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Article ; Online: Can the HB-EGF/EGFR pathway restore injured neurons?

Adrain, Colin / Badenes, Marina

2024

Abstract: Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a transmembrane protein that, when cleaved by metalloproteases through a process called ectodomain shedding, binds to the EGF receptor (EGFR), activating downstream signaling. The HB- ... ...

Abstract	Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a transmembrane protein that, when cleaved by metalloproteases through a process called ectodomain shedding, binds to the EGF receptor (EGFR), activating downstream signaling. The HB-EGF/EGFR pathway is crucial in development and is involved in numerous pathophysiological processes. In this issue of The FEBS Journal, Sireci et al. reveal a previously unexplored function of the HB-EGF/EGFR pathway in promoting neuronal progenitor proliferation and sensory neuron regeneration in the zebrafish olfactory epithelium in response to injury.
Language	English
Publishing date	2024-04-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.17143
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Article ; Online: iRhom2 and TNF: Partners or enemies?

Badenes, Marina / Adrain, Colin

Science signaling

2019 Volume 12, Issue 605

Abstract: iRhom2 is an essential cofactor for ADAM17, the metalloprotease that sheds both the proinflammatory cytokine tumor necrosis factor-α (TNF-α) and TNF receptors (TNFRs) from the cell surface. In this issue ... ...

Abstract	iRhom2 is an essential cofactor for ADAM17, the metalloprotease that sheds both the proinflammatory cytokine tumor necrosis factor-α (TNF-α) and TNF receptors (TNFRs) from the cell surface. In this issue of
MeSH term(s)	ADAM17 Protein ; Cholestasis ; Humans ; Liver Cirrhosis ; Receptors, Tumor Necrosis Factor ; Signal Transduction ; Tumor Necrosis Factor-alpha
Chemical Substances	Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha ; ADAM17 Protein (EC 3.4.24.86)
Language	English
Publishing date	2019-10-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review ; Comment
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.aaz0444
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: RHBDL4-triggered downregulation of COPII adaptor protein TMED7 suppresses TLR4-mediated inflammatory signaling.

Knopf, Julia D / Steigleder, Susanne S / Korn, Friederike / Kühnle, Nathalie / Badenes, Marina / Tauber, Marina / Theobald, Sebastian J / Rybniker, Jan / Adrain, Colin / Lemberg, Marius K

Nature communications

2024 Volume 15, Issue 1, Page(s) 1528

Abstract: The toll-like receptor 4 (TLR4) is a central regulator of innate immunity that primarily recognizes bacterial lipopolysaccharide cell wall constituents to trigger cytokine secretion. We identify the intramembrane protease RHBDL4 as a negative regulator ... ...

Abstract	The toll-like receptor 4 (TLR4) is a central regulator of innate immunity that primarily recognizes bacterial lipopolysaccharide cell wall constituents to trigger cytokine secretion. We identify the intramembrane protease RHBDL4 as a negative regulator of TLR4 signaling. We show that RHBDL4 triggers degradation of TLR4's trafficking factor TMED7. This counteracts TLR4 transport to the cell surface. Notably, TLR4 activation mediates transcriptional upregulation of RHBDL4 thereby inducing a negative feedback loop to reduce TLR4 trafficking to the plasma membrane. This secretory cargo tuning mechanism prevents the over-activation of TLR4-dependent signaling in an in vitro Mycobacterium tuberculosis macrophage infection model and consequently alleviates septic shock in a mouse model. A hypomorphic RHBDL4 mutation linked to Kawasaki syndrome, an ill-defined inflammatory disorder in children, further supports the pathophysiological relevance of our findings. In this work, we identify an RHBDL4-mediated axis that acts as a rheostat to prevent over-activation of the TLR4 pathway.
MeSH term(s)	Animals ; Child ; Humans ; Mice ; Adaptor Proteins, Signal Transducing/metabolism ; Cell Membrane/metabolism ; Down-Regulation ; Lipopolysaccharides/metabolism ; Signal Transduction ; Toll-Like Receptor 4/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Lipopolysaccharides ; TLR4 protein, human ; Toll-Like Receptor 4 ; Rhbdl3 protein, mouse (EC 3.4.21.105)
Language	English
Publishing date	2024-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45615-2
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Article ; Online: The ADAM17 sheddase complex regulator iTAP/Frmd8 modulates inflammation and tumor growth.

