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Article: SIALIDASE (NEURAMINIDASE) ACTIVITY OF STANDARD AND INCOMPLETE VIRUS.

SETO, J T

2003 Volume 90, Page(s) 420–422

MeSH term(s)	Chemical Phenomena ; Chemistry ; Defective Viruses ; Electrons ; Microscopy ; Microscopy, Electron ; Neuraminidase ; Orthomyxoviridae ; Research
Chemical Substances	Neuraminidase (EC 3.2.1.18)
Language	English
Publishing date	2003-02-17
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/0304-4165(64)90213-2
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Article: EFFECT OF SIALIDASE ANTISERUM ON TOXICITY OF INFLUENZA VIRUS.

SETO, J T

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)

2003 Volume 118, Page(s) 1043–1046

MeSH term(s)	HeLa Cells ; Humans ; Immune Sera ; Neuraminidase ; Orthomyxoviridae ; Research ; Tissue Culture Techniques ; Virus Cultivation
Chemical Substances	Immune Sera ; Neuraminidase (EC 3.2.1.18)
Language	English
Publishing date	2003-09-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.3181/00379727-118-30040
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Article ; Online: α-Actinin-3 deficiency alters muscle adaptation in response to denervation and immobilization.

Garton, F C / Seto, J T / Quinlan, K G R / Yang, N / Houweling, P J / North, K N

Human molecular genetics

2014 Volume 23, Issue 7, Page(s) 1879–1893

Abstract: Homozygosity for a common null polymorphism (R577X) in the ACTN3 gene results in the absence of the fast fibre-specific protein, α-actinin-3 in ∼16% of humans worldwide. α-Actinin-3 deficiency is detrimental to optimal sprint performance and benefits ... ...

Abstract	Homozygosity for a common null polymorphism (R577X) in the ACTN3 gene results in the absence of the fast fibre-specific protein, α-actinin-3 in ∼16% of humans worldwide. α-Actinin-3 deficiency is detrimental to optimal sprint performance and benefits endurance performance in elite athletes. In the general population, α-actinin-3 deficiency is associated with reduced muscle mass, strength and fast muscle fibre area, and poorer muscle function with age. The Actn3 knock-out (KO) mouse model mimics the human phenotype, with fast fibres showing a shift towards slow/oxidative metabolism without a change in myosin heavy chain (MyHC) isoform. We have recently shown that these changes are attributable to increased activity of the calcineurin-dependent signalling pathway in α-actinin-3 deficient muscle, resulting in enhanced response to exercise training. This led us to hypothesize that the Actn3 genotype influences muscle adaptation to disuse, irrespective of neural innervation. Separate cohorts of KO and wild-type mice underwent 2 weeks immobilization and 2 and 8 weeks of denervation. Absence of α-actinin-3 resulted in reduced atrophic response and altered adaptation to disuse, as measured by a change in MyHC isoform. KO mice had a lower threshold to switch from the predominantly fast to a slower muscle phenotype (in response to immobilization) and a higher threshold to switch to a faster muscle phenotype (in response to denervation). We propose that this change is mediated through baseline alterations in the calcineurin signalling pathway of Actn3 KO muscle. Our findings have important implications for understanding individual responses to muscle disuse/disease and training in the general population.
MeSH term(s)	Actinin/deficiency ; Actinin/genetics ; Adult ; Aged ; Aged, 80 and over ; Animals ; Athletic Performance ; Calcineurin/metabolism ; Denervation ; Energy Metabolism/genetics ; Female ; Hindlimb Suspension ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Muscle Fibers, Fast-Twitch/physiology ; Muscle Strength/genetics ; Muscle, Skeletal/innervation ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiology ; Muscular Atrophy/genetics ; Muscular Diseases/genetics ; Myosin Heavy Chains/genetics ; Physical Conditioning, Animal ; Polymorphism, Single Nucleotide ; Protein Isoforms ; Signal Transduction/genetics ; Young Adult
Chemical Substances	Actn3 protein, mouse ; Protein Isoforms ; Actinin (11003-00-2) ; Calcineurin (EC 3.1.3.16) ; Myosin Heavy Chains (EC 3.6.4.1)
Language	English
Publishing date	2014-04-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddt580
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Article ; Online: Exploring the relationship between α-actinin-3 deficiency and obesity in mice and humans.

