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Article ; Online: Systemic and cellular metabolism: the cause of and remedy for disease?

Adrain, Colin

2021 Volume 288, Issue 12, Page(s) 3624–3627

Abstract: The word 'metabolism' is derived from the Greek word μεταβολή (metabolē), denoting 'change'. True to this definition, it is now appreciated that a cell or tissue cannot change its behaviour without altering its metabolism. Hence, most key cell decision- ... ...

Abstract	The word 'metabolism' is derived from the Greek word μεταβολή (metabolē), denoting 'change'. True to this definition, it is now appreciated that a cell or tissue cannot change its behaviour without altering its metabolism. Hence, most key cell decision-making processes are tightly coupled to metabolic change. Conversely, perturbations in metabolite abundance or flux can alter cellular (and whole-body) function profoundly, giving rise to disease. This Special Issue on Systemic and Cellular Metabolism and Disease provides an integrative perspective on the importance of metabolism for health and disease alike. Spanning several orders of scale (from metabolites, proteins, organelles, organs/tissues and whole-body physiology), these review articles cover a breadth of topics, including the importance of metabolites as signalling regulators, metabolic disease, immunity, organelle function/dysfunction, ageing and neurodegenerative disease. One of the emergent themes is that just as metabolism is the fulcrum of biology, metabolic perturbances underpin most forms of acute, chronic, infectious and non-infectious human disease; ageing and senescence could be similarly viewed. Arguably most diseases are metabolic diseases; hence, modulating metabolism may help to 'change' disease outcomes.
MeSH term(s)	AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Adipose Tissue, Brown/metabolism ; Aging/genetics ; Aging/metabolism ; Animals ; Gene Expression Regulation ; Humans ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Metabolic Diseases/genetics ; Metabolic Diseases/metabolism ; Metabolic Diseases/pathology ; Metabolic Networks and Pathways/genetics ; Mitochondria/genetics ; Mitochondria/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; RNA, Circular/genetics ; RNA, Circular/metabolism ; Signal Transduction
Chemical Substances	Interferon Regulatory Factors ; RNA, Circular ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2021-06-21
Publishing country	England
Document type	Editorial ; 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.16033
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Article ; Online: Can the HB-EGF/EGFR pathway restore injured neurons?

Adrain, Colin / Badenes, Marina

The FEBS journal

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: Pseudoenzymes: dead enzymes with a lively role in biology.

Adrain, Colin

The FEBS journal

2020 Volume 287, Issue 19, Page(s) 4102–4105

Abstract: This Special Issue comprises twelve authoritative reviews that highlight an understudied but rapidly developing area of biology: catalytically inactive enzyme homologs. These pseudoenzymes, sometimes called 'dead enzymes', are found within most enzyme ... ...

Abstract	This Special Issue comprises twelve authoritative reviews that highlight an understudied but rapidly developing area of biology: catalytically inactive enzyme homologs. These pseudoenzymes, sometimes called 'dead enzymes', are found within most enzyme families and generally arose via gene duplication events. Dead enzymes have lost their enzymatic capacity, often via the evolutionary loss of key catalytic residues. However, as this Special Issue highlights, pseudoenzymes are far from being functionally 'dead'. In fact, they fulfill a range of critical biochemical roles, frequently appearing more versatile as biochemical regulators than their catalytic cousins. The functions of dead enzymes from diverse enzyme families often follow recurring themes, including allosteric regulation of their catalytically active counterparts, acting as signaling scaffolds, or as inhibitors that recognize and sequester the substrates of their catalytic homologs. As well as highlighting the breadth and depth of dead enzyme biology, this Special Issue emphasizes the power of pseudoenzymes as key biochemical regulators in health and disease and potentially as more tractable drug targets than some enzymes themselves. We hope you find these reviews enlivening, and we thank the authors for these excellent contributions.
MeSH term(s)	Enzymes/chemistry ; Humans ; Proteins/chemistry ; Proteins/metabolism
Chemical Substances	Enzymes ; Proteins
Language	English
Publishing date	2020-10-07
Publishing country	England
Document type	Editorial ; Introductory Journal Article ; 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.15535
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Systemic and cellular metabolism: the cause of and remedy for disease?

Adrain, Colin

FEBS journal. 2021 June, v. 288, no. 12

2021

Abstract: The word ‘metabolism’ is derived from the Greek word μεταβολή (metabolē), denoting ‘change’. True to this definition, it is now appreciated that a cell or tissue cannot change its behaviour without altering its metabolism. Hence, most key cell decision‐ ... ...

