast cancer patients & control subjects

Regulatory Peptides ◽

10.1016/0167-0115(92)90572-c ◽

1992 ◽

Vol 39 (2-3) ◽

pp. 262

Author(s):

J. Nelson ◽

P. McAleese ◽

F. Zhong ◽

N.V. McFerran ◽

W. Odling-Smee

Keyword(s):

Breast Cancer ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Cancer Patients ◽

Egf Receptor ◽

Breast Cancer Patients ◽

Receptor Ligands ◽

Control Subjects ◽

Epidermal Growth

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FRMD8 promotes inflammatory and growth factor signalling by stabilising the iRhom/ADAM17 sheddase complex

10.1101/255802 ◽

2018 ◽

Author(s):

Ulrike Künzel ◽

Adam G. Grieve ◽

Yao Meng ◽

Sally A. Cowley ◽

Matthew Freeman

Keyword(s):

Growth Factor ◽

Cell Surface ◽

Inflammatory Cytokine ◽

Egf Receptor ◽

Receptor Ligands ◽

Ferm Domain ◽

Human Macrophages ◽

Mouse Tissues ◽

N Terminus ◽

Growth Factor Signalling

AbstractMany intercellular signals are synthesised as transmembrane precursors that are released by proteolytic cleavage (‘shedding’) from the cell surface. ADAM17, a membrane-tethered metalloprotease, is the primary shedding enzyme responsible for the release of the inflammatory cytokine TNFα and several EGF receptor ligands. ADAM17 exists in complex with the rhomboid-like iRhom proteins, which act as cofactors that regulate ADAM17 substrate shedding. Here we report that the poorly characterised FERM domain-containing protein FRMD8 is a new component of iRhom2/ADAM17 sheddase complex. FRMD8 binds to the cytoplasmic N-terminus of iRhoms, and is necessary to stabilise the iRhoms and ADAM17 beyond the Golgi. In the absence of FRMD8, iRhom2 and ADAM17 are degraded via the endolysosomal pathway, resulting in the reduction of ADAM17-mediated shedding. We have confirmed the pathophysiological significance of FRMD8 in iPSC-derived human macrophages and mouse tissues, thus demonstrating its role in the regulated release of multiple cytokine and growth factor signals.

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Different Epidermal Growth Factor (EGF) Receptor Ligands Show Distinct Kinetics and Biased or Partial Agonism for Homodimer and Heterodimer Formation

Journal of Biological Chemistry ◽

10.1074/jbc.m114.586826 ◽

2014 ◽

Vol 289 (38) ◽

pp. 26178-26188 ◽

Cited By ~ 63

Author(s):

Jennifer L. Macdonald-Obermann ◽

Linda J. Pike

Keyword(s):

Growth Factor ◽

Epidermal Growth Factor ◽

Egf Receptor ◽

Receptor Ligands ◽

Partial Agonism ◽

Epidermal Growth

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Insulin Signaling in Intestinal Stem and Progenitor Cells as an Important Determinant of Physiological and Metabolic Traits in Drosophila

Cells ◽

10.3390/cells9040803 ◽

2020 ◽

Vol 9 (4) ◽

pp. 803 ◽

Cited By ~ 1

Author(s):

Olha M. Strilbytska ◽

Uliana V. Semaniuk ◽

Kenneth B. Storey ◽

Ihor S. Yurkevych ◽

Oleh Lushchak

Keyword(s):

Progenitor Cells ◽

Insulin Signaling ◽

Egf Receptor ◽

The Body ◽

Receptor Ligands ◽

Adipokinetic Hormone ◽

Peripheral Tissues ◽

Genes Encoding ◽

Stem And Progenitor Cells ◽

Multicellular Organisms

The insulin–IGF-1 signaling (IIS) pathway is conserved throughout multicellular organisms and regulates many traits, including aging, reproduction, feeding, metabolism, stress resistance, and growth. Here, we present evidence of a survival-sustaining role for IIS in a subset of gut cells in Drosophila melanogaster, namely the intestinal stem cells (ISCs) and progenitor cells. Using RNAi to knockdown the insulin receptor, we found that inhibition of IIS in ISCs statistically shortened the lifespan of experimental flies compared with non-knockdown controls, and also shortened their survival under starvation or malnutrition conditions. These flies also showed decreased reproduction and feeding, and had lower amounts of glycogen and glucose in the body. In addition, increased expression was observed for the Drosophila transcripts for the insulin-like peptides dilp2, dilp5, and dilp6. This may reflect increased insulin signaling in peripheral tissues supported by up-regulation of the target of the brain insulin gene (tobi). In contrast, activation of IIS (via knockdown of the insulin pathway inhibitor PTEN) in intestinal stem and progenitor cells decreased fly resistance to malnutrition, potentially by affecting adipokinetic hormone signaling. Finally, Pten knockdown to enhance IIS also activated JAK–STAT signaling in gut tissue by up-regulation of upd2, upd3, and soc36 genes, as well as genes encoding the EGF receptor ligands spitz and vein. These results clearly demonstrate that manipulating insulin levels may be used to modulate various fly traits, which are important determinants of organismal survival.

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