Houweling, P J / Berman, Y D / Turner, N / Quinlan, K G R / Seto, J T / Yang, N / Lek, M / Macarthur, D G / Cooney, G / North, K N

International journal of obesity (2005)

2017 Volume 41, Issue 7, Page(s) 1154–1157

Abstract: Obesity is a worldwide health crisis, and the identification of genetic modifiers of weight gain is crucial in understanding this complex disorder. A common null polymorphism in the fast fiber-specific gene ACTN3 (R577X) is known to influence skeletal ... ...

Abstract	Obesity is a worldwide health crisis, and the identification of genetic modifiers of weight gain is crucial in understanding this complex disorder. A common null polymorphism in the fast fiber-specific gene ACTN3 (R577X) is known to influence skeletal muscle function and metabolism. α-Actinin-3 deficiency occurs in an estimated 1.5 billion people worldwide, and results in reduced muscle strength and a shift towards a more efficient oxidative metabolism. The X-allele has undergone strong positive selection during recent human evolution, and in this study, we sought to determine whether ACTN3 genotype influences weight gain and obesity in mice and humans. An Actn3 KO mouse has been generated on two genetic backgrounds (129X1/SvJ and C57BL/6J) and fed a high-fat diet (HFD, 45% calories from fat). Anthropomorphic features (including body weight) were examined and show that Actn3 KO 129X1/SvJ mice gained less weight compared to WT. In addition, six independent human cohorts were genotyped for ACTN3 R577X (Rs1815739) and body mass index (BMI), waist-to-hip ratio-adjusted BMI (WHRadjBMI) and obesity-related traits were assessed. In humans, ACTN3 genotype alone does not contribute to alterations in BMI or obesity.
MeSH term(s)	Actinin/deficiency ; Actinin/genetics ; Actinin/metabolism ; Animals ; Diet, High-Fat ; Female ; Gene Expression ; Genotype ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Obesity/genetics ; Obesity/physiopathology ; RNA, Messenger/genetics ; Weight Gain/genetics ; Weight Gain/physiology
Chemical Substances	ACTN3 protein, human ; Actn3 protein, mouse ; RNA, Messenger ; Actinin (11003-00-2)
Language	English
Publishing date	2017-03-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	752409-2
ISSN	1476-5497 ; 0307-0565
ISSN (online)	1476-5497
ISSN	0307-0565
DOI	10.1038/ijo.2017.72
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Article: Determinants of organ tropism of Sendai virus.

Tashiro, M / Seto, J T

Frontiers in bioscience : a journal and virtual library

1997 Volume 2, Page(s) d588–91

Abstract: Wild-type Sendai virus is exclusively pneumotropic in mice. Protease activation mutants, ts-f1 and F1-R, were isolated from persistently infected tissue culture cells. Additional mutants were isolated from wild-type Sendai virus with phenotypes similar ... ...

Abstract	Wild-type Sendai virus is exclusively pneumotropic in mice. Protease activation mutants, ts-f1 and F1-R, were isolated from persistently infected tissue culture cells. Additional mutants were isolated from wild-type Sendai virus with phenotypes similar to the pantropic mutant, F1-R. The genome of the mutants was sequenced and mutations were revealed in several proteins encoded by the genes. Three of the six mutations in the fusion (F) proteins were considered prime candidates for the determinant of pantropism. Characterization of the mutants led to the finding that the exchange (Ser to Pro) residue 115 next to the cleavage site of the F protein was the primary determinant that resulted in the enhanced cleavability of the F protein. Another important finding was bipolar budding of F1-R in polarized epithelial cells and mouse bronchial epithelium. This has been attributed to two mutations in the matrix (M) protein, at residues 128 (Asp to Gly) and 210 (Ile to Thr). Thus, the determinants of pantropism of F1-R are protease activation of the F protein and biopolar budding attributed to the mutated M protein.
MeSH term(s)	Animals ; Bronchi/virology ; Mice ; Mutation ; Organ Specificity ; Sendai virus/genetics ; Sendai virus/growth & development ; Serine Endopeptidases/metabolism ; Tryptases ; Viral Fusion Proteins/genetics ; Viral Fusion Proteins/metabolism ; Viral Matrix Proteins/genetics ; Viral Matrix Proteins/metabolism
Chemical Substances	Viral Fusion Proteins ; Viral Matrix Proteins ; Serine Endopeptidases (EC 3.4.21.-) ; tryptase Clara (EC 3.4.21.-) ; Tryptases (EC 3.4.21.59)
Language	English
Publishing date	1997-12-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2141320-4
ISSN	1093-9946
ISSN	1093-9946
DOI	10.2741/a214
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Article: Electron microscopy and serology of staphylococcus phages.