Abstract	The word ‘metabolism’ is derived from the Greek word μεταβολή (metabolē), denoting ‘change’. True to this definition, it is now appreciated that a cell or tissue cannot change its behaviour without altering its metabolism. Hence, most key cell decision‐making processes are tightly coupled to metabolic change. Conversely, perturbations in metabolite abundance or flux can alter cellular (and whole‐body) function profoundly, giving rise to disease. This Special Issue on Systemic and Cellular Metabolism and Disease provides an integrative perspective on the importance of metabolism for health and disease alike. Spanning several orders of scale (from metabolites, proteins, organelles, organs/tissues and whole‐body physiology), these review articles cover a breadth of topics, including the importance of metabolites as signalling regulators, metabolic disease, immunity, organelle function/dysfunction, ageing and neurodegenerative disease. One of the emergent themes is that just as metabolism is the fulcrum of biology, metabolic perturbances underpin most forms of acute, chronic, infectious and non‐infectious human disease; ageing and senescence could be similarly viewed. Arguably most diseases are metabolic diseases; hence, modulating metabolism may help to ‘change’ disease outcomes.
Keywords	cell differentiation ; human diseases ; immunity ; metabolic diseases ; metabolism ; metabolites ; neurodegenerative diseases ; organelles
Language	English
Dates of publication	2021-06
Size	p. 3624-3627.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	EDITORIAL
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16033
Database	NAL-Catalogue (AGRICOLA)

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Article: Pseudoenzymes: dead enzymes with a lively role in biology

Adrain, Colin

FEBS journal. 2020 Oct., v. 287, no. 19

2020

Abstract: This Special Issue comprises twelve authoritative reviews that highlight an understudied but rapidly developing area of biology: catalytically inactive enzyme homologs. These pseudoenzymes, sometimes called ‘dead enzymes’, are found within most enzyme ... ...

Abstract	This Special Issue comprises twelve authoritative reviews that highlight an understudied but rapidly developing area of biology: catalytically inactive enzyme homologs. These pseudoenzymes, sometimes called ‘dead enzymes’, are found within most enzyme families and generally arose via gene duplication events. Dead enzymes have lost their enzymatic capacity, often via the evolutionary loss of key catalytic residues. However, as this Special Issue highlights, pseudoenzymes are far from being functionally ‘dead’. In fact, they fulfill a range of critical biochemical roles, frequently appearing more versatile as biochemical regulators than their catalytic cousins. The functions of dead enzymes from diverse enzyme families often follow recurring themes, including allosteric regulation of their catalytically active counterparts, acting as signaling scaffolds, or as inhibitors that recognize and sequester the substrates of their catalytic homologs. As well as highlighting the breadth and depth of dead enzyme biology, this Special Issue emphasizes the power of pseudoenzymes as key biochemical regulators in health and disease and potentially as more tractable drug targets than some enzymes themselves. We hope you find these reviews enlivening, and we thank the authors for these excellent contributions.
Keywords	drugs ; enzymes ; gene duplication
Language	English
Dates of publication	2020-10
Size	p. 4102-4105.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	NAL-AP-2-clean ; EDITORIAL
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15535
Database	NAL-Catalogue (AGRICOLA)

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Z 2006/704: Show issues

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Article ; Online: Organelle homeostasis: from cellular mechanisms to disease

Burbridge, Emma / Adrain, Colin

The FEBS Journal. 2022 Nov., v. 289, no. 22 p.6822-6831

2022

Abstract: The major criterion that distinguishes eukaryotes from prokaryotes is the presence of organelles in the former. Organelles provide a compartment in which biochemical processes are corralled within bespoke biophysical conditions and act as storage depots, ...

Abstract	The major criterion that distinguishes eukaryotes from prokaryotes is the presence of organelles in the former. Organelles provide a compartment in which biochemical processes are corralled within bespoke biophysical conditions and act as storage depots, powerhouses, waste storage/recycling units and innate immune signalling hubs. A key challenge faced by organelles is to define, and then retain, their identity; this is mediated by complex proteostasis mechanisms including the import of an organelle‐specific proteome, the exclusion of non‐organellar proteins and the removal of misfolded proteins via dedicated quality control mechanisms. This Special Issue on Organelle Homeostasis provides an engaging, eclectic, yet integrative, perspective on organelle homeostasis in a range of organelles including those from the secretory and endocytic pathways, mitochondria, the autophagy‐lysosomal pathway and the nucleus and its sub‐compartments. Some lesser‐known organelles including migrasomes (organelles that are released by migrating cells) and GOMED (a Golgi‐specific form of autophagy) are also introduced. In the spirit of the principles of organelle biology, we hope you find the reviews in this Issue both encapsulating and captivating, and we thank the authors for their excellent contributions.
Keywords	autophagy ; eukaryotic cells ; homeostasis ; imports ; mitochondria ; prokaryotic cells ; proteome ; quality control
Language	English
Dates of publication	2022-11
Size	p. 6822-6831.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	EDITORIAL
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16667
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Organelle homeostasis: from cellular mechanisms to disease.