Badenes, Marina / Burbridge, Emma / Oikonomidi, Ioanna / Amin, Abdulbasit / de Carvalho, Érika / Kosack, Lindsay / Mariano, Camila / Domingos, Pedro / Faísca, Pedro / Adrain, Colin

Life science alliance

2023 Volume 6, Issue 4

Abstract: The metalloprotease ADAM17 is a sheddase of key molecules, including TNF and epidermal growth factor receptor ligands. ADAM17 exists within an assemblage, the "sheddase complex," containing a rhomboid pseudoprotease (iRhom1 or iRhom2). iRhoms control ... ...

Abstract	The metalloprotease ADAM17 is a sheddase of key molecules, including TNF and epidermal growth factor receptor ligands. ADAM17 exists within an assemblage, the "sheddase complex," containing a rhomboid pseudoprotease (iRhom1 or iRhom2). iRhoms control multiple aspects of ADAM17 biology. The FERM domain-containing protein iTAP/Frmd8 is an iRhom-binding protein that prevents the precocious shunting of ADAM17 and iRhom2 to lysosomes and their consequent degradation. As pathophysiological role(s) of iTAP/Frmd8 have not been addressed, we characterized the impact of iTAP/Frmd8 loss on ADAM17-associated phenotypes in mice. We show that iTAP/Frmd8 KO mice exhibit defects in inflammatory and intestinal epithelial barrier repair functions, but not the collateral defects associated with global ADAM17 loss. Furthermore, we show that iTAP/Frmd8 regulates cancer cell growth in a cell-autonomous manner and by modulating the tumor microenvironment. Our work suggests that pharmacological intervention at the level of iTAP/Frmd8 may be beneficial to target ADAM17 activity in specific compartments during chronic inflammatory diseases or cancer, while avoiding the collateral impact on the vital functions associated with the widespread inhibition of ADAM17.
MeSH term(s)	Animals ; Mice ; ADAM17 Protein/genetics ; ADAM17 Protein/metabolism ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Inflammation ; Neoplasms/genetics ; Tumor Microenvironment
Chemical Substances	ADAM17 Protein (EC 3.4.24.86) ; Carrier Proteins ; iRhom2 protein, mouse ; Frmd8 protein, mouse
Language	English
Publishing date	2023-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202201644
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Article ; Conference proceedings: Crosstalk between metabolism and immunity: the 3rd Annual Research Symposium of Instituto Gulbenkian de Ciência

Amin, Abdulbasit / Neves‐Costa, Ana / Pedroso, Dora / Colaço, Henrique / Coelho, Inês / Mahú, Inês / Badenes, Marina / Duarte, Nádia

FEBS journal. 2020 Nov., v. 287, no. 21

2020

Abstract: The ‘Crosstalks of immunity and metabolism’ Symposium was focused on how the intercommunication between different organs and the immune system affects organismal health. At this meeting, experts in immunology and metabolic research provided novel ... ...

Abstract	The ‘Crosstalks of immunity and metabolism’ Symposium was focused on how the intercommunication between different organs and the immune system affects organismal health. At this meeting, experts in immunology and metabolic research provided novel insights into the growing field of immunometabolism. This report attempts to review and integrate views, ideas, propositions, and conclusions that emanated from the symposium.
Keywords	immune system ; immunity ; metabolism
Language	English
Dates of publication	2020-11
Size	p. 4602-4606.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Conference proceedings
Note	NAL-AP-2-clean ; JOURNAL ARTICLE
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15368
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Metastasis is impaired by endothelial-specific Dll4 loss-of-function through inhibition of epithelial-to-mesenchymal transition and reduction of cancer stem cells and circulating tumor cells.

Mendonça, Liliana / Trindade, Alexandre / Carvalho, Catarina / Correia, Jorge / Badenes, Marina / Gigante, Joana / Duarte, António

Clinical & experimental metastasis

2019 Volume 36, Issue 4, Page(s) 365–380

Abstract: Systemic inhibition of Dll4 has been shown to thoroughly reduce cancer metastasis. The exact cause of this effect and whether it is endothelial mediated remains to be clarified. Therefore, we proposed to analyze the impact of endothelial Dll4 loss-of- ... ...