KAESBERG, P / SETO, J T / WILSON, J B

Journal of bacteriology

2003 Volume 72, Issue 6, Page(s) 847–850

MeSH term(s)	Electrons ; Micrococcus ; Microscopy ; Microscopy, Electron ; Staphylococcus Phages ; Staphylococcus aureus
Language	English
Publishing date	2003-08-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2968-3
ISSN	1098-5530 ; 0021-9193
ISSN (online)	1098-5530
ISSN	0021-9193
DOI	10.1128/jb.72.6.847-850.1956
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Article: Some biological characteristics of Asian influenza isolates.

SETO, J T / HICKEY, B J / RASMUSSEN, A F

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)

2003 Volume 100, Issue 4, Page(s) 672–676

MeSH term(s)	Asian Continental Ancestry Group ; Humans ; Influenza, Human ; Orthomyxoviridae
Language	English
Publishing date	2003-09-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.3181/00379727-100-24740
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Article: Determinants of organ tropism of sendai virus.

Tashiro, M / McQueen, N L / Seto, J T

Frontiers in bioscience : a journal and virtual library

1999 Volume 4, Page(s) D642–5

Abstract	Wild-type Sendai virus is exclusively pneumotropic in mice. Protease activation mutants, ts-f1 and F1-R, were isolated from persistently infected tissue culture cells. Additional mutants were isolated from wild-type Sendai virus with phenotypes similar to the pantropic mutant, F1-R. The genome of the mutants was sequenced and mutations were revealed in several proteins encoded by the genes. Three of the six mutations in the fusion (F) proteins were considered prime candidates for the determinant of pantropism. Characterization of the mutants led to the finding that the exchange (Ser to Pro) residue 115 next to the cleavage site of the F protein was the primary determinant that resulted in the enhanced cleavability of the F protein. Another important finding was bipolar budding of F1-R in polarized epithelial cells and mouse bronchial epithelium. This has been attributed to two mutations in the matrix (M) protein, at residues 128 (Asp to Gly) and 210 (Ile to Thr). Thus the determinants of pantropism of F1-R are protease activation of the F protein and bipolar budding attributed to the mutated M protein and enhanced disruption of microtubules.
MeSH term(s)	Amino Acid Substitution ; Animals ; Dogs ; Endopeptidases/metabolism ; Mice ; Mutation ; Organ Specificity ; Respirovirus/genetics ; Respirovirus/metabolism ; Respirovirus/pathogenicity ; Tropism/genetics ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism ; Viral Fusion Proteins/genetics ; Viral Fusion Proteins/metabolism
Chemical Substances	Viral Envelope Proteins ; Viral Fusion Proteins ; Endopeptidases (EC 3.4.-)
Language	English
Publishing date	1999-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	2141320-4
ISSN	1093-9946
ISSN	1093-9946
DOI	10.2741/tashiro
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Article: Molecular biology of the pathogenesis of Sendai viruses.

Seto, J T / Tashiro, M

Behring Institute Mitteilungen

1991 , Issue 89, Page(s) 54–58

Abstract: Protease activation mutant (ts-f1) was isolated from persistently infected cells, and a pantropic mutant, F1-R, was derived from ts-f1. The mutants have been found to be extremely useful for investigations on the molecular biology of paramyxoviruses. The ...

