LIVIVO - Search results -

Search results

Result 1 - 10 of total 1246

Search options

Article ; Online: Leptin prevents aberrant targeting of tau to hippocampal synapses via PI 3 kinase driven inhibition of GSK3β.

Hamilton, Kirsty / Morrow, Kate / Markantoni, Ermione / Harvey, Jenni

2023 Volume 167, Issue 4, Page(s) 520–537

Abstract: Amyloid-β (Aβ) and hyper-phosphorylated tau are key hallmarks of Alzheimer's disease (AD), with an accumulation of both proteins linked to hippocampal synaptic dysfunction. Recent evidence indicates that Aβ drives mis-localisation of tau from axons to ... ...

Abstract	Amyloid-β (Aβ) and hyper-phosphorylated tau are key hallmarks of Alzheimer's disease (AD), with an accumulation of both proteins linked to hippocampal synaptic dysfunction. Recent evidence indicates that Aβ drives mis-localisation of tau from axons to synapses, resulting in AMPA receptor (AMPAR) internalisation and impaired excitatory synaptic function. These tau-driven synaptic impairments are thought to underlie the cognitive deficits in AD. Consequently, limiting the synapto-toxic effects of tau may prevent AD-related cognitive deficits. Increasing evidence links leptin dysfunction with higher AD risk, and numerous studies have identified neuroprotective properties of leptin in AD models of Aβ-induced toxicity. However, it is unclear if leptin protects against tau-related synaptic dysfunction. Here we show that Aβ
MeSH term(s)	Humans ; Glycogen Synthase Kinase 3 beta/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Leptin/pharmacology ; Alzheimer Disease/metabolism ; Synapses/metabolism ; Amyloid beta-Peptides/metabolism ; Hippocampus/metabolism ; Phosphorylation ; tau Proteins/metabolism
Chemical Substances	Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Leptin ; Amyloid beta-Peptides ; tau Proteins
Language	English
Publishing date	2023-10-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15980
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ui II Zs.170: 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)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Book ; Thesis: Bedeutung der katalytischen PI-3-Kinase Untereinheit p110delta für Wachstumsfaktor-induzierte zelluläre Reaktionen von pulmonal arteriellen glatten Gefäßmuskelzellen und Hypoxie-induzierte pulmonale Hypertonie

Skoruppa, Christopher / Rosenkranz, Stephan / Pfitzer, Gabriele

2021

Institution	Universitätsklinikum Köln / Klinik und Poliklinik für Kardiologie, Pneumologie, Angiologie und Internistische Intensivmedizin
Author's details	vorgelegt von Christopher Skoruppa ; 1. Gutachter: Universitätsprofessor Dr. med. S.H. Rosenkranz, 2. Gutachterin: Universitätsprofessorin Dr. med. G. Pfitzer ; aus dem Herzzentrum der Universität zu Köln, Klinik und Poliklinik für Innere Medizin III
Subject code	610
Language	German
Size	86 Seiten, Illustrationen, Deagramme
Publishing place	Köln
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Dissertation, Universität zu Köln, 2020
HBZ-ID	HT020870803
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
2021 D 173	order for loan	Magazin

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Book ; Thesis: Bedeutung der PI 3-Kinase Untereinheit p110[alpha] für die Neointimaformation nach Ballonangioplastie

Moreira Jesus Adler, Joana Frazão Faria

2017

Author's details	vorgelegt von Joana Frazão Faria Moreira Jesus Adler
Language	German
Size	70 Seiten, Illustrationen, Diagramme
Publishing place	Köln
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Dissertation, Universität zu Köln, 2017
HBZ-ID	HT019493658
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
2017 D 1169	order for loan	Magazin

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Serum Beta-Defensin-2 is a biomarker for psoriasis but not subclinical atherosclerosis: Role of IL17a, PI-3 kinase and Rac1.