Abstract	Systemic inhibition of Dll4 has been shown to thoroughly reduce cancer metastasis. The exact cause of this effect and whether it is endothelial mediated remains to be clarified. Therefore, we proposed to analyze the impact of endothelial Dll4 loss-of-function on metastasis induction on three early steps of the metastatic process, regulation of epithelial-to-mesenchymal transition (EMT), cancer stem cell (CSC) frequency and circulating tumor cell (CTC) number. For this, Lewis Lung Carcinoma (LLC) cells were used to model mouse tumor metastasis in vivo, by subcutaneous transplantation into endothelial-specific Dll4 loss-of-function mice. We observed that endothelial-specific Dll4 loss-of-function is responsible for the tumor vascular regression that leads to the reduction of tumor burden. It induces an increase in tumoral blood vessel density, but the neovessels are poorly perfused, with increased leakage and reduced perivascular maturation. Unexpectedly, although hypoxia was increased in the tumor, the number and burden of macro-metastasis was significantly reduced. This is likely to be a consequence of the observed reduction in both EMT and CSC numbers caused by the endothelial-specific Dll4 loss-of-function. This multifactorial context may explain the concomitantly observed reduction of the circulating tumor cell count. Furthermore, our results suggest that endothelial Dll4/Notch-function mediates tumor hypoxia-driven increase of EMT. Therefore, it appears that endothelial Dll4 may constitute a promising target to prevent metastasis.
MeSH term(s)	Adaptor Proteins, Signal Transducing/physiology ; Animals ; Calcium-Binding Proteins/physiology ; Carcinoma, Lewis Lung/blood supply ; Carcinoma, Lewis Lung/pathology ; Cell Hypoxia ; Endothelial Cells/physiology ; Epithelial-Mesenchymal Transition ; Mice ; Neoplasm Metastasis/prevention & control ; Neoplastic Cells, Circulating ; Neoplastic Stem Cells/physiology ; Platelet Endothelial Cell Adhesion Molecule-1/analysis ; Receptors, Notch/physiology ; Signal Transduction ; Tumor Burden
Chemical Substances	Adaptor Proteins, Signal Transducing ; Calcium-Binding Proteins ; DLL4 protein, human ; Pecam1 protein, mouse ; Platelet Endothelial Cell Adhesion Molecule-1 ; Receptors, Notch
Language	English
Publishing date	2019-05-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604952-7
ISSN	1573-7276 ; 0262-0898
ISSN (online)	1573-7276
ISSN	0262-0898
DOI	10.1007/s10585-019-09973-2
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Article ; Online: Semaphorin 4B is an ADAM17-cleaved adipokine that inhibits adipocyte differentiation and thermogenesis.

Amin, Abdulbasit / Badenes, Marina / Tüshaus, Johanna / de Carvalho, Érika / Burbridge, Emma / Faísca, Pedro / Trávníčková, Květa / Barros, André / Carobbio, Stefania / Domingos, Pedro M / Vidal-Puig, Antonio / Moita, Luís F / Maguire, Sarah / Stříšovský, Kvido / Ortega, Francisco J / Fernández-Real, José Manuel / Lichtenthaler, Stefan F / Adrain, Colin

Molecular metabolism

2023 Volume 73, Page(s) 101731

Abstract: Objective: The metalloprotease ADAM17 (also called TACE) plays fundamental roles in homeostasis by shedding key signaling molecules from the cell surface. Although its importance for the immune system and epithelial tissues is well-documented, little is ...

Abstract	Objective: The metalloprotease ADAM17 (also called TACE) plays fundamental roles in homeostasis by shedding key signaling molecules from the cell surface. Although its importance for the immune system and epithelial tissues is well-documented, little is known about the role of ADAM17 in metabolic homeostasis. The purpose of this study was to determine the impact of ADAM17 expression, specifically in adipose tissues, on metabolic homeostasis. Methods: We used histopathology, molecular, proteomic, transcriptomic, in vivo integrative physiological and ex vivo biochemical approaches to determine the impact of adipose tissue-specific deletion of ADAM17 upon adipocyte and whole organism metabolic physiology. Results: ADAM17 Conclusions: Our findings identify a novel ADAM17-dependent axis, regulated by beta-adrenoceptors and mediated by the ADAM17-cleaved form of SEMA4B, that modulates energy balance in adipocytes by inhibiting adipocyte differentiation, thermogenesis and lipid catabolism.
MeSH term(s)	Animals ; Mice ; Adipocytes, Brown/metabolism ; Adipokines/metabolism ; Cell Differentiation ; Lipids ; Proteomics ; Receptors, Adrenergic, beta/metabolism ; Semaphorins/genetics ; Semaphorins/metabolism ; Thermogenesis/physiology
Chemical Substances	Adipokines ; Lipids ; Receptors, Adrenergic, beta ; Semaphorins ; semaphorin 4B, mouse
Language	English
Publishing date	2023-04-28
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2023.101731
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Article ; Online: Crosstalk between metabolism and immunity: the 3rd Annual Research Symposium of Instituto Gulbenkian de Ciência.