Abstract	Protease activation mutant (ts-f1) was isolated from persistently infected cells, and a pantropic mutant, F1-R, was derived from ts-f1. The mutants have been found to be extremely useful for investigations on the molecular biology of paramyxoviruses. The genome of the mutants has been sequenced and mutations were revealed in several proteins encoded by the genes. Three of the six mutations in the fusion (F) proteins were considered prime candidates for the determinants of pantropism. Characterization of the revertants, that are no longer pantropic and derived from F1-R, revealed that the mutation at amino acid residue (115 Arg to Pro) of the F protein is responsible for pantropism. Another important finding was bipolar budding of F1-R in polarized epithelial cells and mouse bronchial epithelium. It has been postulated that mutation(s) in the matrix (M) protein may be associated with bipolar budding since the revertants retained this phenotype of F1-R.
MeSH term(s)	Animals ; Cell Line ; Endopeptidases/metabolism ; Parainfluenza Virus 1, Human/genetics ; Parainfluenza Virus 1, Human/pathogenicity ; Viral Proteins/genetics ; Virulence/genetics
Chemical Substances	Viral Proteins ; Endopeptidases (EC 3.4.-)
Language	English
Publishing date	1991-07
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
ISSN	0301-0457
ISSN	0301-0457
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Article: A gene for speed: contractile properties of isolated whole EDL muscle from an alpha-actinin-3 knockout mouse.

Chan, S / Seto, J T / MacArthur, D G / Yang, N / North, K N / Head, S I

American journal of physiology. Cell physiology

2008 Volume 295, Issue 4, Page(s) C897–904

Abstract: The actin-binding protein alpha-actinin-3 is one of the two isoforms of alpha-actinin that are found in the Z-discs of skeletal muscle. alpha-Actinin-3 is exclusively expressed in fast glycolytic muscle fibers. Homozygosity for a common polymorphism in ... ...

Abstract	The actin-binding protein alpha-actinin-3 is one of the two isoforms of alpha-actinin that are found in the Z-discs of skeletal muscle. alpha-Actinin-3 is exclusively expressed in fast glycolytic muscle fibers. Homozygosity for a common polymorphism in the ACTN3 gene results in complete deficiency of alpha-actinin-3 in about 1 billion individuals worldwide. Recent genetic studies suggest that the absence of alpha-actinin-3 is detrimental to sprint and power performance in elite athletes and in the general population. In contrast, alpha-actinin-3 deficiency appears to be beneficial for endurance athletes. To determine the effect of alpha-actinin-3 deficiency on the contractile properties of skeletal muscle, we studied isolated extensor digitorum longus (fast-twitch) muscles from a specially developed alpha-actinin-3 knockout (KO) mouse. alpha-Actinin-3-deficient muscles showed similar levels of damage to wild-type (WT) muscles following lengthening contractions of 20% strain, suggesting that the presence or absence of alpha-actinin-3 does not significantly influence the mechanical stability of the sarcomere in the mouse. alpha-Actinin-3 deficiency does not result in any change in myosin heavy chain expression. However, compared with alpha-actinin-3-positive muscles, alpha-actinin-3-deficient muscles displayed longer twitch half-relaxation times, better recovery from fatigue, smaller cross-sectional areas, and lower twitch-to-tetanus ratios. We conclude that alpha-actinin-3 deficiency results in fast-twitch, glycolytic fibers developing slower-twitch, more oxidative properties. These changes in the contractile properties of fast-twitch skeletal muscle from alpha-actinin-3-deficient individuals would be detrimental to optimal sprint and power performance, but beneficial for endurance performance.
MeSH term(s)	Actinin/genetics ; Actinin/metabolism ; Animals ; Gene Expression Regulation/physiology ; Mice ; Mice, Knockout ; Muscle Contraction/genetics ; Muscle Contraction/physiology ; Muscle Fatigue/genetics ; Muscle Fatigue/physiology ; Muscle Fibers, Fast-Twitch/physiology ; Muscle Fibers, Slow-Twitch/physiology ; Muscle, Skeletal/physiology
Chemical Substances	Actn3 protein, mouse ; Actinin (11003-00-2)
Language	English
Publishing date	2008-07-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00179.2008
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