Burbridge, Emma / Adrain, Colin

The FEBS journal

2021 Volume 289, Issue 22, Page(s) 6822–6831

Abstract	The major criterion that distinguishes eukaryotes from prokaryotes is the presence of organelles in the former. Organelles provide a compartment in which biochemical processes are corralled within bespoke biophysical conditions and act as storage depots, powerhouses, waste storage/recycling units and innate immune signalling hubs. A key challenge faced by organelles is to define, and then retain, their identity; this is mediated by complex proteostasis mechanisms including the import of an organelle-specific proteome, the exclusion of non-organellar proteins and the removal of misfolded proteins via dedicated quality control mechanisms. This Special Issue on Organelle Homeostasis provides an engaging, eclectic, yet integrative, perspective on organelle homeostasis in a range of organelles including those from the secretory and endocytic pathways, mitochondria, the autophagy-lysosomal pathway and the nucleus and its sub-compartments. Some lesser-known organelles including migrasomes (organelles that are released by migrating cells) and GOMED (a Golgi-specific form of autophagy) are also introduced. In the spirit of the principles of organelle biology, we hope you find the reviews in this Issue both encapsulating and captivating, and we thank the authors for their excellent contributions.
MeSH term(s)	Endoplasmic Reticulum/metabolism ; Organelles/metabolism ; Golgi Apparatus/metabolism ; Lysosomes/metabolism ; Mitochondria ; Homeostasis
Language	English
Publishing date	2021-09-27
Publishing country	England
Document type	Editorial
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16667
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The complex life of rhomboid pseudoproteases.

Adrain, Colin / Cavadas, Miguel

The FEBS journal

2020 Volume 287, Issue 19, Page(s) 4261–4283

Abstract: Rhomboid pseudoproteases are catalytically inactive members of the rhomboid superfamily. The founding members, rhomboids, were first identified in Drosophila as serine intramembrane proteases that cleave transmembrane proteins, enabling signaling. This ... ...

Abstract	Rhomboid pseudoproteases are catalytically inactive members of the rhomboid superfamily. The founding members, rhomboids, were first identified in Drosophila as serine intramembrane proteases that cleave transmembrane proteins, enabling signaling. This led to the discovery of the wider rhomboid superfamily, a clan that in metazoans is dominated by pseudoproteases. These so-called rhomboid pseudoproteases inherited from their catalytically active ancestors a conserved rhomboid-like domain and a propensity to regulate signaling. Lacking catalytic activity, they developed new 'pseudoenzyme' functions that include regulating the trafficking, turnover, and activity of their client proteins. Rhomboid pseudoproteases have preeminent roles in orchestrating immune cell activation, antiviral responses, and cytokine release in response to microbial infection, or in chronic diseases, and have also been implicated in growth factor signaling, cancer, and, more recently, metabolism. Here, we discuss the mechanism(s) of action of rhomboid pseudoproteases, contrasted with rhomboid proteases. We also highlight the roles of rhomboid pseudoproteases in mammalian physiology, which, quite paradoxically among pseudoenzymes, is understood much better than active rhomboids.
MeSH term(s)	Animals ; Humans ; Membrane Proteins/metabolism ; Peptide Hydrolases
Chemical Substances	Membrane Proteins ; Peptide Hydrolases (EC 3.4.-)
Keywords	covid19
Language	English
Publishing date	2020-10-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15548
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The complex life of rhomboid pseudoproteases

Adrain, Colin / Cavadas, Miguel

FEBS journal. 2020 Oct., v. 287, no. 19

2020

Abstract	Rhomboid pseudoproteases are catalytically inactive members of the rhomboid superfamily. The founding members, rhomboids, were first identified in Drosophila as serine intramembrane proteases that cleave transmembrane proteins, enabling signaling. This led to the discovery of the wider rhomboid superfamily, a clan that in metazoans is dominated by pseudoproteases. These so‐called rhomboid pseudoproteases inherited from their catalytically active ancestors a conserved rhomboid‐like domain and a propensity to regulate signaling. Lacking catalytic activity, they developed new ‘pseudoenzyme’ functions that include regulating the trafficking, turnover, and activity of their client proteins. Rhomboid pseudoproteases have preeminent roles in orchestrating immune cell activation, antiviral responses, and cytokine release in response to microbial infection, or in chronic diseases, and have also been implicated in growth factor signaling, cancer, and, more recently, metabolism. Here, we discuss the mechanism(s) of action of rhomboid pseudoproteases, contrasted with rhomboid proteases. We also highlight the roles of rhomboid pseudoproteases in mammalian physiology, which, quite paradoxically among pseudoenzymes, is understood much better than active rhomboids.
Keywords	Drosophila ; catalytic activity ; cytokines ; mammals ; metabolism ; proteinases ; serine
Language	English
Dates of publication	2020-10
Size	p. 4261-4283.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	NAL-AP-2-clean ; REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15548
Database	NAL-Catalogue (AGRICOLA)

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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
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