Amin, Abdulbasit / Neves-Costa, Ana / Pedroso, Dora / Colaço, Henrique / Coelho, Inês / Mahú, Inês / Badenes, Marina / Duarte, Nádia

The FEBS journal

2020 Volume 287, Issue 21, Page(s) 4602–4606

Abstract: The 'Crosstalks of immunity and metabolism' Symposium was focused on how the intercommunication between different organs and the immune system affects organismal health. At this meeting, experts in immunology and metabolic research provided novel ... ...

Abstract	The 'Crosstalks of immunity and metabolism' Symposium was focused on how the intercommunication between different organs and the immune system affects organismal health. At this meeting, experts in immunology and metabolic research provided novel insights into the growing field of immunometabolism. This report attempts to review and integrate views, ideas, propositions, and conclusions that emanated from the symposium.
MeSH term(s)	Animals ; Energy Metabolism/immunology ; Humans ; Immune System/immunology ; Immunity, Innate/immunology ; Inflammation/immunology
Language	English
Publishing date	2020-06-04
Publishing country	England
Document type	Congress ; Research Support, Non-U.S. Gov't
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15368
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Article ; Online: Delta-like 4/Notch signaling promotes Apc

Badenes, Marina / Trindade, Alexandre / Pissarra, Hugo / Lopes-da-Costa, Luís / Duarte, António

BMC cancer

2017 Volume 17, Issue 1, Page(s) 50

Abstract: Background: Delta like 4 (Dll4)/Notch signaling is a key regulator of tumor angiogenesis. Additionally, the role of Dll4 has been studied on tumor stem cells. However, as these cells are implicated in tumor angiogenesis, it is conceivable that the ... ...

Abstract	Background: Delta like 4 (Dll4)/Notch signaling is a key regulator of tumor angiogenesis. Additionally, the role of Dll4 has been studied on tumor stem cells. However, as these cells are implicated in tumor angiogenesis, it is conceivable that the effect of Dll4 on these cells may be a consequence of its angiogenic function. Our aim was to evaluate the expression and dissect the functions of Dll4 in the Apc Methods: We evaluated the protein expression pattern of Dll4 and other Notch members in the Apc Results: All Notch pathway members were present in the normal small and large intestine and in the adenomas of the same regions. Dll4, all Notch receptors and Hes1 expression seemed upregulated in the tumors, with some regional differences. The same members and Hes5, instead of Hes1, presented ectopic expression in the tumor parenchyma. Dll4 expression was most pronounced in the tumor cells but it was also present in the tumor blood vessels and in other stromal cells. Ubiquitous and endothelial-specific Dll4 deletion led to an equivalent reduction of tumor growth because of a similarly marked tumoral angiogenic phenotype promoting non-productive vasculature and consequently hypoxia and apoptosis. The ubiquitous Dll4 inhibition led to a stronger decrease of tumor multiplicity than the endothelial-specific deletion by further reducing tumor proliferation and tumor stem cell density through upregulation of the cyclin-dependent kinase inhibitors 1C and 1B and downregulation of Myc, Cyclin D1 and D2 independently of β-catenin activation. This phenotype was associated to the observed increased epithelial differentiation deviated towards the secretory lineages by Atoh1 and Klf4 upregulation only in the ubiquitous Dll4 mutants. Conclusions: Dll4 seems to promote Apc
MeSH term(s)	Adenomatous Polyposis Coli Protein/metabolism ; Animals ; Cell Proliferation/physiology ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Cyclin-Dependent Kinases/metabolism ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Intercellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Receptors, Notch/metabolism ; Signal Transduction/physiology ; beta Catenin/metabolism
Chemical Substances	Adenomatous Polyposis Coli Protein ; DLL4 protein, mouse ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Receptors, Notch ; adenomatous polyposis coli protein, mouse ; beta Catenin ; Cyclin-Dependent Kinases (EC 2.7.11.22)
Language	English
Publishing date	2017--13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-016-3036-0
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Article ; Online: Erratum to: Delta-like 4/Notch signaling promotes Apc

Badenes, Marina / Trindade, Alexandre / Pissarra, Hugo / Lopes-da-Costa, Luís / Duarte, António

BMC cancer

2017 Volume 17, Issue 1, Page(s) 205

Language	English
Publishing date	2017--21
Publishing country	England
Document type	Journal Article ; Published Erratum
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-017-3202-z
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