Pantoja, C J / Li, H / Rodante, J / Keel, A / Sorokin, A V / Svedbom, A / Teague, H L / Stahle, M / Mehta, N N / Playford, M P

JEADV clinical practice

2023 Volume 3, Issue 1, Page(s) 150–159

Abstract: ... kinase (PI3-kinase) and Rac1 GTPase-dependent manner.: Conclusions: Our findings expand ... kinase/Rac signaling axis in regulating BD2 levels in keratinocytes. ... observed. Furthermore, we demonstrate that IL-17A-driven BD2 expression occurs in a Phosphatidylinositol 3 ...

Abstract	Background: Beta-defensins (BDs) are antimicrobial peptides secreted upon epithelial injury. Both chemotactic and antimicrobial properties of BDs function as initial steps in host defense and prime the adaptive immune system in the body. Psoriasis, a chronic immune-mediated inflammatory disease, has both visible cutaneous manifestations as well as known associations with higher incidence of cardiometabolic complications and vascular inflammation. Objectives: We aimed to investigate the circulating expression of beta-defensin-2 (BD2) in psoriasis at baseline compared to control subjects, along with changes in BD2 levels following biologic treatment at one-year. The contribution of BD2 to subclinical atherosclerosis is also assessed. In addition, we have sought to unravel signaling mechanisms linking inflammation with BD2 expression. Methods: Multimodality imaging as well inflammatory biomarker assays were performed in biologic naïve psoriasis (n=71) and non-psoriasis (n=53) subjects. A subset of psoriasis patients were followed for one-year after biological intervention (anti-Tumor Necrosis Factor-α (TNFα), n=30; anti-Interleukin17A (IL17A), n=21). Measurements of circulating BD2 were completed by Enzyme-Linked Immunosorbent Assay (ELISA). Using HaCaT transformed keratinocytes, expression of BD2 upon cytokine treatment was assessed by quantitative polymerase chain reaction (qPCR) and ELISA. Results: Herein, we confirm that human circulating BD2 levels associate with psoriasis, which attenuate upon biologic interventions (anti-TNFα, anti-IL-17A). A link between circulating BD2 and sub-clinical atherosclerosis markers was not observed. Furthermore, we demonstrate that IL-17A-driven BD2 expression occurs in a Phosphatidylinositol 3-kinase (PI3-kinase) and Rac1 GTPase-dependent manner. Conclusions: Our findings expand on the potential role of BD2 as a tractable biomarker in psoriasis patients and describes the role of an IL-17A-PI3-kinase/Rac signaling axis in regulating BD2 levels in keratinocytes.
Language	English
Publishing date	2023-10-27
Publishing country	England
Document type	Journal Article
ISSN	2768-6566
ISSN (online)	2768-6566
DOI	10.1002/jvc2.278
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Receptor tyrosine kinase-Ras-PI 3 kinase-Akt signaling network in glioblastoma multiforme.

Tuncel, Gulten / Kalkan, Rasime

Medical oncology (Northwood, London, England)

2018 Volume 35, Issue 9, Page(s) 122

Abstract: ... Ras-PI 3 kinase-Akt signaling network, focusing on the potential molecular targets for anti-signaling ... approaches in designing novel therapies for GBM. In this review, we summarize the receptor tyrosine kinase ...

Abstract	Glioblastoma multiforme (GBM) is the most malignant form of the brain tumors and shows different genetic and epigenetic abnormalities. Gene amplification, genetic instability, disruption of apoptotic pathways, deregulated oncogene expression, invasive phenotypical changes, abnormal angiogenesis, and epigenetic changes have all been described in GBMs. These abnormalities indicate that a number of different signaling pathways are deregulated in GBM. Increasing number of studies provide a better understanding of the tumor biology, genetic, and epigenetic background of the GBM. Also, current research provides us useful approaches in designing novel therapies for GBM. In this review, we summarize the receptor tyrosine kinase-Ras-PI 3 kinase-Akt signaling network, focusing on the potential molecular targets for anti-signaling molecular therapies in this pathway.
MeSH term(s)	Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor Protein-Tyrosine Kinases/metabolism ; Signal Transduction/physiology ; ras Proteins/metabolism
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2018-08-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1201189-7
ISSN	1559-131X ; 0736-0118 ; 1357-0560
ISSN (online)	1559-131X
ISSN	0736-0118 ; 1357-0560
DOI	10.1007/s12032-018-1185-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1899: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: PI(3,5)P

