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Article: The Role of Pseudo-Orthocaspase (SyOC) of

Lema A, Saul / Klemenčič, Marina / Völlmy, Franziska / Altelaar, Maarten / Funk, Christiane

2021 Volume 12, Page(s) 634366

Abstract: Caspases are proteases, best known for their involvement in the execution of apoptosis-a subtype of programmed cell death, which occurs only in animals. These proteases are composed of two structural building blocks: a proteolytically active p20 domain ... ...

Abstract	Caspases are proteases, best known for their involvement in the execution of apoptosis-a subtype of programmed cell death, which occurs only in animals. These proteases are composed of two structural building blocks: a proteolytically active p20 domain and a regulatory p10 domain. Although structural homologs appear in representatives of all other organisms, their functional homology, i.e., cell death depending on their proteolytical activity, is still much disputed. Additionally, pseudo-caspases and pseudo-metacaspases, in which the catalytic histidine-cysteine dyad is substituted with non-proteolytic amino acid residues, were shown to be involved in cell death programs. Here, we present the involvement of a pseudo-orthocaspase (SyOC), a prokaryotic caspase-homolog lacking the p10 domain, in oxidative stress in the model cyanobacterium
Language	English
Publishing date	2021-02-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2021.634366
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Article ; Online: Systemic LRG1 Expression in Melanoma is Associated with Disease Progression and Recurrence.

Hoefsmit, Esmee P / Völlmy, Franziska / Rozeman, Elisa A / Reijers, Irene L M / Versluis, Judith M / Hoekman, Liesbeth / van Akkooi, Alexander C J / Long, Georgina V / Schadendorf, Dirk / Dummer, Reinhard / Altelaar, Maarten / Blank, Christian U

Cancer research communications

2023 Volume 3, Issue 4, Page(s) 672–683

Abstract: The response rates upon neoadjuvant immune checkpoint blockade (ICB) in stage III melanoma are higher as compared with stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might ...

Abstract	The response rates upon neoadjuvant immune checkpoint blockade (ICB) in stage III melanoma are higher as compared with stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might be a mechanism responsible for lower response rates in late-stage disease, and also potentially with disease recurrence in early-stage disease. Plasma and serum samples of cohorts of patients with melanoma were analyzed for circulating proteins using mass spectrometry proteomic profiling and Olink proteomic assay. A cohort of paired samples of patients with stage III that progressed to stage IV disease ( Significance: LRG1 could serve as a potential target and as a biomarker to identify patients with high risk for disease recurrence, and consequently benefit from additional therapies and intensive follow-up.
MeSH term(s)	Humans ; Proteomics ; Disease Progression ; Prognosis ; Melanoma ; Biomarkers ; Glycoproteins
Chemical Substances	Biomarkers ; LRG1 protein, human ; Glycoproteins
Language	English
Publishing date	2023-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-23-0015
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Article ; Online: Farnesylated heat shock protein 40 is a component of membrane-bound RISC in

Sjögren, Lars / Floris, Maïna / Barghetti, Andrea / Völlmy, Franziska / Linding, Rune / Brodersen, Peter

The Journal of biological chemistry

2018 Volume 293, Issue 43, Page(s) 16608–16622

Abstract: ARGONAUTE1 (AGO1) binds directly to small regulatory RNA and is a key effector protein of post-transcriptional gene silencing mediated by microRNA (miRNA) and small interfering RNA (siRNA) ... ...

Abstract	ARGONAUTE1 (AGO1) binds directly to small regulatory RNA and is a key effector protein of post-transcriptional gene silencing mediated by microRNA (miRNA) and small interfering RNA (siRNA) in
MeSH term(s)	Arabidopsis/genetics ; Arabidopsis/metabolism ; Arabidopsis Proteins/genetics ; Arabidopsis Proteins/metabolism ; Argonaute Proteins/genetics ; Argonaute Proteins/metabolism ; HSP40 Heat-Shock Proteins/genetics ; HSP40 Heat-Shock Proteins/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Prenylation ; RNA, Plant/genetics ; RNA, Plant/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; RNA-Induced Silencing Complex/genetics ; RNA-Induced Silencing Complex/metabolism
Chemical Substances	Arabidopsis Proteins ; Argonaute Proteins ; HSP40 Heat-Shock Proteins ; MicroRNAs ; RNA, Plant ; RNA, Small Interfering ; RNA-Induced Silencing Complex
Language	English
Publishing date	2018-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA118.003887
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Article ; Online: The Q-junction and the inflammatory response are critical pathological and therapeutic factors in CoQ deficiency.

