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Article ; Online: A novel unbiased method reveals progressive podocyte globotriaosylceramide accumulation and loss with age in females with Fabry disease.

Najafian, Behzad / Silvestroni, Aurelio / Sokolovskiy, Alexey / Tøndel, Camilla / Svarstad, Einar / Obrisca, Bogdan / Ismail, Gener / Holida, Myrl D / Mauer, Michael

Kidney international

2022 Volume 102, Issue 1, Page(s) 173–182

Abstract: While females can suffer serious complications of Fabry disease, most studies are limited to males to avoid confounding by mosaicism. Here, we developed a novel unbiased method for quantifying globotriaosylceramide (GL3) inclusion volume in affected ... ...

Abstract	While females can suffer serious complications of Fabry disease, most studies are limited to males to avoid confounding by mosaicism. Here, we developed a novel unbiased method for quantifying globotriaosylceramide (GL3) inclusion volume in affected podocytes (F+) in females with Fabry disease independent of mosaicism leading to important new observations. All podocytes in male patients with Fabry are F+. The probability of observing random profiles from F+ podocytes without GL3 inclusions (estimation error) was modeled from electron microscopic studies of 99 glomeruli from 40 treatment-naïve males and this model was applied to 28 treatment-naïve females. Also, podocyte structural parameters were compared in 16 age-matched treatment-naïve males and females with classic Fabry disease and 11 normal individuals. A 4
MeSH term(s)	Fabry Disease/complications ; Female ; Humans ; Male ; Podocytes ; Proteinuria/etiology ; Trihexosylceramides
Chemical Substances	Trihexosylceramides ; globotriaosylceramide (71965-57-6)
Language	English
Publishing date	2022-04-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2022.03.023
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Zs.A 797: Show issues

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Article ; Online: Differential migratory properties of monocytes isolated from human subjects naïve and non-naïve to Cannabis.

Sexton, Michelle / Silvestroni, Aurelio / Möller, Thomas / Stella, Nephi

Inflammopharmacology

2012 Volume 21, Issue 3, Page(s) 253–259

Abstract: This study evaluates the migratory potential of monocytes isolated from two groups of human subjects: naïve and non-naïve to Cannabis. Phytocannabinoids (pCB), the bioactive agents produced by the plant Cannabis, regulate the phenotype and function of ... ...

Abstract	This study evaluates the migratory potential of monocytes isolated from two groups of human subjects: naïve and non-naïve to Cannabis. Phytocannabinoids (pCB), the bioactive agents produced by the plant Cannabis, regulate the phenotype and function of immune cells by interacting with CB1 and CB2 receptors. It has been shown that agents influencing the phenotype of circulating monocytes influence the phenotype of macrophages and the outcome of immune responses. To date, nothing is known about the acute and long-term effects of pCB on human circulating monocytes. Healthy subjects were recruited for a single blood draw. Monocytes were isolated, fluorescently labeled and their migration quantified using a validated assay that employs near infrared fluorescence and modified Boyden chambers. CB1 and CB2 receptor mRNA expression was quantified by qPCR. Monocytes from all subjects (n = 10) responded to chemokine (c-c motif) ligand 2 (CCL2) and human serum stimuli. Acute application of pCB significantly inhibited both the basal and CCL2-stimulated migration of monocytes, but only in subjects non-naïve to Cannabis. qPCR analysis indicates that monocytes from subjects non-naïve to Cannabis express significantly more CB1 mRNA. The phenotype of monocytes isolated from subjects non-naïve to Cannabis is significantly different from monocytes isolated from subjects naïve to Cannabis. Only monocytes from subjects non-naïve to Cannabis respond to acute exposure to pCB by reducing their overall migratory capacity. Our study suggests that chronic exposure to Cannabis affects the phenotype of circulating monocytes and accordingly could influence outcome of inflammatory responses occurring in injured tissues.
MeSH term(s)	Adult ; Cannabinoids/administration & dosage ; Cannabinoids/pharmacology ; Cannabis/chemistry ; Cell Movement/drug effects ; Female ; Humans ; Male ; Marijuana Smoking/metabolism ; Middle Aged ; Monocytes/drug effects ; Monocytes/metabolism ; Pilot Projects ; Polymerase Chain Reaction ; RNA, Messenger/metabolism ; Receptor, Cannabinoid, CB1/metabolism ; Receptor, Cannabinoid, CB2/metabolism ; Young Adult
Chemical Substances	Cannabinoids ; RNA, Messenger ; Receptor, Cannabinoid, CB1 ; Receptor, Cannabinoid, CB2
Language	English
Publishing date	2012-04-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Validation Study
ZDB-ID	1080058-x
ISSN	1568-5608 ; 0925-4692
ISSN (online)	1568-5608
ISSN	0925-4692
DOI	10.1007/s10787-012-0133-9
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Article ; Online: Distinct neuroinflammatory profile in post-mortem human Huntington's disease.