Sun, Jiachen / Song, Seohyeon / Singaram, Indira / Sharma, Ashutosh / Wang, Wei / Hu, Yusi / Lo, Wen-Ting / Koch, Philipp Alexander / Zhao, Jean J / Haucke, Volker / Gao, Ruixuan / Cho, Wonhwa

bioRxiv : the preprint server for biology

2023

Abstract: ... Among 3'-phosphoinositides, phosphatidylinositol-3,5-bisphosphate (PI(3,5)P ... kinases (PI3K) but the mechanisms underlying their regulation and cross-talk are not fully understood ... and disease. Generation of 3'-phosphoinositides are driven by three families of phosphoinositide 3 ...

Abstract	3'-Phosphoinositides are ubiquitous cellular lipids that play pivotal regulatory roles in health and disease. Generation of 3'-phosphoinositides are driven by three families of phosphoinositide 3-kinases (PI3K) but the mechanisms underlying their regulation and cross-talk are not fully understood. Among 3'-phosphoinositides, phosphatidylinositol-3,5-bisphosphate (PI(3,5)P
Language	English
Publishing date	2023-01-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.25.525550
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: PI(4,5)P

Davies, Elizabeth M / Gurung, Rajendra / Le, Kai Qin / Roan, Katherine T T / Harvey, Richard P / Mitchell, Geraldine M / Schwarz, Quenten / Mitchell, Christina A

Science advances

2023 Volume 9, Issue 13, Page(s) eadd6911

Abstract: ... signaling, is essential for angiogenesis. VEGFR2 activates PI3K, which phosphorylates PI(4,5)P ...

Abstract	Dynamic positioning of endothelial tip and stalk cells, via the interplay between VEGFR2 and NOTCH signaling, is essential for angiogenesis. VEGFR2 activates PI3K, which phosphorylates PI(4,5)P
MeSH term(s)	Animals ; Mice ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Endothelial Cells/metabolism ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Neovascularization, Physiologic/genetics ; Membrane Proteins/metabolism ; RNA, Small Interfering/metabolism ; Receptors, Notch/genetics ; Receptors, Notch/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; beta Catenin ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Calcium-Binding Proteins ; Membrane Proteins ; RNA, Small Interfering ; Receptors, Notch
Language	English
Publishing date	2023-03-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.add6911
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: PI 3-Kinase and the Histone Methyl-Transferase KMT2D Collaborate to Induce Arp2/3-Dependent Migration of Mammary Epithelial Cells.

Rysenkova, Karina D / Gaboriaud, Julia / Fokin, Artem I / Toubiana, Raphaëlle / Bense, Alexandre / Mirdass, Camil / Jin, Mélissa / Ho, Minh Chau N / Glading, Elizabeth / Vacher, Sophie / Courtois, Laura / Bièche, Ivan / Gautreau, Alexis M

Cells

2024 Volume 13, Issue 10

Abstract: ... to reconstitute this process in a particular case. To this end, we combined the activated form of the PI 3-kinase ... in the non-tumorigenic human mammary epithelial cell line MCF10A. We found that PI 3-kinase activation ... in synergy with PI 3-kinase activation. The combination of these two genetic alterations induced expression of the ...