González-García, Pilar / Díaz-Casado, María Elena / Hidalgo-Gutiérrez, Agustín / Jiménez-Sánchez, Laura / Bakkali, Mohammed / Barriocanal-Casado, Eliana / Escames, Germaine / Chiozzi, Riccardo Zenezini / Völlmy, Franziska / Zaal, Esther A / Berkers, Celia R / Heck, Albert J R / López, Luis C

Redox biology

2022 Volume 55, Page(s) 102403

Abstract: Defects in Coenzyme Q (CoQ) metabolism have been associated with primary mitochondrial disorders, neurodegenerative diseases and metabolic conditions. The consequences of CoQ deficiency have not been fully addressed, and effective treatment remains ... ...

Abstract	Defects in Coenzyme Q (CoQ) metabolism have been associated with primary mitochondrial disorders, neurodegenerative diseases and metabolic conditions. The consequences of CoQ deficiency have not been fully addressed, and effective treatment remains challenging. Here, we use mice with primary CoQ deficiency (Coq9
Language	English
Publishing date	2022-07-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102403
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Article ; Online: NODAL/TGFβ signalling mediates the self-sustained stemness induced by PIK3CAH1047R homozygosity in pluripotent stem cells.

Madsen, Ralitsa R / Longden, James / Knox, Rachel G / Robin, Xavier / Völlmy, Franziska / Macleod, Kenneth G / Moniz, Larissa S / Carragher, Neil O / Linding, Rune / Vanhaesebroeck, Bart / Semple, Robert K

Disease models & mechanisms

2021 Volume 14, Issue 3

Abstract: Activating PIK3CA mutations are known 'drivers' of human cancer and developmental overgrowth syndromes. We recently demonstrated that the 'hotspot' PIK3CAH1047R variant exerts unexpected allele dose-dependent effects on stemness in human pluripotent stem ...

Abstract	Activating PIK3CA mutations are known 'drivers' of human cancer and developmental overgrowth syndromes. We recently demonstrated that the 'hotspot' PIK3CAH1047R variant exerts unexpected allele dose-dependent effects on stemness in human pluripotent stem cells (hPSCs). In this study, we combine high-depth transcriptomics, total proteomics and reverse-phase protein arrays to reveal potentially disease-related alterations in heterozygous cells, and to assess the contribution of activated TGFβ signalling to the stemness phenotype of homozygous PIK3CAH1047R cells. We demonstrate signalling rewiring as a function of oncogenic PI3K signalling strength, and provide experimental evidence that self-sustained stemness is causally related to enhanced autocrine NODAL/TGFβ signalling. A significant transcriptomic signature of TGFβ pathway activation in heterozygous PIK3CAH1047R was observed but was modest and was not associated with the stemness phenotype seen in homozygous mutants. Notably, the stemness gene expression in homozygous PIK3CAH1047R hPSCs was reversed by pharmacological inhibition of NODAL/TGFβ signalling, but not by pharmacological PI3Kα pathway inhibition. Altogether, this provides the first in-depth analysis of PI3K signalling in hPSCs and directly links strong PI3K activation to developmental NODAL/TGFβ signalling. This work illustrates the importance of allele dosage and expression when artificial systems are used to model human genetic disease caused by activating PIK3CA mutations. This article has an associated First Person interview with the first author of the paper.
MeSH term(s)	Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Humans ; Mutation/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Pluripotent Stem Cells/metabolism ; Signal Transduction ; Transforming Growth Factor beta
Chemical Substances	Transforming Growth Factor beta ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137)
Language	English
Publishing date	2021-03-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.048298
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Article ; Online: The Q-junction and the inflammatory response are critical pathological and therapeutic factors in CoQ deficiency

Pilar González-García / María Elena Díaz-Casado / Agustín Hidalgo-Gutiérrez / Laura Jiménez-Sánchez / Mohammed Bakkali / Eliana Barriocanal-Casado / Germaine Escames / Riccardo Zenezini Chiozzi / Franziska Völlmy / Esther A. Zaal / Celia R. Berkers / Albert J.R. Heck / Luis C. López

Redox Biology, Vol 55, Iss , Pp 102403- (2022)

2022

Abstract	Defects in Coenzyme Q (CoQ) metabolism have been associated with primary mitochondrial disorders, neurodegenerative diseases and metabolic conditions. The consequences of CoQ deficiency have not been fully addressed, and effective treatment remains challenging. Here, we use mice with primary CoQ deficiency (Coq9R239X), and we demonstrate that CoQ deficiency profoundly alters the Q-junction, leading to extensive changes in the mitochondrial proteome and metabolism in the kidneys and, to a lesser extent, in the brain. CoQ deficiency also induces reactive gliosis, which mediates a neuroinflammatory response, both of which lead to an encephalopathic phenotype. Importantly, treatment with either vanillic acid (VA) or β-resorcylic acid (β-RA), two analogs of the natural precursor for CoQ biosynthesis, partially restores CoQ metabolism, particularly in the kidneys, and induces profound normalization of the mitochondrial proteome and metabolism, ultimately leading to reductions in gliosis, neuroinflammation and spongiosis and, consequently, reversing the phenotype. Together, these results provide key mechanistic insights into defects in CoQ metabolism and identify potential disease biomarkers. Furthermore, our findings clearly indicate that the use of analogs of the CoQ biosynthetic precursor is a promising alternative therapy for primary CoQ deficiency and has potential for use in the treatment of more common neurodegenerative and metabolic diseases that are associated with secondary CoQ deficiency.
Keywords	Coenzyme Q ; Mitochondrial disease ; Therapy ; Omics ; Phenolic compound ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Into the Dark Serum Proteome: Personalized Features of IgG1 and IgA1 Repertoires in Severe COVID-19 Patients.

Bondt, Albert / Hoek, Max / Dingess, Kelly / Tamara, Sem / de Graaf, Bastiaan / Peng, Weiwei / den Boer, Maurits A / Damen, Mirjam / Zwart, Ceri / Barendregt, Arjan / van Rijswijck, Danique M H / Schulte, Douwe / Grobben, Marloes / Tejjani, Khadija / van Rijswijk, Jacqueline / Völlmy, Franziska / Snijder, Joost / Fortini, Francesca / Papi, Alberto /

Volta, Carlo Alberto / Campo, Gianluca / Contoli, Marco / van Gils, Marit J / Spadaro, Savino / Rizzo, Paola / Heck, Albert J R

Molecular & cellular proteomics : MCP

2023 Volume 23, Issue 1, Page(s) 100690

Abstract: Serum proteomics has matured and is now able to monitor hundreds of proteins quantitatively in large cohorts of patients. However, the fine characteristics of some of the most dominant proteins in serum, the immunoglobulins, are in these studies often ... ...

Abstract	Serum proteomics has matured and is now able to monitor hundreds of proteins quantitatively in large cohorts of patients. However, the fine characteristics of some of the most dominant proteins in serum, the immunoglobulins, are in these studies often ignored, due to their vast, and highly personalized, diversity in sequences. Here, we focus exclusively on these personalized features in the serum proteome and distinctively chose to study individual samples from a low diversity population: elderly donors infected by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). By using mass spectrometry-based methods, immunoglobulin IgG1 and IgA1 clonal repertoires were monitored quantitatively and longitudinally in more than 50 individual serum samples obtained from 17 Corona virus disease 2019 patients admitted to intensive care units. These clonal profiles were used to examine how each patient reacted to a severe SARS-CoV-2 infection. All 17 donors revealed unique polyclonal repertoires and substantial changes over time, with several new clones appearing following the infection, in a few cases leading to a few, very high, abundant clones dominating their repertoire. Several of these clones were de novo sequenced through combinations of top-down, middle-down, and bottom-up proteomics approaches. This revealed sequence features in line with sequences deposited in the SARS-CoV-specific antibody database. In other patients, the serological Ig profiles revealed the treatment with tocilizumab, that subsequently dominated their serological IgG1 repertoire. Tocilizumab clearance could be monitored, and a half-life of approximately 6 days was established. Overall, our longitudinal monitoring of IgG1 and IgA1 repertoires of individual donors reveals that antibody responses are highly personalized traits of each patient, affected by the disease and the chosen clinical treatment. The impact of these observations argues for a more personalized and longitudinal approach in patients' diagnostics, both in serum proteomics as well as in monitoring immune responses.
MeSH term(s)	Humans ; Aged ; COVID-19 ; SARS-CoV-2 ; Proteome ; Immunoglobulin G ; Immunoglobulin A ; Antibodies, Viral
Chemical Substances	Proteome ; Immunoglobulin G ; Immunoglobulin A ; Antibodies, Viral
Language	English
Publishing date	2023-12-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2075924-1
ISSN	1535-9484 ; 1535-9476
ISSN (online)	1535-9484
ISSN	1535-9476
DOI	10.1016/j.mcpro.2023.100690
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Article ; Online: NODAL/TGFβ signalling mediates the self-sustained stemness induced by PIK3CAH1047R homozygosity in pluripotent stem cells

Ralitsa R. Madsen / James Longden / Rachel G. Knox / Xavier Robin / Franziska Völlmy / Kenneth G. Macleod / Larissa S. Moniz / Neil O. Carragher / Rune Linding / Bart Vanhaesebroeck / Robert K. Semple

Disease Models & Mechanisms, Vol 14, Iss

2021 Volume 3

Abstract: Activating PIK3CA mutations are known ‘drivers’ of human cancer and developmental overgrowth syndromes. We recently demonstrated that the ‘hotspot’ PIK3CAH1047R variant exerts unexpected allele dose-dependent effects on stemness in human pluripotent stem ...

Abstract	Activating PIK3CA mutations are known ‘drivers’ of human cancer and developmental overgrowth syndromes. We recently demonstrated that the ‘hotspot’ PIK3CAH1047R variant exerts unexpected allele dose-dependent effects on stemness in human pluripotent stem cells (hPSCs). In this study, we combine high-depth transcriptomics, total proteomics and reverse-phase protein arrays to reveal potentially disease-related alterations in heterozygous cells, and to assess the contribution of activated TGFβ signalling to the stemness phenotype of homozygous PIK3CAH1047R cells. We demonstrate signalling rewiring as a function of oncogenic PI3K signalling strength, and provide experimental evidence that self-sustained stemness is causally related to enhanced autocrine NODAL/TGFβ signalling. A significant transcriptomic signature of TGFβ pathway activation in heterozygous PIK3CAH1047R was observed but was modest and was not associated with the stemness phenotype seen in homozygous mutants. Notably, the stemness gene expression in homozygous PIK3CAH1047R hPSCs was reversed by pharmacological inhibition of NODAL/TGFβ signalling, but not by pharmacological PI3Kα pathway inhibition. Altogether, this provides the first in-depth analysis of PI3K signalling in hPSCs and directly links strong PI3K activation to developmental NODAL/TGFβ signalling. This work illustrates the importance of allele dosage and expression when artificial systems are used to model human genetic disease caused by activating PIK3CA mutations. This article has an associated First Person interview with the first author of the paper.
Keywords	pi3k ; pik3ca ; stemness ; pluripotent stem cells ; Medicine ; R ; Pathology ; RB1-214
Subject code	570
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
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Article ; Online: A serum proteome signature to predict mortality in severe COVID-19 patients.

Völlmy, Franziska / van den Toorn, Henk / Zenezini Chiozzi, Riccardo / Zucchetti, Ottavio / Papi, Alberto / Volta, Carlo Alberto / Marracino, Luisa / Vieceli Dalla Sega, Francesco / Fortini, Francesca / Demichev, Vadim / Tober-Lau, Pinkus / Campo, Gianluca / Contoli, Marco / Ralser, Markus / Kurth, Florian / Spadaro, Savino / Rizzo, Paola / Heck, Albert Jr

Life science alliance

2021 Volume 4, Issue 9

Abstract: Here, we recorded serum proteome profiles of 33 severe COVID-19 patients admitted to respiratory and intensive care units because of respiratory failure. We received, for most patients, blood samples just after admission and at two more later time points. ...

Abstract	Here, we recorded serum proteome profiles of 33 severe COVID-19 patients admitted to respiratory and intensive care units because of respiratory failure. We received, for most patients, blood samples just after admission and at two more later time points. With the aim to predict treatment outcome, we focused on serum proteins different in abundance between the group of survivors and non-survivors. We observed that a small panel of about a dozen proteins were significantly different in abundance between these two groups. The four structurally and functionally related type-3 cystatins AHSG, FETUB, histidine-rich glycoprotein, and KNG1 were all more abundant in the survivors. The family of inter-α-trypsin inhibitors, ITIH1, ITIH2, ITIH3, and ITIH4, were all found to be differentially abundant in between survivors and non-survivors, whereby ITIH1 and ITIH2 were more abundant in the survivor group and ITIH3 and ITIH4 more abundant in the non-survivors. ITIH1/ITIH2 and ITIH3/ITIH4 also showed opposite trends in protein abundance during disease progression. We defined an optimal panel of nine proteins for mortality risk assessment. The prediction power of this mortality risk panel was evaluated against two recent COVID-19 serum proteomics studies on independent cohorts measured in other laboratories in different countries and observed to perform very well in predicting mortality also in these cohorts. This panel may not be unique for COVID-19 as some of the proteins in the panel have previously been annotated as mortality markers in aging and in other diseases caused by different pathogens, including bacteria.
MeSH term(s)	Aged ; COVID-19/blood ; COVID-19/mortality ; COVID-19/virology ; Cohort Studies ; Female ; Hospitalization ; Humans ; Immunoglobulins/blood ; Male ; Proteome/metabolism ; SARS-CoV-2/physiology ; Severity of Illness Index ; Survivors
Chemical Substances	Immunoglobulins ; Proteome
Language	English
Publishing date	2021-07-05
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.202101099
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