Silvestroni, Aurelio / Faull, Richard L M / Strand, Andrew D / Möller, Thomas

Neuroreport

2009 Volume 20, Issue 12, Page(s) 1098–1103

Abstract: Neuroinflammation is a prominent feature of many neurodegenerative diseases, however, little is known about neuroinflammation in Huntington's disease. We used quantitative real time-PCR to compare the expression level of neuroinflammation-associated ... ...

Abstract	Neuroinflammation is a prominent feature of many neurodegenerative diseases, however, little is known about neuroinflammation in Huntington's disease. We used quantitative real time-PCR to compare the expression level of neuroinflammation-associated mediators in the striatum, cortex, and cerebellum from post-mortem Huntington's disease patient samples with controls. We found increased expression of several key inflammatory mediators, including CCL2 and IL-10, specifically in the striatum of Huntington's disease patients, the main area affected by this pathology. Remarkably, we also found upregulation of IL-6, IL-8, and MMP9, in the cortex and notably the cerebellum, a brain area commonly thought to be spared by Huntington's disease. Our data suggest that neuroinflammation is a prominent feature associated with Huntington's disease and may constitute a novel target for therapeutic intervention.
MeSH term(s)	Adult ; Aged ; Cerebellum/immunology ; Cerebellum/metabolism ; Cerebral Cortex/immunology ; Cerebral Cortex/metabolism ; Chemokine CCL2/genetics ; Chemokine CCL2/metabolism ; Corpus Striatum/immunology ; Corpus Striatum/metabolism ; Female ; Gene Expression ; Humans ; Huntington Disease/genetics ; Huntington Disease/immunology ; Huntington Disease/metabolism ; Interleukin-10/genetics ; Interleukin-10/metabolism ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Interleukin-8/genetics ; Interleukin-8/metabolism ; Male ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Middle Aged ; RNA, Messenger/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	CCL2 protein, human ; Chemokine CCL2 ; IL10 protein, human ; IL6 protein, human ; Interleukin-1beta ; Interleukin-6 ; Interleukin-8 ; RNA, Messenger ; Tumor Necrosis Factor-alpha ; Interleukin-10 (130068-27-8) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2009-08-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1049746-8
ISSN	1473-558X ; 0959-4965
ISSN (online)	1473-558X
ISSN	0959-4965
DOI	10.1097/WNR.0b013e32832e34ee
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Zs.A 3118: Show issues

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Article: Regulation of cytotoxin expression by converging eukaryotic-type and two-component signalling mechanisms in Streptococcus agalactiae.

Rajagopal, Lakshmi / Vo, Anthony / Silvestroni, Aurelio / Rubens, Craig E

Molecular microbiology

2006 Volume 62, Issue 4, Page(s) 941–957

Abstract: Signal transducing mechanisms are essential for regulation of gene expression in both prokaryotic and eukaryotic organisms. Regulation of gene expression in eukaryotes is accomplished by serine/threonine and tyrosine kinases and cognate phosphatases. In ... ...

Abstract	Signal transducing mechanisms are essential for regulation of gene expression in both prokaryotic and eukaryotic organisms. Regulation of gene expression in eukaryotes is accomplished by serine/threonine and tyrosine kinases and cognate phosphatases. In contrast, gene expression in prokaryotes is controlled by two-component systems that comprise a sensor histidine kinase and a cognate DNA binding response regulator. Pathogenic bacteria utilize two-component systems to regulate expression of their virulence factors and for adaptive responses to the external environment. We have previously shown that the human pathogen Streptococcus agalactiae (Group B Streptococci, GBS) encodes a single eukaryotic-type serine/threonine kinase Stk1, which is important for virulence of the organism. In this study, we aimed to understand how Stk1 contributes to virulence of GBS. Our results indicate that Stk1 expression is important for resistance of GBS to human blood, neutrophils and oxidative stress. Consistent with these observations, Stk1 positively regulates transcription of a cytotoxin, beta-haemolysin/cytolysin (beta-H/C) that is critical for survival of GBS in the bloodstream and for resistance to oxidative stress. Interestingly, positive regulation of beta-H/C by Stk1 requires the two-component regulator CovR. Further, we show that Stk1 can negatively regulate transcription of CAMP factor in a CovR-dependent manner. As Stk1 phosphorylates CovR in vitro, these data suggest that serine/threonine phosphorylation impacts CovR-mediated regulation of GBS gene expression. In summary, our studies provide novel information that a eukaryotic-type serine/threonine kinase regulates two-component-mediated expression of GBS cytotoxins.
MeSH term(s)	Bacterial Proteins/metabolism ; Blood Bactericidal Activity ; Cytotoxins/genetics ; Gene Expression Regulation, Bacterial ; Hemolysin Proteins/genetics ; Hemolysin Proteins/metabolism ; Histidine Kinase ; Humans ; Hydrogen Peroxide ; Phagocytosis ; Pigments, Biological/biosynthesis ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/physiology ; Signal Transduction ; Streptococcus agalactiae/genetics ; Streptococcus agalactiae/immunology ; Streptococcus agalactiae/metabolism ; Transcription Factors/metabolism ; Virulence/genetics
Chemical Substances	Bacterial Proteins ; CAMP protein, Streptococcus ; Cytotoxins ; Hemolysin Proteins ; Pigments, Biological ; Transcription Factors ; Hydrogen Peroxide (BBX060AN9V) ; Protein Kinases (EC 2.7.-) ; Stk1 protein, Streptococcus agalactiae (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Histidine Kinase (EC 2.7.13.1)
Language	English
Publishing date	2006-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	619315-8
ISSN	1365-2958 ; 0950-382X
ISSN (online)	1365-2958
ISSN	0950-382X
DOI	10.1111/j.1365-2958.2006.05431.x
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Article: Regulation of purine biosynthesis by a eukaryotic-type kinase in Streptococcus agalactiae.

Rajagopal, Lakshmi / Vo, Anthony / Silvestroni, Aurelio / Rubens, C E

Molecular microbiology

2005 Volume 56, Issue 5, Page(s) 1329–1346

Abstract: Group B streptococci (GBS) are the principal causal agents of human neonatal pneumonia, sepsis and meningitis. We had previously described the existence of a eukaryotic-type serine/threonine kinase (Stk1) and phosphatase (Stp1) in GBS that regulate ... ...

Abstract	Group B streptococci (GBS) are the principal causal agents of human neonatal pneumonia, sepsis and meningitis. We had previously described the existence of a eukaryotic-type serine/threonine kinase (Stk1) and phosphatase (Stp1) in GBS that regulate growth and virulence of the pathogen. Our previous results also demonstrated that these enzymes reversibly phosphorylated an inorganic pyrophosphatase. To understand the role of these eukaryotic-type enzymes on growth of GBS, we assessed the stk1-mutants for auxotrophic requirements. In this report, we describe that in the absence of the kinase (Stk1), GBS are attenuated for de novo purine biosynthesis and are consequently growth arrested. During growth in media lacking purines, the intracellular G nucleotide pools (GTP, GDP and GMP) are significantly reduced in the Stk1-deficient strains, while levels of A nucleotides (ATP, ADP and AMP) are marginally increased when compared with the isogenic wild-type strain. We provide evidence that the reduced pools of G nucleotides result from altered activity of the IMP utilizing enzymes, adenylosuccinate synthetase (PurA) and IMP dehydrogenase (GuaB) in these strains. We also demonstrate that Stk1 and Stp1 reversibly phosphorylate and consequently regulate PurA activity in GBS. Collectively, these data indicate the novel role of eukaryotic-type kinases in regulation of metabolic processes such as purine biosynthesis.
MeSH term(s)	Adenosine Diphosphate/metabolism ; Adenosine Monophosphate/metabolism ; Adenosine Triphosphate/metabolism ; Adenylosuccinate Synthase/metabolism ; Genetic Complementation Test ; Guanosine Diphosphate/metabolism ; Guanosine Monophosphate/analysis ; Guanosine Triphosphate/metabolism ; IMP Dehydrogenase/metabolism ; Mutation ; Phosphorylation ; Phosphotransferases/genetics ; Phosphotransferases/metabolism ; Purines/biosynthesis ; Streptococcus agalactiae/genetics ; Streptococcus agalactiae/growth & development ; Streptococcus agalactiae/metabolism
Chemical Substances	Purines ; Guanosine Diphosphate (146-91-8) ; Adenosine Monophosphate (415SHH325A) ; Adenosine Diphosphate (61D2G4IYVH) ; Guanosine Monophosphate (85-32-5) ; Guanosine Triphosphate (86-01-1) ; Adenosine Triphosphate (8L70Q75FXE) ; IMP Dehydrogenase (EC 1.1.1.205) ; Phosphotransferases (EC 2.7.-) ; Adenylosuccinate Synthase (EC 6.3.4.4)
Language	English
Publishing date	2005-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	619315-8
ISSN	1365-2958 ; 0950-382X
ISSN (online)	1365-2958
ISSN	0950-382X
DOI	10.1111/j.1365-2958.2005.04620.x
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Article: Identification of serine/threonine kinase substrates in the human pathogen group B streptococcus.

Silvestroni, Aurelio / Jewell, Kelsea A / Lin, Wan-Jung / Connelly, James E / Ivancic, Melanie M / Tao, W Andy / Rajagopal, Lakshmi

Journal of proteome research

2009 Volume 8, Issue 5, Page(s) 2563–2574

Abstract: All living organisms respond to changes in their internal and external environment for their survival and existence. Signaling is primarily achieved through reversible phosphorylation of proteins in both prokaryotes and eukaryotes. A change in the ... ...

Abstract	All living organisms respond to changes in their internal and external environment for their survival and existence. Signaling is primarily achieved through reversible phosphorylation of proteins in both prokaryotes and eukaryotes. A change in the phosphorylation state of a protein alters its function to enable the control of cellular responses. A number of serine/threonine kinases regulate the cellular responses of eukaryotes. Although common in eukaryotes, serine/threonine kinases have only recently been identified in prokaryotes. We have described that the human pathogen Group B Streptococcus (GBS, Streptococcus agalactiae) encodes a single membrane-associated, serine/threonine kinase (Stk1) that is important for virulence of this bacterium. In this study, we used a combination of phosphopeptide enrichment and mass spectrometry to enrich and identify serine (S) and threonine (T) phosphopeptides of GBS. A comparison of S/T phosphopeptides identified from the Stk1 expressing strains to the isogenic stk1 mutant indicates that 10 proteins are potential substrates of the GBS Stk1 enzyme. Some of these proteins are phosphorylated by Stk1 in vitro and a site-directed substitution of the phosphorylated threonine to an alanine abolished phosphorylation of an Stk1 substrate. Collectively, these studies provide a novel approach to identify serine/threonine kinase substrates for insight into their signaling in human pathogens like GBS.
MeSH term(s)	Alanine/genetics ; Alanine/metabolism ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Binding Sites/genetics ; Chromatography, Liquid/methods ; Humans ; Mutagenesis, Site-Directed ; Mutation ; Phosphopeptides/analysis ; Phosphopeptides/isolation & purification ; Phosphopeptides/metabolism ; Phosphorylation ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Proteomics/methods ; Reproducibility of Results ; Streptococcus agalactiae/enzymology ; Streptococcus agalactiae/genetics ; Substrate Specificity ; Tandem Mass Spectrometry/methods ; Threonine/genetics ; Threonine/metabolism
Chemical Substances	Bacterial Proteins ; Phosphopeptides ; Threonine (2ZD004190S) ; Stk1 protein, Streptococcus agalactiae (EC 2.7.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Alanine (OF5P57N2ZX)
Language	English
Publishing date	2009-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2078618-9
ISSN	1535-3893
ISSN	1535-3893
DOI	10.1021/pr900069n
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Zs.A 6189: Show issues

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Article ; Online: The p53 transcription factor modulates microglia behavior through microRNA-dependent regulation of c-Maf.

Su, Wei / Hopkins, Stephanie / Nesser, Nicole K / Sopher, Bryce / Silvestroni, Aurelio / Ammanuel, Simon / Jayadev, Suman / Möller, Thomas / Weinstein, Jonathan / Garden, Gwenn A

Journal of immunology (Baltimore, Md. : 1950)

2013 Volume 192, Issue 1, Page(s) 358–366

Abstract: Neuroinflammation occurs in acute and chronic CNS injury, including stroke, traumatic brain injury, and neurodegenerative diseases. Microglia are specialized resident myeloid cells that mediate CNS innate immune responses. Disease-relevant stimuli, such ... ...

Abstract	Neuroinflammation occurs in acute and chronic CNS injury, including stroke, traumatic brain injury, and neurodegenerative diseases. Microglia are specialized resident myeloid cells that mediate CNS innate immune responses. Disease-relevant stimuli, such as reactive oxygen species (ROS), can influence microglia activation. Previously, we observed that p53, a ROS-responsive transcription factor, modulates microglia behaviors in vitro and in vivo, promoting proinflammatory functions and suppressing downregulation of the inflammatory response and tissue repair. In this article we describe a novel mechanism by which p53 modulates the functional differentiation of microglia both in vitro and in vivo. Adult microglia from p53-deficient mice have increased expression of the anti-inflammatory transcription factor c-Maf. To determine how p53 negatively regulates c-Maf, we examined the impact of p53 on known c-Maf regulators. MiR-155 is a microRNA that targets c-Maf. We observed that cytokine-induced expression of miR-155 was suppressed in p53-deficient microglia. Furthermore, Twist2, a transcriptional activator of c-Maf, is increased in p53-deficient microglia. We identified recognition sites in the 3' untranslated region of Twist2 mRNA that are predicted to interact with two p53-dependent microRNAs: miR-34a and miR-145. In this article, we demonstrate that miR-34a and -145 are regulated by p53 and negatively regulate Twist2 and c-Maf expression in microglia and the RAW macrophage cell line. Taken together, these findings support the hypothesis that p53 activation induced by local ROS or accumulated DNA damage influences microglia functions and that one specific molecular target of p53 in microglia is c-Maf.
MeSH term(s)	Animals ; Brain Ischemia/genetics ; Brain Ischemia/metabolism ; Cell Line ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Male ; Mice ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Microglia/metabolism ; Models, Biological ; Phenotype ; Proto-Oncogene Proteins c-maf/genetics ; Proto-Oncogene Proteins c-maf/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Twist-Related Protein 1/genetics ; Twist-Related Protein 1/metabolism
Chemical Substances	MicroRNAs ; Mirn155 microRNA, mouse ; Proto-Oncogene Proteins c-maf ; Repressor Proteins ; Tumor Suppressor Protein p53 ; Twist-Related Protein 1 ; Twist2 protein, mouse
Language	English
Publishing date	2013-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1301397
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: Characterization of the melA locus for alpha-galactosidase in Lactobacillus plantarum.

Silvestroni, Aurelio / Connes, Cristelle / Sesma, Fernando / De Giori, Graciela Savoy / Piard, Jean-Christophe

Applied and environmental microbiology

2002 Volume 68, Issue 11, Page(s) 5464–5471

Abstract: Alpha-galactosides are abundant sugars in legumes such as soy. Because of the lack of alpha-galactosidase (alpha-Gal) in the digestive tract, humans are unable to digest these sugars, which consequently induce flatulence. To develop the consumption of ... ...

Abstract	Alpha-galactosides are abundant sugars in legumes such as soy. Because of the lack of alpha-galactosidase (alpha-Gal) in the digestive tract, humans are unable to digest these sugars, which consequently induce flatulence. To develop the consumption of the otherwise highly nutritional soy products, the use of exogenous alpha-Gal is promising. In this framework, we characterized the melA gene for alpha-Gal in Lactobacillus plantarum. The melA gene encodes a cytoplasmic 84-kDa protein whose enzymatically active form occurs as oligomers. The melA gene was cloned and expressed in Escherichia coli, yielding an active alpha-Gal. We show that melA is transcribed from its own promoter, yielding a monocistronic mRNA, and that it is regulated at the transcriptional level, i.e., it is induced by melibiose but is not totally repressed by glucose. Posttranscriptional regulation by the carbon source could also occur. Upstream of melA, a putative galactoside transporter, designated RafP, was identified that shows high homology to LacS, the unique transporter for both alpha- and beta-galactosides in Streptococcus thermophilus. rafP is also expressed as a monocistronic mRNA. Downstream of melA, the lacL and lacM genes were identified that encode a heterodimeric beta-galactosidase. A putative galM gene identified in the same cluster suggests the presence of a galactose operon. These results indicate that the genes involved in galactoside catabolism are clustered in L. plantarum ATCC 8014. This first genetic characterization of melA and of its putative associated transporter, rafP, in a lactobacillus opens doors to various applications both in the manufacture of soy-derived products and in probiotic and nutraceutical issues.
MeSH term(s)	Amino Acid Sequence ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Base Sequence ; DNA, Bacterial/analysis ; Galactosides/metabolism ; Lactobacillus/enzymology ; Lactobacillus/genetics ; Lactobacillus/metabolism ; Molecular Sequence Data ; Multigene Family ; Raffinose/metabolism ; Sequence Homology, Amino Acid ; Symporters/genetics ; Symporters/metabolism ; Transcription, Genetic ; alpha-Galactosidase/genetics ; alpha-Galactosidase/metabolism ; beta-Galactosidase/genetics ; beta-Galactosidase/metabolism
Chemical Substances	Bacterial Proteins ; DNA, Bacterial ; Galactosides ; Symporters ; melibiose permease (9055-24-7) ; alpha-Galactosidase (EC 3.2.1.22) ; beta-Galactosidase (EC 3.2.1.23) ; Raffinose (N5O3QU595M)
Language	English
Publishing date	2002-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	223011-2
ISSN	1098-5336 ; 0099-2240
ISSN (online)	1098-5336
ISSN	0099-2240
DOI	10.1128/AEM.68.11.5464-5471.2002
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Article ; Online: Dysregulated miRNA biogenesis downstream of cellular stress and ALS-causing mutations: a new mechanism for ALS.

The EMBO journal

2015 Volume 34, Issue 21, Page(s) 2633–2651

Abstract: Interest in RNA dysfunction in amyotrophic lateral sclerosis (ALS) recently aroused upon discovering causative mutations in RNA-binding protein genes. Here, we show that extensive down-regulation of miRNA levels is a common molecular denominator for ... ...

Abstract	Interest in RNA dysfunction in amyotrophic lateral sclerosis (ALS) recently aroused upon discovering causative mutations in RNA-binding protein genes. Here, we show that extensive down-regulation of miRNA levels is a common molecular denominator for multiple forms of human ALS. We further demonstrate that pathogenic ALS-causing mutations are sufficient to inhibit miRNA biogenesis at the Dicing step. Abnormalities of the stress response are involved in the pathogenesis of neurodegeneration, including ALS. Accordingly, we describe a novel mechanism for modulating microRNA biogenesis under stress, involving stress granule formation and re-organization of DICER and AGO2 protein interactions with their partners. In line with this observation, enhancing DICER activity by a small molecule, enoxacin, is beneficial for neuromuscular function in two independent ALS mouse models. Characterizing miRNA biogenesis downstream of the stress response ties seemingly disparate pathways in neurodegeneration and further suggests that DICER and miRNAs affect neuronal integrity and are possible therapeutic targets.
MeSH term(s)	Amyotrophic Lateral Sclerosis/drug therapy ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/pathology ; Animals ; Base Sequence ; Cytoplasmic Granules/metabolism ; DEAD-box RNA Helicases/metabolism ; Down-Regulation ; Drug Evaluation, Preclinical ; Enoxacin/pharmacology ; Female ; HEK293 Cells ; Humans ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; Motor Neurons/metabolism ; RNA Interference ; RNA Processing, Post-Transcriptional ; Ribonuclease III/metabolism ; Stress, Physiological ; Superoxide Dismutase/genetics ; Superoxide Dismutase-1
Chemical Substances	MicroRNAs ; SOD1 protein, human ; Enoxacin (325OGW249P) ; Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1) ; DICER1 protein, human (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2015-09-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.201490493
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Article ; Online: Reduction of non-digestible oligosaccharides in soymilk: application of engineered lactic acid bacteria that produce alpha-galactosidase.

LeBlanc, Jean Guy / Silvestroni, Aurelio / Connes, Cristelle / Juillard, Vincent / de Giori, Graciela Savoy / Piard, Jean-Christophe / Sesma, Fernando

Genetics and molecular research : GMR

2004 Volume 3, Issue 3, Page(s) 432–440

Abstract: Human consumption of soy-derived products has been limited by the presence of non-digestible oligosaccharides (NDO), such as the alpha-galactooligosaccharides raffinose and stachyose. Most mammals, including man, lack pancreatic alpha-galactosidase ( ... ...

Abstract	Human consumption of soy-derived products has been limited by the presence of non-digestible oligosaccharides (NDO), such as the alpha-galactooligosaccharides raffinose and stachyose. Most mammals, including man, lack pancreatic alpha-galactosidase (alpha-Gal), which is necessary for the hydrolysis of these sugars. However, such NDO can be fermented by gas-producing microorganisms present in the cecum and large intestine, which in turn can induce flatulence and other gastrointestinal disorders in sensitive individuals. The use of microorganisms expressing alpha-Gal is a promising solution to the elimination of NDO before they reach the large intestine. In the present study, lactic acid bacteria engineered to degrade NDO have been constructed and are being used as a tool to evaluate this solution. The alpha-Gal structural genes from Lactobacillus plantarum ATCC8014 (previously characterized in our laboratory) and from guar have been cloned and expressed in Lactococcus lactis. The gene products were directed to different bacterial compartments to optimize their possible applications. The alpha-Gal-producing strains are being evaluated for their efficiency in degrading raffinose and stachyose: i) in soymilk fermentation when used as starters and ii) in situ in the upper gastrointestinal tract when administered to animals orally, as probiotic preparations. The expected outcomes and possible complications of this project are discussed.
MeSH term(s)	Animals ; Cultured Milk Products ; Digestion ; Fermentation ; Food, Genetically Modified ; Lactobacillus plantarum/growth & development ; Lactobacillus plantarum/metabolism ; Lactococcus lactis/growth & development ; Lactococcus lactis/metabolism ; Oligosaccharides/metabolism ; Probiotics ; Raffinose/metabolism ; Rodentia ; Soy Milk/chemistry ; alpha-Galactosidase/genetics ; alpha-Galactosidase/metabolism
Chemical Substances	Oligosaccharides ; stachyose (25VX64653N) ; alpha-Galactosidase (EC 3.2.1.22) ; Raffinose (N5O3QU595M)
Language	English
Publishing date	2004-09-30
Publishing country	Brazil
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2114039-X
ISSN	1676-5680 ; 1676-5680
ISSN (online)	1676-5680
ISSN	1676-5680
Database	MEDical Literature Analysis and Retrieval System OnLINE

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