Abstract	Breast cancer develops upon sequential acquisition of driver mutations in mammary epithelial cells; however, how these mutations collaborate to transform normal cells remains unclear in most cases. We aimed to reconstitute this process in a particular case. To this end, we combined the activated form of the PI 3-kinase harboring the H1047R mutation with the inactivation of the histone lysine methyl-transferase KMT2D in the non-tumorigenic human mammary epithelial cell line MCF10A. We found that PI 3-kinase activation promoted cell-cycle progression, especially when growth signals were limiting, as well as cell migration, both in a collective monolayer and as single cells. Furthermore, we showed that KMT2D inactivation had relatively little influence on these processes, except for single-cell migration, which KMT2D inactivation promoted in synergy with PI 3-kinase activation. The combination of these two genetic alterations induced expression of the
MeSH term(s)	Humans ; Cell Movement/genetics ; Epithelial Cells/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Histone-Lysine N-Methyltransferase/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Actin-Related Protein 2-3 Complex/metabolism ; Actin-Related Protein 2-3 Complex/genetics ; Female ; Mammary Glands, Human/metabolism ; Mammary Glands, Human/cytology ; DNA-Binding Proteins/metabolism ; DNA-Binding Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasm Proteins/genetics ; Mutation/genetics ; Cell Line
Chemical Substances	KMT2D protein, human ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Actin-Related Protein 2-3 Complex ; DNA-Binding Proteins ; Neoplasm Proteins
Language	English
Publishing date	2024-05-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13100876
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The second PI(3,5)P

Biological chemistry

2023 Volume 404, Issue 4, Page(s) 241–254

Abstract: The Phosphatidylinositol 3-phosphate 5-kinase Type III PIKfyve is the main source for selectively ... generated phosphatidylinositol 3,5-bisphosphate (PI(3,5)P ...

Abstract	The Phosphatidylinositol 3-phosphate 5-kinase Type III PIKfyve is the main source for selectively generated phosphatidylinositol 3,5-bisphosphate (PI(3,5)P
MeSH term(s)	Phosphatidylinositol 4,5-Diphosphate/chemistry ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; KCNQ1 Potassium Channel/chemistry ; KCNQ1 Potassium Channel/genetics ; KCNQ1 Potassium Channel/metabolism ; Binding Sites ; Mutation ; Cell Membrane/metabolism
Chemical Substances	Phosphatidylinositol 4,5-Diphosphate ; KCNQ1 Potassium Channel
Language	English
Publishing date	2023-02-23
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1334659-3
ISSN	1437-4315 ; 1431-6730 ; 1432-0355
ISSN (online)	1437-4315
ISSN	1431-6730 ; 1432-0355
DOI	10.1515/hsz-2022-0247
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.50: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The WW domain of IQGAP1 binds directly to the p110α catalytic subunit of PI 3-kinase.

Bardwell, A Jane / Paul, Madhuri / Yoneda, Kiku C / Andrade-Ludeña, María D / Nguyen, Oanh T / Fruman, David / Bardwell, Lee

The Biochemical journal

2023

Abstract: ... directly to the p110α catalytic subunit of phosphoinositide 3-kinase (PI3K). In contrast, the WW domain ...

Abstract	IQGAP1 is a multi-domain cancer-associated protein that serves as a scaffold protein for multiple signaling pathways. Numerous binding partners have been found for the calponin homology, IQ and GAP-related domains in IQGAP1. Identification of a binding partner for its WW domain has proven elusive, however, even though a cell-penetrating peptide derived from this domain has marked anti-tumor activity. Here, using in vitro binding assays with human proteins and co-precipitation from human cells, we show that the WW domain of human IQGAP1 binds directly to the p110α catalytic subunit of phosphoinositide 3-kinase (PI3K). In contrast, the WW domain does not bind to ERK1/2, MEK1/2, or the p85α regulatory subunit of PI3K when p85α is expressed alone. However, the WW domain is able to bind to the p110α/p85α heterodimer when both subunits are co-expressed, as well as to the mutationally activated p110α/p65α heterodimer. We present a model of the structure of the IQGAP1 WW domain, and experimentally identify key residues in the hydrophobic core and beta strands of the WW domain that are required for binding to p110α. These findings contribute to a more precise understanding of IQGAP1-mediated scaffolding, and of how IQGAP1-derived therapeutic peptides might inhibit tumorigenesis.
Language	English
Publishing date	2023-05-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20220493
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.110: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito